tag:blogger.com,1999:blog-33935095041801562972024-03-19T14:14:51.545-07:00SUHASIS ONLINEMy Study and ResearchAnonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.comBlogger19125tag:blogger.com,1999:blog-3393509504180156297.post-16521594585441732962012-07-31T14:05:00.000-07:002012-07-31T14:34:44.149-07:00Dead Man Returns: The Lazarus Phenomenon ( A second chance)<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="background-color: black; color: #bf9000;"><span style="font-family: 'Eras Demi ITC', sans-serif;">First,
you receive a phone call from the hospital. The officials reveal to you that
your loved one has been pronounced dead. What would your reaction be if 2 hours
later, the doctor calls you again to tell you that your loved one back alive?
Puzzled? Numb? Going to get a second doctor’s opinion whether your loved one is
really alive or dead by checking the name once again? Simply overjoyed? Call
the doctor again and ask him to use a different stethoscope? Or maybe, call all
your friends and relatives to have a “Welcome back, party?”</span><span style="font-family: 'Eras Demi ITC', sans-serif; font-size: 11pt; line-height: 115%;">.....Well, a series of perplexed thoughts are
sure to run wild in our thoughts if this happens to our families. Of course,
the variations, your heart beat rate and the intensity differs from
individuals.</span><span class="apple-converted-space"><span style="font-family: Georgia, serif; font-size: 8pt; line-height: 115%;"> </span></span></span></div>
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<span style="background-color: black; color: #bf9000;"><span style="font-family: 'Eras Demi ITC', sans-serif;">Imagine
the joy, of having to call out your relatives and friends again to notify that
your loved dead is back from the dead. As for their reaction, your guess is as
good as mine. After all, some would still want to see him/her and pat on the
back and may want to say, “Hey, your lifeline has just been renewed and
extended for an indefinite period of time, don't screw up your life and health
with your second chance.”</span><o:p></o:p></span></div>
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<span style="background-color: black; color: #bf9000; font-family: 'Eras Demi ITC', sans-serif;">...It’s called the
Lazarus Phenomenon (sometimes called Lazarus syndrome) , and goes to prove what
a fantastic machine the human body really is.</span></div>
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<h2 style="text-align: left;">
<span class="apple-converted-space"><span style="background-color: black; font-family: 'Eras Demi ITC', sans-serif; line-height: 115%;"><span style="color: magenta; font-size: x-large;">What is Lazarus Phenomenon?</span></span></span></h2>
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<span style="background-color: black; color: #bf9000;"><span style="font-family: 'Eras Demi ITC', sans-serif;">The Lazarus phenomenon is described as delayed “Return Of
Spontaneous Circulation” (ROSC) after cessation of cardiopulmonary
resuscitation (CPR). This was first reported in the medical literature in 1982</span>,
and the term Lazarus phenomenon was first used by Bray in 1993. The term
was coined from the story of Lazarus, who was resurrected by Jesus Christ
four days after his death.<o:p></o:p></span></div>
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<span style="background-color: black; color: #bf9000; font-family: 'Eras Demi ITC', sans-serif;">Even though Lazarus phenomenon is rare, it is probably
under reported. There is no doubt that Lazarus phenomenon is a reality but so
far the scientific explanations have been inadequate. So far the only plausible
explanation at least in some cases is auto-positive end-expiratory pressure
(PEEP) and impaired venous return. In patients with pulseless electrical
activity (PEA) or asystole, dynamic hyperinflation should be considered as a
cause and a short period of apnoea (30-60 seconds) should be tried before
stopping resuscitation. Since ROSC occurred within 10 minutes in most cases,
patients should be passively monitored for at least 10 minutes after the cessation
of CPR before confirming death.</span><o:p></o:p></div>
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<h2 style="text-align: left;">
<b><span style="background-color: black; color: magenta; font-size: x-large;">Case Report</span></b></h2>
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<span style="background-color: black; color: #bf9000;">A 66-yr-old man, weighing 80 kg, was emergently brought to the operating
room (OR) with a suspected leaking abdominal aortic aneurysm. His past history
included hypertension and a transient ischemic attack 4 yr earlier. He also had
a 50-pack/yr smoking history and chronic renal insufficiency (creatinine 2.3
mg/dL). He had no history of metabolic disorder. He had received 2600 mL of
lactated Ringer’s solution before arrival in the OR. Vital signs on arrival included
a heart rate of 120 bpm and a systolic blood pressure of 60 mm Hg. The patient
was pale, mottled, diaphoretic, and tachypneic. Rapid administration of warmed
IV fluids via two rapid infusion systems increased his systolic blood pressure
to 120 mm Hg.<o:p></o:p></span></div>
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<span style="background-color: black; color: #bf9000;">Induction of anaesthesia
proceeded uneventfully with d-tubocurarine 3 mg, fentanyl 250 <span style="font-family: 'Lucida Sans Unicode', sans-serif;">μ</span>g, etomidate 20 mg, and succinylcholine 160 mg IV before rapid sequence
endotracheal intubation. Maintenance of anesthesia included inhalation of
isoflurane (as tolerated by blood pressure) in 100% oxygen. Pancuronium 6 mg
was given for continued neuromuscular blockade. With induction of anesthesia,
the vital signs remained stable (systolic blood pressure 110–120 mm Hg by
automated cuff pressure) and surgical incision promptly followed at 5.30 p.m.
An arterial blood gas drawn at this time revealed hemoglobin 8.1 g/dL, K<sup><span style="border: 1pt none windowtext; padding: 0cm;">+</span></sup> 3.8 mEq/L, glucose 185 mg/dL, pHa 7.24, Pa<span style="text-transform: uppercase;">CO</span><sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub> 41 mm Hg,
Pa<span style="text-transform: uppercase;">O</span><sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub> 479 mm Hg,
HCO<sub><span style="border: 1pt none windowtext; padding: 0cm;">3</span></sub>16 mEq/L, and base excess −10.6 mEq/L. At this time,
the end-tidal CO<sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub> was 29 mm Hg.
Electrocardiogram (ECG) showed a cardiac rhythm of sinus tachycardia.<o:p></o:p></span></div>
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<span style="background-color: black; color: #bf9000;">At 5.48 p.m. the surgeon placed a
cross-clamp across the suprarenal aorta. This led to an increase in systolic
pressure to 160 mm Hg, but no apparent changes on the ECG. At 5.53 p.m. the
clamp was shifted to an infrarenal position. At 5.59 p.m., the cardiac rhythm
suddenly deteriorated into ventricular tachycardia, which rapidly progressed to
ventricular fibrillation. Chest compressions were initiated, and the patient
was ventilated with 100% oxygen. This resuscitation continued for the next 17
min during which time the patient received a total of nine countershocks of 360
J each. Additionally, a total of 5 mg of epinephrine, 4 mg of atropine, 2 g of
CaCl<sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub>, 400 mg of lidocaine, 150 mEq of NaHCO<sub><span style="border: 1pt none windowtext; padding: 0cm;">3</span></sub> and 2 g of MgSO4 were given IV. Chest
compressions were initially thought to be effective as the end-tidal CO<sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub>was maintained at 25–32 mm Hg. No arterial line was
yet available to observe a waveform or to draw blood gases, and no single-stick
arterial blood gas was drawn during the resuscitation. Despite the
resuscitation efforts, the underlying rhythm continued to be asystole. This was
confirmed by the palpation of a flaccid and pulseless (in the absence of chest
compressions) proximal aorta. End-tidal CO<sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub> had
diminished to 8–10 mm Hg, and the pupils were widely dilated. Because of the
patient’s complete lack of response and the apparent deterioration by end-tidal
CO<sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub>, the attending surgeon and anesthesiologist
mutually agreed to discontinue the resuscitation. The patient was pronounced
dead at 6.17p.m.<o:p></o:p></span></div>
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<span style="background-color: black;"><span style="color: #bf9000;">With cessation of the
resuscitation, the IV medications and infusions were discontinued. The monitors
were turned off, and the ventilator was disconnected although the endotracheal
tube was left <i>in situ</i>. The surgeon stayed at the operating table,
using the opportunity to teach residents and students. At 6.27p.m., 10 min
after the pronounced death of the patient, the surgeon announced that he had
begun to feel a pulse in the proximal aorta above the level of the aortic
cross-clamp. Ventilation with 100% oxygen was recommenced and revealed an
end-tidal CO<sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub> of 29 mm Hg. The ECG was reconnected and
showed a sinus rhythm of 90 bpm. Systolic blood pressure was 90 mm Hg by
automated cuff. A radial arterial line was now inserted successfully, and at
0630, arterial blood gases were: hemoglobin 9.5 mg/dL, K<sup><span style="border: 1pt none windowtext; padding: 0cm;">+</span></sup> 3.5 mEq/L, glucose 323 mg/dL, pHa 7.17, Pa<span style="text-transform: uppercase;">CO</span><sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub> 54.4 mm Hg,
Pa<span style="text-transform: uppercase;">O</span><sub><span style="border: 1pt none windowtext; padding: 0cm;">2</span></sub> 438 mm Hg,
and base excess −8.0 mEq/L. An esophageal temperature probe was inserted and
measured 33.4°C. It was decided to proceed with the operation although
neurologic prognosis was anticipated to be bleak. The patient was
hemodynamically stable throughout the remainder of the procedure, requiring no
inotropic support. Total fluid administration for the operation was 16 U of
packed red blood cells, 8 U of fresh frozen plasma, 20 U of platelets, and 12 L
of crystalloid solutions. Despite warming of all IV fluids and blood products
and the use of a forced air warming blanket, the patient’s temperature ranged
between 33° and 34°C for the remainder of the operation. The leaking aneurysm
was resected uneventfully and the patient was transported to the intensive care
unit.</span><span style="color: #1d1b11;"><o:p></o:p></span></span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhdL5cthOohKAv7Z9sT6Q-896-N5iz2gnFC6E-95itfe6BNEE1H4sjL_qSq5nyDyN_K2lrdl2UmmFiw4urbN7C_VmBlGQpu0vhQeVQkgPODHeoHBReuxKB-WaUWdTsT_JEX3HCHYHC3h20I/s1600/625d47410555a092f95d06a3_1.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="213" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhdL5cthOohKAv7Z9sT6Q-896-N5iz2gnFC6E-95itfe6BNEE1H4sjL_qSq5nyDyN_K2lrdl2UmmFiw4urbN7C_VmBlGQpu0vhQeVQkgPODHeoHBReuxKB-WaUWdTsT_JEX3HCHYHC3h20I/s320/625d47410555a092f95d06a3_1.jpg" width="320" /></a></div>
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<span style="background-color: black; color: #bf9000;">Postoperatively, the patient was maintained on mechanical ventilation
for several days in the intensive care unit. The postoperative course was
complicated by mild renal insufficiency and two bouts of atrial arrhythmias
(both of which were self-limiting). Remarkably, the patient improved
dramatically and, after tracheal extubation, was found to be completely
neurologically intact. He appeared to have no short- or long-term memory
deficits. He also had no recall of any events of the day of operation except
for being initially brought into the OR.<o:p></o:p></span></div>
<div class="MsoNormal" style="margin: 9pt 0cm; text-align: justify; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;">He was discharged home on postoperative Day 13 in excellent condition
with no apparent neurologic deficit. Follow-up at 5 wk revealed that the
patient had fully recovered, and had resumed full physical activities and his
lifestyle of prior to the surgery.</span><span style="color: #1d1b11;"><o:p></o:p></span></div>
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<h2 style="border: none; margin: 6pt 0cm; padding: 0cm; vertical-align: baseline;">
<span style="background-color: black; color: magenta; font-size: x-large;">PROPOSED
MECH</span><span style="background-color: black; color: magenta; font-size: x-large;">ANISMS</span><span style="color: #1d1b11; font-size: 16pt;"><o:p></o:p></span></h2>
</div>
<div id="p-14" style="margin: 9pt 0cm; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">T</span><span style="background-color: black; color: #bf9000; font-size: 11pt;">he exact mechanism of delayed ROSC is unclear and it is possible that more
than one mechanism is involved. </span><span style="background-color: black; color: #bf9000; font-size: 11pt;">Dynamic hyperinflation of the lung causing
increased positive end expiratory pressure (PPEP) is one of the proposed
mechanisms, which has some supporting evidence in patients with obstructive
airways disease.<o:p></o:p></span></div>
<h3 style="font-style: inherit; margin: 0cm 3pt 0.0001pt 0cm; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;">
Positive end
expiratory pressure</span><span style="color: #1d1b11;"><o:p></o:p></span></h3>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhcpXPYdxqr3kOkb1JtSSxI8N-VXG4RzpWKq7412g_Wej8TIU1AxCoIra03tQQpL3C5VfOxsU0uNc3ENaKE7sitQP_XnbdfzMqod2HCvNsMDkURvK5IbbGvh1DKl16Ib5B9oc2Td9-8uzkW/s1600/vnt26.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><span style="background-color: black;"><img border="0" height="292" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhcpXPYdxqr3kOkb1JtSSxI8N-VXG4RzpWKq7412g_Wej8TIU1AxCoIra03tQQpL3C5VfOxsU0uNc3ENaKE7sitQP_XnbdfzMqod2HCvNsMDkURvK5IbbGvh1DKl16Ib5B9oc2Td9-8uzkW/s320/vnt26.jpg" width="320" /></span></a></div>
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<span style="background-color: black; color: #bf9000; font-size: 11pt;">Rapid manual
ventilation without adequate time for exhalation during CPR can lead to dynamic
hyperinflation of lungs. Dynamic hyperinflation may lead to gas trapping and an
increase in the end-expiratory pressure (called auto-PEEP) leading to delayed
venous return, low cardiac output and even cardiac arrest in patients with
obstructive airways disease.<o:p></o:p></span></div>
<div id="p-16" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">The link between
mechanical ventilation of patients with obstructive ventilatory defects and
circulatory failure was first demonstrated in 1982.<span class="apple-converted-space"> </span>One report describes a patient with
respiratory failure due to asthma whose blood pressure was undetectable five
minutes after initiating artificial ventilation with a tidal volume of 700 mL
and respiratory rate of 25 breaths per minute. Even after inotropes the
systolic blood pressure did not exceed 70 mm Hg. The ventilator was adjusted to
a respiratory rate of six breaths per minute and a tidal volume of 400 mL and
the blood pressure gradually rose to 126/84 mm Hg.<o:p></o:p></span></div>
<div id="p-17" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">The physiology of
severe auto-PEEP is similar to pericardial tamponade, where circulation can
only be restored after removing the obstacle to cardiac filling. Auto-PEEP is a
possible cause of pulseless electrical activity (PEA), and rapid ventilation
during CPR should be avoided. Hypovolaemia and decreased myocardial
contractility could exaggerate its effect on venous return and cardiac output.
Some authors recommend discontinuing the ventilation transiently for 10 to 30
seconds in PEA to allow venous return.<o:p></o:p></span></div>
<div id="p-18" style="font-size: inherit; font-style: inherit; margin: 9pt 0cm; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">It is tempting to apply this theory even to patients without obstructive
airways disease. Dynamic hyperinflation can theoretically happen in any
situation where rapid manual ventilation is carried out. One could argue that
in the presence of decreased cardiac output—as in myocardial infarction and
hypovolaemia—dynamic hyperinflation could compromise the cardiac output even
more, leading to cardiac arrest.<o:p></o:p></span></div>
<div id="p-19" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">Even though
auto-PEEP due to dynamic hyperinflation seems most plausible and has some
evidence in patients with obstructive airways disease, this alone would not
explain all cases of delayed ROSC. In one report, CPR was terminated after 30
minutes and the patient was in asystole. Because the patient had MRSA and CPR
was performed without proper infection control measures, the physician involved
in the CPR went to shower and change clothes, leaving the patient still being
ventilated in the intensive care unit. Returning five minutes later, he found
the patient with a perfusable rhythm. The patient died two days later.<o:p></o:p></span></div>
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<span style="background-color: black; color: #bf9000;">
Delayed action of
drugs <o:p></o:p></span></h3>
<div id="p-20" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">Some authors
suggest delayed action of drugs administered during CPR as a mechanism for
delayed ROSC.<span class="apple-converted-space"> </span>It is possible that
drugs injected through a peripheral vein are inadequately delivered centrally
due to impaired venous return, and when venous return improves after stopping
the dynamic hyperinflation, delivery of drugs could contribute to return of
circulation. In some cases, however, drugs are actually administered through a
central line. Even though this theory is plausible it would be impossible to
either prove or disprove.<o:p></o:p></span></div>
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<span style="background-color: black; color: #bf9000;"><br /></span></h3>
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<span style="background-color: black; color: #bf9000;">
Hyperkalaemia<o:p></o:p></span></h3>
<div id="p-21" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">There are few
reports of delayed ROSC in the presence of hyperkalaemia.<span class="apple-converted-space"> </span>It is a well-known fact that
intracellular hyperkalaemia could persist longer, rendering the myocardium
retractile for long periods of time. There is a report on a 68-year-old lady
with cardiac arrest due to hyperkalaemia who did not respond to CPR and
conventional treatment up to 100 minutes, but later responded to dialysis and
made a complete recovery.<span class="apple-converted-space"> </span>So even
though prolonged cardiac arrest refractory to conventional treatment could
respond to dialysis, it is unlikely that hyperkalaemia on its own could explain
delayed ROSC after cessation of CPR.<o:p></o:p></span></div>
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<span style="background-color: black; color: #bf9000;"><br /></span></h3>
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<span style="background-color: black; color: #bf9000;">
Myocardial stunning<o:p></o:p></span></h3>
<div id="p-22" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">Prolonged
myocardial dysfunction can occur following myocardial ischaemia, taking up to
several hours before normal function returns.<span class="apple-converted-space"> </span>Of
the 38 cases, 13 had myocardial infarction, and at least seven had hypovolaemia
which could have contributed to transient myocardial ischaemia and stunning.<o:p></o:p></span></div>
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<span style="background-color: black; color: #bf9000;"><br /></span></h3>
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<span style="background-color: black; color: #bf9000;">
Transient asystole<o:p></o:p></span></h3>
<div id="p-23" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="font-size: 11pt;"><span style="background-color: black; color: #bf9000;">Asystole or PEA
following countershock of prolonged VF is common and occurs in around 60% of
patients.<span class="apple-converted-space"> </span>Even though restoration
of circulation occurs in 16% of patients, the prognosis is poor: only 0-3% are
discharged alive. It is possible that asystole or PEA after countershock could
be transient before a perfusable rhythm restores circulation. Transient asystole
following defibrillation would explain at least one case, where CPR was
interrupted after a last cardioversion attempt resulting in asystole, and ROSC
occurred soon after.<span class="apple-converted-space"> </span>However,
transient asystole would not explain delayed ROSC in majority of patients in
whom the duration of asystole was much longer. In another case, CPR was stopped
while the patient was still in ventricular fibrillation and haemodynamic
activity returned few moments later.<span class="apple-converted-space"> </span>The
authors of the case rightly point out that CPR should not be halted in a
patient with ventricular fibrillation.</span><span style="color: #1d1b11;"><o:p></o:p></span></span></div>
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<span style="background-color: black; font-size: 11pt;"><br /></span></div>
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</div>
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<h2 style="border: none; margin: 6pt 0cm; padding: 0cm; vertical-align: baseline;">
<span style="background-color: black; color: magenta; font-size: x-large;">CONSEQUENCES
OF DELAYED RETU</span><span style="background-color: black; color: magenta; font-size: x-large;">RN OF SPONTANEOUS CIRCULATION</span><span style="color: #1d1b11; font-size: 16pt;"><o:p></o:p></span></h2>
</div>
<div id="p-24" style="color: #1d1b11; font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; font-size: 11pt;"><br /></span></div>
<div id="p-24" style="font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">Delayed ROSC
can lead to serious professional and legal consequences. Questions will be
asked abo</span><span style="background-color: black; color: #bf9000; font-size: 11pt;">ut whether CPR has been conducted properly and whether it was stopped
too soon. The medical team might be accused of negligence and incompetence and
even be sued for damages if a patient survives with severe disability.<span class="apple-converted-space"> </span>A doctor involved in resuscitation and
certification of death followed by delayed ROSC has recently been accused of
culpable homicide.<o:p></o:p></span></div>
<div id="p-25" style="font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; font-size: 11pt;"><span style="color: #bf9000;">The conduct
of ALS can only be assessed from the case record, so it is vital to record the
events during cardiac arrest as accurately as possible. When to discontinue CPR
is still a medical decision and so it is absolutely essential to get a
consensus from the arrest team and to document the reason for termination of
CPR. Some authors recommend measurement of end-tidal carbon dioxide during CPR.
Values above 10-15 mmHg indicate a favourable prognosis and should preclude
termination of CPR.<span style="border: 1pt none windowtext; padding: 0cm;"> </span>This technology is not widely
available outside the intensive care setting, but should be considered in
difficult clinical situations. Whether this would identify patients in whom
delayed ROSC might occur is nevertheless questionable.</span><span style="color: #1d1b11;"><o:p></o:p></span></span></div>
<div id="p-25" style="color: #1d1b11; font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="font-size: 11pt;"><br /></span></div>
<div id="p-25" style="margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
</div>
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<h2 style="border: none; margin: 6pt 0cm; padding: 0cm; vertical-align: baseline;">
<span style="background-color: black; color: magenta; font-size: x-large;">HOW WOULD ONE
RECOGNIZE DEATH?</span><span style="background-color: white; color: #1d1b11; font-size: 16pt;"><o:p></o:p></span></h2>
<div>
<span style="background-color: black; color: magenta; font-size: x-large;"><br /></span></div>
</div>
<div id="p-26" style="font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh9UBQ1wgZy4-ybscTtlUEDlXvKVlhnioAu9_Jv4nlrW93GD5ePAFgebVfQLZwi-H1O1_TgAfb4ofP5zXK_i6WSxn3BDKcQAg03AIOR6aqg6vTfRiSoUFNZH0KZLOiKFRfi1WJM2CvfmR5H/s1600/230px-CPR_training-04.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh9UBQ1wgZy4-ybscTtlUEDlXvKVlhnioAu9_Jv4nlrW93GD5ePAFgebVfQLZwi-H1O1_TgAfb4ofP5zXK_i6WSxn3BDKcQAg03AIOR6aqg6vTfRiSoUFNZH0KZLOiKFRfi1WJM2CvfmR5H/s1600/230px-CPR_training-04.jpg" /></a></div>
<span style="background-color: black; color: #bf9000; font-size: 11pt;">It is
important to realize that death is not an event, but a process. The conference
of Medical Royal Colleges in the UK advocated that death is a process during
which various organs supporting the continuation of life fail.<span style="border: 1pt none windowtext; padding: 0cm;"> </span>Cessation of circulation and respiration is such an
example. The physical findings to support this—absence of heartbeat and
respiration—are the traditional and the most widely used criteria to certify
death. Since these findings alone are not a sign of definitive death, it is
quite possible to declare death in the interval between cessation of CPR and
delayed ROSC.<o:p></o:p></span></div>
<div id="p-27" style="font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="font-size: 11pt;"><span style="background-color: black; color: #bf9000;"><br /></span></span><br />
<span style="font-size: 11pt;"><span style="background-color: black; color: #bf9000;">Because
delayed ROSC occurred within 10 minutes in most cases, many authors recommend
that patients should be passively monitored for at least 10 minutes following
unsuccessful CPR. During that period the family should be informed that CPR had
been stopped because of poor response and further efforts are not in the best
interests of the patient. It should also be mentioned that the patient is being
closely monitored to establish death beyond any doubt. Death should not be
certified in any patient immediately after stopping CPR, and one should wait at
least 10 minutes, if not longer, to verify and confirm death beyond doubt. This
is in line with what was said by W H Sweet in 1978:‘ the time honoured criteria
of the stoppage of the heart beat and circulation are indicative of death only
when they persist long enough for the brain to die</span><span style="background-color: black; color: #bf9000;">.</span><span style="color: #1d1b11;"><o:p></o:p></span></span></div>
<div id="p-27" style="color: #1d1b11; font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; font-size: 11pt;"><br /></span></div>
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</div>
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<h2 style="border: none; margin: 6pt 0cm; padding: 0cm; vertical-align: baseline;">
<span style="background-color: black; color: magenta; font-size: x-large;">NON-MEDICAL
LITERATURE</span><span style="color: #1d1b11; font-size: 16pt;"><o:p></o:p></span></h2>
</div>
<h3 style="color: #1d1b11; font-size: inherit; font-style: inherit; margin: 0cm 3pt 0.0001pt 0cm; outline-style: none; vertical-align: baseline;">
</h3>
<h3 style="font-size: inherit; font-style: inherit; margin: 0cm 3pt 0.0001pt 0cm; outline-style: none; vertical-align: baseline;">
<span style="color: #bf9000;"><span style="background-color: black;">
Newspapers<o:p></o:p></span></span></h3>
<div id="p-28" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">In addition to
medical literature, there are many newspaper articles, websites and a few
</span><span style="background-color: black; color: #bf9000; font-size: 11pt;">anecdotes in medical journals describing patients who were certified dead, but
later found to be alive. Many of these articles refer to these incidents as
‘Lazarus phenomenon’. There is even a movie called<span class="apple-converted-space"> </span><em style="font-size: inherit; line-height: inherit; outline-style: none; text-align: inherit;"><span style="border: 1pt none windowtext; padding: 0cm;">Lazarus
phenomenon</span></em><span class="apple-converted-space"> </span>describing
two cases of resurrection after death. However, the authenticity of one of
these cases has been questioned.<o:p></o:p></span></div>
<div style="font-size: inherit; margin: 0cm 0cm 0.0001pt; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;"><br /></span></div>
<h3 style="font-size: inherit; margin: 0cm 3pt 0.0001pt 0cm; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;">
Websites<o:p></o:p></span></h3>
<div id="p-31" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">A website (<a href="http://www.snopes.com/horrors/gruesome/buried.asp" style="font-size: inherit; font-style: inherit; line-height: inherit; outline-style: none; text-align: inherit;"><span style="border: 1pt none windowtext; padding: 0cm;">www.snopes.com/horrors/gruesome/buried.asp</span></a>) describing
people who have been buried alive by mistake in the last few centuries provides
entertaining reading. In olden days a number of illnesses could cause coma and
there was a danger of hasty disposal of the body especially in those with
infectious diseases.<o:p></o:p></span></div>
<div style="font-size: inherit; margin: 0cm 0cm 0.0001pt; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;"><br /></span></div>
<h3 style="font-size: inherit; font-style: inherit; margin: 0cm 3pt 0.0001pt 0cm; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;">
Literature<o:p></o:p></span></h3>
<div id="p-32" style="font-size: inherit; font-style: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">Edgar Allan Poe's
most hair-raising tale is<span class="apple-converted-space"> </span><em style="font-size: inherit; line-height: inherit; outline-style: none; text-align: inherit;"><span style="border: 1pt none windowtext; padding: 0cm;">The Premature Burial</span></em>, in which a young wife was
incorrectly pronounced dead and kept in a coffin in the family vault. When the
vault was opened a few years later to receive another coffin, a shrouded
skeleton was found in the doorway suggested that the lady had survived and
eventually died unable to open the vault door. It is believed that he based his
story on a widely reported incident that took place around that time.<o:p></o:p></span></div>
<div id="p-33" style="font-size: inherit; font-style: inherit; margin: 9pt 0cm; outline-style: none; text-align: inherit; vertical-align: baseline;">
<span style="font-size: 11pt;"><span style="background-color: black; color: #bf9000;">It seems that the chances of being buried alive were not so remote in
1800s. The fear of being buried alive was so prevalent that many people
specified in their wills that tests must be carried out to confirm their death,
such as pouring hot liquids on the skin, touching the skin with red-hot irons,
or making surgical incisions prior to the burial. A coffin was invented and
patented in 1897 to allow a person accidentally buried alive to summon help
through a system of flags and bells. The fear of being buried alive is called
‘taphophobia’ in the medical literature. There was even a Society for the
Prevention of Burial Before Death, which recognized the difficulties in
diagnosing death and issued educational leaflets to assist members of the
society.</span><span style="background-color: white; color: #1d1b11;"><o:p></o:p></span></span></div>
<div id="p-33" style="font-style: inherit; margin: 9pt 0cm; outline-style: none; text-align: inherit; vertical-align: baseline;">
</div>
<div style="border-bottom-color: rgb(153, 153, 153); border-bottom-width: 1.5pt; border-style: none none dotted; padding: 0cm;">
<h2 style="border: none; margin: 6pt 0cm; padding: 0cm; vertical-align: baseline;">
<span style="background-color: black; color: magenta; font-size: x-large;">LAZARUS IN
OTHER CONTEXTS</span><span style="color: #1d1b11; font-size: 16pt;"><o:p></o:p></span></h2>
</div>
<div id="p-34" style="color: #1d1b11; font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; font-size: 11pt;"><br /></span></div>
<div id="p-34" style="font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000; font-size: 11pt;">The term
Lazarus has also been used to describe many other unexpected and scientifically
unex</span><span style="background-color: black; color: #bf9000; font-size: 11pt;">plainable phenomena. Lazarus complex describes the psychological sequence
in the survivors of cardiac arrest, near-death experiences and unexpected
remission in AIDS.<span class="apple-converted-space"> </span>Lazarus
syndrome is described in paediatric palliative care, when a child is expected
to die but unexpectedly goes into remission.<span class="apple-converted-space"> </span>Spontaneous
movement in brain dead and spinal cord injury patients has been described as
Lazarus sign.<span class="apple-converted-space"> </span>Survival of species
after mass extinction has been called Lazarus effect.<span class="apple-converted-space"> </span>The term Lazarus phenomenon was also
used for unexpected survival of renal graft patients.<span style="border: 1pt none windowtext; padding: 0cm;"> <o:p></o:p></span></span></div>
<div style="font-size: inherit; margin: 0cm 0cm 0.0001pt; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;"><br /></span></div>
<div id="p-35" style="font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="color: #bf9000; font-size: 11pt;"><span style="background-color: black;">Lazarus
premonition describes an unexpected state of brief resurrection in terminally
ill patients, when they experience an increase in vitality, appetite and
general improvement.<span class="apple-converted-space"> </span>This was
recognized at least a thousand years ago in the medieval Chinese literature and
was described as<span class="apple-converted-space"> </span><em style="font-size: inherit; line-height: inherit; outline-style: none; text-align: inherit;"><span style="border: 1pt none windowtext; padding: 0cm;">hui guang fan zhao</span></em>, meaning reflected rays of setting
sun. Recently a ‘Lazarus Pill’ (Zolpidem, a non-benzodiazepine sedative) has
aroused medical interest in patients with persistent vegetative state. This was
following a report where a patient with persistent vegetative state showed a
brief remarkable neurological response to zolpidem.</span><span style="border: 1pt none windowtext; padding: 0cm;"><o:p></o:p></span></span></div>
<div id="p-35" style="font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; font-size: 11pt;"><br /></span></div>
<div id="p-35" style="margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
</div>
<div style="border-bottom-color: rgb(153, 153, 153); border-bottom-width: 1.5pt; border-style: none none dotted; padding: 0cm;">
<h2 style="border: none; margin: 6pt 0cm; padding: 0cm; vertical-align: baseline;">
<span style="background-color: black; color: magenta; font-size: x-large;">RESURRECTION</span><span style="color: #1d1b11; font-size: 16pt;"><o:p></o:p></span></h2>
</div>
<div id="p-36" style="color: #1d1b11; font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; font-size: 11pt;"><br /></span></div>
<div id="p-36" style="font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="font-size: 11pt;"><span style="background-color: black; color: #bf9000;">There are
many other resurrections in addition to that of Lazarus. Three resurrections
are recorded in the Old Testament, one each by Elijah, Elisha and Elisha's
bones. There are many resurrections in the New Testament, four by Jesus
(including Lazarus) and one each by Paul and Peter.<span class="apple-converted-space"> </span>In Hindu mythology Sathyavan's wife
Savithri convinces the Lord of death (Yamaraj) to resurrect Sathyavan following
his death after being caught under a falling tree. These stories illustrate
that humanity's preoccupation with death and resurrection is universal. The
greatest example of Lazarus phenomenon is probably the death and resurrection
of Jesus Christ himself.</span><span style="color: #1d1b11;"><o:p></o:p></span></span></div>
<div id="p-36" style="color: #1d1b11; font-size: inherit; margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
<span style="background-color: black; font-size: 11pt;"><br /></span></div>
<div id="p-36" style="margin: 0cm 0cm 0.0001pt; outline-style: none; vertical-align: baseline;">
</div>
<div style="border-bottom-color: rgb(153, 153, 153); border-bottom-width: 1.5pt; border-style: none none dotted; padding: 0cm;">
<h2 style="border: none; margin: 6pt 0cm; padding: 0cm; vertical-align: baseline;">
<span style="background-color: black; color: magenta; font-size: x-large;">KEY POINTS</span><span style="background-color: white; color: #1d1b11; font-size: 16pt;"><o:p></o:p></span></h2>
</div>
<div style="font-size: inherit; margin: 9pt 14.4pt 9pt 27.6pt; outline-style: none; text-indent: -18pt; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;"><span style="font-family: Symbol; font-size: 10pt;">·<span style="font-family: 'Times New Roman'; font-size: 7pt;">
</span></span><span style="font-size: 11pt;">Lazarus phenomenon is described as delayed ROSC after cessation of CPR;<o:p></o:p></span></span></div>
<div id="p-39" style="font-size: inherit; font-style: inherit; margin: 9pt 14.4pt 9pt 27.6pt; outline-style: none; text-align: inherit; text-indent: -18pt; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;"><span style="font-family: Symbol; font-size: 10pt;">·<span style="font-family: 'Times New Roman'; font-size: 7pt;">
</span></span><span style="font-size: 11pt;">Dynamic hyperinflation should be considered as a reversible of cause of
PEA;<o:p></o:p></span></span></div>
<div id="p-40" style="font-size: inherit; font-style: inherit; margin: 9pt 14.4pt 9pt 27.6pt; outline-style: none; text-align: inherit; text-indent: -18pt; vertical-align: baseline;">
<span style="background-color: black; color: #bf9000;"><span style="font-family: Symbol; font-size: 10pt;">·<span style="font-family: 'Times New Roman'; font-size: 7pt;">
</span></span><span style="font-size: 11pt;">Patients should be observed for at least 10 minutes using blood pressure
and ECG monitoring after the cessation of CPR before confirming death.<o:p></o:p></span></span></div>
<div style="font-size: inherit; margin: 0cm 0cm 0.0001pt; vertical-align: baseline;">
<span style="background-color: black;"><br /></span></div>
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<br /></div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com3tag:blogger.com,1999:blog-3393509504180156297.post-73588291137316205692012-07-29T02:33:00.001-07:002012-07-29T02:33:09.997-07:00Orofacial manifestations of hematological disorders: Anemia and hemostatic disorders<div dir="ltr" style="text-align: left;" trbidi="on">
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<tr><td class="pageSub" height="15px" style="background-image: url(http://www.ijdr.in/images/ps.gif); background-position: 5px 50%; background-repeat: no-repeat no-repeat; border-bottom-color: rgb(238, 238, 238); border-bottom-style: solid; border-bottom-width: 2px; color: #302a7b; font-family: Arial, Verdana, sans-serif; font-weight: bold; height: 30px; padding-left: 20px;" width="85%"><span style="font-size: x-large;"> Abstract</span></td><td align="right" class="inthis"> </td><td height="15px" width="15%"></td></tr>
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The aim of this paper is to review the literature and identify orofacial manifestations of hematological diseases, with particular reference to anemias and disorders of hemostasis. A computerized literature search using MEDLINE was conducted for published articles on orofacial manifestations of hematological diseases, with emphasis on anemia. Mesh phrases used in the search were: oral diseases AND anaemia; orofacial diseases AND anaemia; orofacial lesions AND anaemia; orofacial manifestations AND disorders of haemostasis. The Boolean operator "AND" was used to combine and narrow the searches. Anemic disorders associated with orofacial signs and symptoms include iron deficiency anemia, Plummer-Vinson syndrome, megaloblastic anemia, sickle cell anemia, thalassaemia and aplastic anemia. The manifestations include conjunctiva and facial pallor, atrophic glossitis, angular stomatitis, dysphagia, magenta tongue, midfacial overgrowth, osteoclerosis, osteomyelitis and paraesthesia/anesthesia of the mental nerve. Orofacial petechiae, conjunctivae hemorrhage, nose-bleeding, spontaneous and post-traumatic gingival hemorrhage and prolonged post-extraction bleeding are common orofacial manifestations of inherited hemostatic disorders such as von Willebrand's disease and hemophilia. A wide array of anemic and hemostatic disorders encountered in internal medicine has manifestations in the oral cavity and the facial region. Most of these manifestations are non-specific, but should alert the hematologist and the dental surgeon to the possibilities of a concurrent disease of hemopoiesis or hemostasis or a latent one that may subsequently manifest itself.</div>
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<tr><td class="pageSub" style="background-image: url(http://www.ijdr.in/images/ps.gif); background-position: 5px 50%; background-repeat: no-repeat no-repeat; border-bottom-color: rgb(238, 238, 238); border-bottom-style: solid; border-bottom-width: 2px; color: #302a7b; font-family: Arial, Verdana, sans-serif; font-weight: bold; height: 30px; padding-left: 20px;"><span style="font-size: large;">Orofacial Manifestations of Anemia</span></td><td align="right" class="inthis"> </td><td align="right" width="15%"><br /></td></tr>
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<br style="font-size: 12px;" /><br style="font-size: 12px;" /><b>Iron deficiency anemia</b><br /><br />Iron deficiency anemia is the most common hematological disorder. It may manifest in the orofacial region as atrophic glossitis, mucosal pallor and angular cheilitis. Atrophic glossitis "flattening of the tongue papillae" resulting in a smooth and erythematous tongue may mimic migratory glossitis (Table 1). Migratory glossitis, also known as geographic tongue, is a condition of unknown etiology that affects 12% of the population. It results in lesions on the tongue that are erythematous, non-indurate, atrophic and bordered by a slightly elevated, distinct rim that varies in color from gray to white. In atrophic glossitis, these areas do not have a white keratotic border and they increase in size rather than changing in position. In more severe cases, the tongue may be tender. Angular stomatitis (painful fissures at the corners of the mouth) and cheilosis (dry scaling of the lips and corners of the mouth) are also common findings associated with iron deficiency anemia. Angular cheilitis, however, is often associated with fungal infections (Candida albicans), lip-sucking and dehydration. Treatment must focus on correcting the deficiency state and providing adequate energy, protein, fluids and nutrients to promote healing. When angular cheilitis is due to opportunistic infections brought on by decreased resistance secondary to nutrient deficiencies, treatment should focus on antifungal therapy, correction of the nutrient deficiency and diet modification to make eating a more comfortable experience.<br />
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<b style="font-size: 12px; text-align: -webkit-center;">Table 1: Orofacial manifestations of anemias</b>
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<b>The <span class="spl" style="background-color: #cdd8ba; border: 3px dotted rgb(255, 255, 255); font-family: Arial, Verdana, sans-serif; font-style: italic; margin-left: 2px; margin-right: 2px;"> Plummer-Vinson syndrome</span></b><br /><br />This is otherwise called the Patterson-Brown-Kelly syndrome or sideropenic dysphagia. It is a symptom complex caused by iron deficiency. This syndrome manifests as atrophic glossitis, or angular cheilitis, and, occasionally, hyperkeratotic lesions are seen in the oral mucosa. It is also associated with koilonychias (or spoon nails), pagophagia and dysphagia due to pharyngoesophageal ulcerations and esophageal webs.<br /><br /><b>Megaloblastic anemia</b><br /><br />This may be caused by a vitamin B12 deficiency (commonly from pernicious anemia, surgical resection of the ileum or small intestinal diverticula) or by a folic acid deficiency (most commonly from malnutrition). Vitamin B12 deficiency manifests in the oral cavity as part of megaloblastic changes in the entire gastrointestinal tract, which are so well demonstrated morphologically in the bone marrow. The oral manifestations of painful atrophy of the entire oral mucous membranes and tongue (glossitis), stomatitis as well as mucosal ulceration (recurrent aphthous ulcers) in vitamin B12 and folate deficiency have long been recognized (Table 1). These oral changes may occur in the absence of symptomatic anemia or of macrocytosis. "Magenta tongue," which is said to be rather characteristic, may herald a B12 deficiency. <br /><br /><b>Sickle cell anemia</b><br /><br />Sickle cell disease is generically used to describe a group of disorders characterized by the production of abnormal hemoglobin S (HBS). The entities include sickle cell anemia (HbSS), sickle cell Hb C disease (HbSC) and sickle cell-β thalassaemia.<br /><br />Sickle cell anemia (HbSS) is the most common type and represents the homozygous form where the individuals inherit a double dose of the abnormal gene that codes for hemoglobin S. The sickle hemoglobin abnormality is caused by substitution of valine for glutamic acid in the sixth position from the NH <sub>2</sub> terminal end of the β-globin chain. With decreased oxygen tension, the abnormal hemoglobin polymerizes, forming fluid polymers (tactoids) that cause the red cells to deform into a characteristic sickle shape that may plug different areas of the microcirculation or large vessels.<br /><br />The hallmark features of sickle cell disease are chronic hemolytic anemia and vaso-occlusion resulting in ischemic tissue injury. While a wide spectrum of complications result from these, the major manifestation of concern is "sickle crisis" of aplastic, hemolytic or painful (vaso-occlusive) types leading to devastating multisystem complications, including stroke, pulmonary disease, delayed growth, osteomyelitis, organ damage and psychosocial dysfunction. All tissues and organs within the body are at risk of damage due to sickling.<br /><br />Although relatively uncommon, a number of orofacial changes have also been observed in sickle cell disease. When it occurs, the basic pathogenicity is similar to that in other organs. These orofacial changes in HbSS as reported in the literature include midfacial overgrowth attributable to marrow hyperplasia, other skull and jaw changes such as increased thickening of the skull and osteoporotic changes, mandibular infarction that may be followed by osteosclerosis, osteomyelitis of the mandible, anesthesia or paraesthesia of the mental nerve, asymptomatic pulpal necrosis, orofacial pain, enamel hypomineralization and diastema (Table 1). These dentofacial deformities are radiographically characterized by a step-ladder appearance of the alveolar bone and areas of decreased densities and coarse trabecular pattern most easily seen between the root apices of the teeth and the inferior border of the mandible.<br /><br />Mandibular osteomyelitis is an oral complication commonly observed in patients with sickle cell anemia, which is rarely manifested with other complications, making both its diagnosis and treatment easy. The mandible is the most affected part of the face because the blood supply is relatively insufficient when compared with the maxilla. Intravascular impairment can result in both ischemic infarct and osteonecrosis thus allowing bacterial proliferation by Streptococcus or <span class="spl" style="background-color: #cdd8ba; border: 3px dotted rgb(255, 255, 255); font-family: Arial, Verdana, sans-serif; font-style: italic; margin-left: 2px; margin-right: 2px;"> Salmonella </span> Aches in the mandible can be preceded by widespread painful crises and be accompanied by neuropathy involving the inferior alveolar nerve and paraesthesia of the lower lip.<br /><br />The possibility of blood extravasations and hematoma secondary to sickle cell anemia-induced hemorrhage should be considered as a working diagnosis of a facial swelling in sickle cell disease. Scipio <i>et al</i>. reported a case of a 14-year-old boy with sickle cell-related hemorrhage who developed an acute facial swelling, mimicking facial cellulitis of dental origin. Surgical exploration, however, revealed a large hematoma between the periosteum and the lateral aspect of the ramus of the mandible. Pools of blood were also found within the buccinators muscle. The boy also exhibited gingival enlargement, which was considered to be an outcome of repeated hemorrhagic episodes and fibrous repair. Gingival biopsies reported the presence of erythrocyte-filled intraepithelial blood vessels in the gingival epithelium.<br /><br />Saint Clair de Velasquez and Rivera reported, in a study, that the most common soft tissue oral manifestation of sickle cell anemia in a Venezuelan population was buccal mucosa pallor, while the most common hard tissue finding was enlarged medullary spaces.<br /><br />The increased number of malocclusions in patients with sickle cell disease can be related to muscular imbalance, absence of labial sealing or changes in the osseous base thus leading to increased orthodontic intervention.<br /><br /><b>Thalassaemia</b><br /><br />These are a group of inherited hemolytic anemia involving defects in the synthesis of either the αor the β polypeptide chains of hemoglobin (α-thalassaemia, β-thalassaemia). Based on genetic and clinical entities, thalassaemia are classified as homozygous, heterozygous or compound heterozygous. The heterozygous form of the disease (thalassaemia minor) is mild and usually asymptomatic, the only manifestation being hypochromic microcytic anemia.<br /><br />Homozygous β-thalassaemia, also known as Cooley's anemia or Mediterranean anemia, is chiefly seen in Mediterranean populations with prevalence as high as 15-20% in Greece, Turkey, Cyprus and southern Italy.<br /><br />The homozygous form of β-thalassaemia (thalassaemia major) exhibits the most severe clinical symptoms with marked orofacial deformities. The onset of symptoms occurs early in infancy and the patients are severely anemic and have a short life expectancy. Patients with the most severe form of the disease rarely survive into adulthood because of cardiac failure, chronic anemia and hypoxia. However, with modern management, the prognosis has greatly improved.<br /><br />The most common orofacial manifestations are due to intense compensatory hyperplasia of the marrow and expansion of the marrow cavity (Table 1) and a facial appearance known as "chipmunk" face: enlargement of the maxilla, bossing of the skull and prominent molar eminences. Overdevelopment of the maxilla frequently results in an increased over jet and spacing of maxillary teeth and other degrees of malocclusion.<br /><br /><b>Aplastic anemia</b><br /><br />Aplastic anemia commonly presents with oral manifestation and can be the first clinical manifestation of the disease (Table 1). The most common orofacial manifestation of the disease is multiple hemorrhages, which most often develop in patients with platelet counts <25 × 10 <sup>9</sup> /liter. (Figure 1) a and b shows multiple orofacial hemorrhages in a 12-year-old patient with aplastic anemia. The other common manifestations are oral ulceration, candidiasis and viral infection. </div>
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<b style="font-size: 12px; text-align: -webkit-center;">Figure 1: (a) A 12-year-old boy with aplastic anemia. Note the subconjunctival ecchymosis. (b) The same patient as in Figure 1a. Note ecchymosis of the lower lip and cheek as well as sublingual hematoma</b>
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<b>Orofacial manifestations of disorders of hemostasis</b><br /><br />Interaction of several basic mechanisms produces normal hemostasis, which can be divided into four general phases: the vascular phase; the platelet phase; the coagulation cascade phase, consisting of intrinsic, extrinsic and common pathways; and the fibrinolytic phase. <br /><br />An abnormal tendency to hemorrhage or thromboembolism occurs in the mixed group of disorders known as hemostatic disorders. All hemorrhagic hemostatic disorders, both inherited and acquired, may produce a variety of orofacial manifestations, including petechiae, nose bleeding, spontaneous and post-traumatic gingival hemorrhages and prolonged post-extraction bleeding (Table 2). Minimal trauma, such as occurs in eating or in tooth brushing, may be sufficient to provoke gingival hemorrhage, which, when it does, is characterized by its persistence rather than its profusion, and the total volume of blood loss may be important. </div>
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<b style="font-size: 12px; text-align: -webkit-center;">Table 2: Orofacial manifestation of some disorders of hemostasis</b>
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<b>Vascular disorders of hemostasis</b><br /><br />The vascular disorders are a heterogenous group of conditions characterized by easy bruising and spontaneous bleeding from the small vessels. Frequently, the bleeding is mainly in the skin, causing petechiae, ecchymoses or both and in some cases there is bleeding also from the mucous membrane. Vascular defect of hemostasis may be acquired or inherited. Most cases of bleeding from the vascular defect alone are not severe or life threatening. Hereditary hemorrhagic telangiectasia and <span class="spl" style="background-color: #cdd8ba; border: 3px dotted rgb(255, 255, 255); font-family: Arial, Verdana, sans-serif; font-style: italic; margin-left: 2px; margin-right: 2px;"> Ehlers-Danlos syndrome</span> in which some patients express the characteristic facial appearance of large eyes, small chin, thin nose and lips, lobeless ears are examples of hereditary vascular disorders that may present with petechiae or ecchymotic lesions on the lips, tongue and oral mucosa and epistaxis.<br /><br /><b>Platelet disorders in hemostasis</b><br /><br />Abnormal bleeding associated with thrombocytopenia (low platelet count) or abnormal platelet function is characterized by spontaneous skin purpura, mucosal hemorrhages and prolonged bleeding after trauma.<br /><br />Facial petechiae, conjunctivae hemorrhage and hemorrhagic bullae in the oral mucous membrane occur in primary deficiency of platelets. These features are also seen in secondary thrombocytopenia due to the myelophthisic syndrome, autoimmune disorder, aplastic anemia (Figure 1) a and b, infections, collagen vascular disease, disseminated intravascular coagulopathy and drugs. These features may be seen in von Willebrand's disease (VWD) and have also been observed in severe hemophilia.<br /><br />Thrombocytopenia secondary to an autoimmunologic disorder is called idiopathic thrombocytopenic purpura (ITP). It is an autoimmune disease characterized by the production of antibodies against ones own platelets. These antibodies adhere to the platelets and are recognized and destroyed by the reticuloendothelial system. Consequently, the platelet count gradually diminishes and is insufficient for the maintenance of primary hemostasis. Several reports have documented cases of ITP presenting as post-extraction hemorrhage.<br /><br />Disorders of platelet function are suspected in patients who show skin and mucosal hemorrhages and in whom the bleeding time is prolonged despite a normal platelet count. Glanzmann thrombasthenia (GT) is an exceedingly rare but well-defined inherited disorder of platelet function caused by a defect in the glycoprotein IIb/IIIa complex. The association of GT with consanguinity has been noted, especially in geographic regions in which such intermarriage is common. In most patients, GT is diagnosed during early infancy or before the age of 5 years. Common manifestations of this hemorrhagic disorder are gingival hemorrhage, purpura, epistaxis, petechiae and menorrhagia. Bernard-Soulier syndrome and grey platelet syndrome are the other well-defined, inherited disorders of platelet function while the use of antiplatelet drugs like aspirin and clopidogrel, uremia and hyperglobulinemia are some acquired disorders of platelet function with similar orofacial manifestations.<br /><br /><b>Coagulation disorders of hemostasis</b><br /><br />In the 2007 World federation of hemophilia global survey where 89% of the world population was covered, 52,545 persons were identified with VWD, 105,018 with hemophilia A, 21,384 with hemophilia B, while 18,762 persons were identified with other bleeding disorders. In this survey, the total number of people identified with bleeding disorders was 213,904.<br /><br /><b>von Willebrand's disease</b><br /><br />VWD is one of the most common hereditary coagulation abnormalities in humans and shows a worldwide distribution. It is classified into type 1, type 2A, 2B, 2M, 2N disease. Type 1 disease is the most common form of VWD, accounting for approximately 80% of all cases. It is transmitted as an autosomal-dominant trait and thus there may be evidence of a family history of excessive bleeding. Most forms of the disease show incomplete penetrance of the phenotype and variable expressivity of bleeding symptoms within families. In contrast, the severe type 3 form of the disease shows a recessive pattern of inheritance with parents that do not usually manifest clinical symptoms. Type 2N VWD, in which isolated low FVIII levels occur, also shows a recessive pattern of inheritance and, thus, here again, a family history may be absent.<br /><br />The diagnosis of VWD is established by finding a prolonged bleeding time, a low level of factor VIII procoagulant activity and abnormally low levels of factor VIII - von Willebrand protein by immunologic assay and diminished platelet aggregation in response to ristocetin. The clinical bleeding symptoms of this disorder are notoriously heterogeneous and may range from virtually no symptom to mild symptoms to a disease resembling factor VIII deficiency and include oral mucosal bleeding, soft tissue hemorrhage, menorrhagia in women and rare hemarthrosis. Continuous oral bleeding over long periods of time fosters deposits of hemosiderin and other blood degradation products on the tooth surfaces, turning them brown. If the history suggests VWD and oral surgery is contemplated in these patients, hematology consultation should be obtained and the patient's blood should be typed.<br /><br /><b>Hemophilia</b><br /><br />Hemophilia is an X-linked hereditary disorder. Hemophilia A is a deficiency of factor VIII while hemophilia B (Christmas disease) is a deficiency of factor IX. Factors VIII and IX are important in the intrinsic phase of blood coagulation and their deficiency is considered severe when plasma activity of the deficient factor is <1 IU/dl (normal range, 50-100), moderate if it ranges between 2 and 5 IU/dl and mild if it is between 6 and 40 IU/dl.<br /><br />The deficiency of factors VIII and XI is characterized by bleeding from multiple sites, frequently manifested in the mouth as gingival and post-extraction hemorrhages. Hemophiliacs may experience many episodes of oral bleeding over their lifetime. Sonis and Musselman reported an average 29.1 bleeding events per year, serious enough to require factor replacement in F VIII-deficient patients, of which 9% involved oral structures. Location of oral bleeding according to Sonis and Musselman are labial frenum, 60%; tongue, 23%; buccal mucosa, 17%; gingiva and palate, 0.5%. Bleeding occurrences were most frequent in patients with severe hemophilia, followed by moderate and then mild hemophilia, and most often resulted from traumatic injury. Bleeding events may also be induced by poor oral hygiene practices and iatrogenic factors. Kaneda and colleagues reported frequency of oral hemorrhage by location in individuals' deficient of F VIII and F IX as follows: gingiva, 64%; dental pulp, 13%; tongue, 7.5%; lip, 7%; palate, 2%; buccal mucosa, 1%. Many minor oral bleeds, such as those from the gingiva or dental pulp, can be controlled by local measures while more major forms will require factor replacement.<br /><br />Hemarthrosis is a common complication in a hemophiliacs' weight-bearing joints, yet it rarely occurs in the temporomandibular joint (TMJ). There are very few reported case of TMJ hemarthrosis. Chronic hemophilic TMJ arthropathy may also occur, which requires arthrotomy, arthroscopic adhesion lysis, factor replacement, splint therapy and physical therapy. The treatment of patients with either hemophilia A or hemophilia B involves the replacement of the deficient clotting factors by intravenous infusion to either control or prevent bleeding. Patients with mild factor VIII deficiency may be treated with DDAVP to raise the factor VIII level.<br /><br />There is a group of rare inherited coagulation disorders that may present significant difficulties in diagnosis and management, and with similar orofacial manifestations of hemophilia and VWD. These rare disorders include defects of fibrinogen, prothrombin, factor V, combined deficiency of factors V and VIII, factor VII, factor X, deficiency of vitamin K-dependent factors (II, VII, IX, X), factor XI, factor XII and factor XIII deficiency. The overall frequency of these disorders in the general population is low (with the exception of factor XI deficiency). Homozygous deficiency varies from 1 in 500,000 for factor VII deficiency to 1 in 2 million for prothrombin. All the disorders are autosomally inherited and, with the exception of factor XI deficiency, generally have no significant clinical manifestations in heterozygotes. Severe deficiencies are more likely to be found in populations where marriage between blood relatives is common and, in rare cases, individuals may inherit more than one disorder.<br /><br />Factor XI deficiency, also known as hemophilia C, is the most common of the rare disorders and has a more variable bleeding tendency than hemophilia A or B. The deficiency is particularly common in Ashkenazi Jews, where the carrier rate is 8-9%. Severely deficient individuals (FXI<10 IU/dl) have a mild bleeding tendency after surgery, especially in areas with high fibrinolytic potential such as the mouth, the nose and the genitourinary tract. Spontaneous bleeding is rare, and hemarthroses are not a feature.<br /><br />Preventive and restorative dental care, particularly for the patient with hereditary hemostatic disorder, is of paramount importance for the fact that advanced dental conditions and subsequent treatments have proven to be more complicated and risky. Quite often, dental health is neglected by hemophiliacs for fear of bleeding during procedures. Surprisingly, even dental specialists avoid these candidates and contribute to the conversion of a simple dental patient to an oral surgical patient. The complexities involved in diagnosing a bleeding disorder and the rarity of a standardized protocol to handle such patients contribute to this problem.</div>
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<br style="font-size: 12px;" /><br style="font-size: 12px;" />A wide array of disorders of red cells and hemostasis encountered in internal medicine has manifestations in the oral cavity and the facial region. Most of these manifestations are non-specific, but should alert the hematologist and the dental surgeon to the possibilities of a concurrent disease of hemopoiesis or hemostasis or a latent one that may subsequently manifest itself. These manifestations must be properly recognized if the patient must receive appropriate diagnosis and referral for treatment. Proper diagnosis is essential to initiate the correct treatment.<br /><br /><br />
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com3tag:blogger.com,1999:blog-3393509504180156297.post-51299496893514405482012-07-29T00:26:00.004-07:002012-07-29T01:42:30.596-07:00Gorlin-Goltz syndrome<div dir="ltr" style="text-align: left;" trbidi="on">
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<b><span style="background-color: black; color: #943634; font-family: Arial, sans-serif;"><span style="font-size: x-large;">Abstract</span><span style="font-size: medium;"><o:p></o:p></span></span></b></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Gorlin-Goltz syndrome is an inherited
autosomal dominant disorder with complete penetrance and extreme variable
expressivity. The authors present a case of an 11-year-old girl with typical
features of Gorlin-Goltz syndrome with special respect to medical and dental
problems which include multiple bony cage deformities like spina bifida with
scoliosis having convexity to the left side, presence of an infantile uterus
and multiple odonogenic keratocysts in the maxillofacial region</span><span style="background-color: black;">.<o:p></o:p></span></span></div>
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<b><span style="background-color: black; color: #943634; font-family: Arial, sans-serif;"><span style="font-size: x-large;">Introduction</span><span style="font-size: medium;"><o:p></o:p></span></span></b></div>
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</span><span style="font-family: Arial, sans-serif;">The
Gorlin-Goltz syndrome or nevoid basal cell carcinoma (BCC) syndrome or nevus
epitheliomatodes multiplex, or nevoid basal-cell epithelioma-jaw cyst-bifid rib
syndrome is an uncommon, autosomal dominant disorder affecting multiple organ
systems which include skeletal, eye, skin, reproductive, and neural system,
although all the features are rarely observed in a single patient.</span></span><span style="font-family: Arial, sans-serif;"><span style="background-color: black;"> It
is principally characterized by cutaneous BCCs (seen in 50-97% of people with
the syndrome), multiple keratocysts (present in 75% of people), and skeletal
anomalies. The incidence of this disorder is estimated to be 1 in 50,000 to
150,000 in the general population, varying from region to region. Many of the
symptoms were first described by Jarish and White in 1894, while in 1960 Robert
J Gorlin and Robert W. Goltz defined the condition as a syndrome comprising the
principal triad of multiple basal cell nevi, jaw keratocyst, and skeletal
anomalies. </span><span style="background-color: black;">It appears in all ethnic
groups, but most often in Whites; males and females are equally affected.</span><span style="background-color: white;"><o:p></o:p></span></span></div>
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<span style="background-color: black;"><b><span style="color: #5795cc; font-family: Arial, sans-serif; font-size: 9pt;"> </span></b><b><span style="color: #943634; font-family: Arial, sans-serif;"><span style="font-size: x-large;">Case Report</span><span style="font-size: medium;"><o:p></o:p></span></span></b></span></div>
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</span><span style="font-family: Arial, sans-serif;">An
11-year-old female patient attended the Department of Oral and Maxillofacial
surgery, Dr. R. Ahmed Dental College and Hospital, with a chief complaint of
delay in the eruption of permanent teeth. A brief medical history revealed that
during late infancy (11 months) she was diagnosed to have rickets and treated
for the same. Apart from this, her past history was uneventful. Her psychomotor
development was normal and her school performance was above average.</span><span style="font-family: Arial, sans-serif;"><br />
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At the Department the patient was completely
examined. On inspection, the patient appeared to have sprengel deformity </span><span style="font-family: 'Times New Roman', serif;">(Figure 1)</span><span style="font-family: Arial, sans-serif;">. AP view of the chest revealed multiple bony cage
abnormalities. Significant findings elicited were spina bifida of C5 and C6
vertebrae with scoliosis having convexity to the left side and left and right 4</span><span style="font-family: Arial, sans-serif;"> <sup>th</sup> and 5<sup>th</sup> ribs partially fused with narrow intercostal space </span><span style="font-family: 'Times New Roman', serif;">(Figure 2)</span><span style="font-family: Arial, sans-serif;">. Complete blood count was done and appeared to be
within normal limits. Panoramic radiograph revealed multiple radiolucent areas
in the region suggestive of a cyst</span><span style="font-family: Arial, sans-serif;"> </span><span style="font-family: 'Times New Roman', serif;">(Figure
3)</span><span style="font-family: Arial, sans-serif;">.
Aspirates of right ramus region of mandible and the biochemical analysis revealed
a total protein content of 0.8 g/dl, suggestive of a keratocyst. Enucleation
with open dressing (packing the cavity with iodoform gauze) of the right ramus
region cyst was done. Enucleation of the left body mandible cyst was done. The
cystic lining was sent for histopathologic examination and was confirmed as
odontogenic keratocyst.<o:p></o:p></span></span></div>
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<b><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Figure 2: Arrows showing odontogenic keratocyst</span><span style="background-color: white;"><o:p></o:p></span></span></b></div>
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<b><span style="font-family: Arial, sans-serif; font-size: 11pt; line-height: 115%;">Figure 3: AP chest and neck radiograph showing spina
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<span style="background-color: black; font-family: Arial, sans-serif;">The patient was advised to get an ultrasonography of the
abdomen which revealed a small nodular structure in uterine fossa giving an
impression of an<span class="apple-converted-space"> </span><i>infantile
uterus</i>. Left ovary could not be visualized.</span><span style="font-family: Arial, sans-serif;"><br />
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The patient was also referred to a tertiary care
centre for genetic evaluation where karyotyping from blood was done and no
detectable abnormality was elicited.</span><br />
<br /><span style="background-color: black;">
Based on the clinical, radiographic, and
histologic findings, and referring to the diagnostic criteria for nevoid BCC
syndrome established by Evans</span><span class="apple-converted-space" style="background-color: black;"> </span><i style="background-color: black;">et
al</i><span style="background-color: black;">, and modified by Kimonos</span><span class="apple-converted-space" style="background-color: black;"> </span><i style="background-color: black;">et
al.</i><span class="apple-converted-space" style="background-color: black;"> </span><span style="background-color: black;">in 1997, the patient was
diagnosed as having Gorlin-Goltz syndrome.</span><o:p></o:p></span></div>
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</span><span style="font-family: Arial, sans-serif;">Gorlin-Goltz
syndrome is an autosomal dominant disorder with high penetrance and variable
expressivity. It is caused by the mutations in the patched tumor suppressor
gene (PTCH), a human homologue of the</span><span style="font-family: Arial, sans-serif;"> <i>Drosophila</i> gene mapped to the long arm of chromosome 9q22.3-q31.
Gorlin-Goltz syndrome's typical malformative patterns suggest that the main
function is to control the growth and development of normal tissues. It is
associated with multiple keratocysts in patients in the second decade of their
life. In the case presented here, one of the first signs was multiple cystic
lesions involving the maxilla and mandible, which have been histopathologically
diagnosed as odontogenic keratocysts. The association with odontogenic
keratocysts, however, is not clearly understood and appears in more than 90% of
the cases. All the other disorders are less frequent. Acral pits that are often
overlooked during physical examination have a characteristic dermoscopy with
red globules that are mainly distributed in parallel lines inside
flesh-colored, irregular-shaped, and slightly depressed lesions. Dermoscopy
improves the visualization of these pits.<br />
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Despite the name of the syndrome, multiple BCCs
occur only in 50% of the cases. They may vary in number from a few to 1000 and
range in size from 1 to 30 mm in diameter. BCC most often involves face and
non-exposed areas such as the back and chest. Management of superficial BCC
without hair follicle involvement can be accomplished by the topical
application of 0.1% Retinoin cream, 5% 5-Florouracil cream, 5% Imiquimod cream,
cryosurgery, and surgical excision.<br />
<br />
The diagnostic criteria for nevoid BCC were
established by Evans <i>et al</i>, and modified by Kimonis <i>et al.</i> in
1973. According to them, diagnosis of Gorlin-Goltz syndrome can be established
when two major or one major and two minor criteria are present which are
described below.<br />
<br />
<b>Major criteria</b><br />
<br />
<br />
</span><span style="font-family: 'Times New Roman', serif;"><o:p></o:p></span></span></div>
<ol start="1" type="1">
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">More
than two BCCs or one BCC under the age of 20 years.<o:p></o:p></span></li>
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">Histologically
proven odontogenic keratocyst of the jaw.<o:p></o:p></span></li>
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">Three
or more cutaneous palmar or plantar pits.<o:p></o:p></span></li>
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">Bifid,
fused or markedly splayed ribs.<o:p></o:p></span></li>
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">First
degree relative with nevoid basal cell carcinomas.<o:p></o:p></span></li>
</ol>
<div class="MsoNormal" style="margin-bottom: 0.0001pt;">
<span style="background-color: black;"><b><span style="font-family: Arial, sans-serif;">Minor
criteria</span></b><span style="font-family: Arial, sans-serif;"><br />
<br />
This consists of any one of the following
features.<br />
<br />
<br />
</span><span style="font-family: 'Times New Roman', serif;"><o:p></o:p></span></span></div>
<ol start="1" type="1">
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">Proven
macrocephaly, after adjustment for height.<o:p></o:p></span></li>
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">One
of the several orofacial congenital malformations: cleft lip or palate,
frontal bossing, 'coarse face', moderate or sever hypertelorism.<o:p></o:p></span></li>
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">Other
skeletal abnormalities: sprengel deformity, marked pectus deformity,
marked syndactyly of the digits.<o:p></o:p></span></li>
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">Radiological
abnormalities: Bridging of the sella turcica, vertebral anomalies such as
hemivertebrae, fusion or elongation of the vertebral bodies, modeling
defects of the hands and feet, or flame shaped lucencies of the hands or
feet.<o:p></o:p></span></li>
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">Ovarian
fibroma.<o:p></o:p></span></li>
<li class="MsoNormal" style="text-align: justify;"><span style="background-color: black; font-family: Arial, sans-serif;">Medulloblastoma.<o:p></o:p></span></li>
</ol>
<div class="MsoNormal">
<span style="background-color: black;"><span style="font-family: Arial, sans-serif;">In
this article, the authors have presented a case having two major
(histologically proven odontogenic keratocyst of the jaw and bifed, fused or
markedly splayed ribs) and one minor criteria (sprengel deformity).</span><span style="font-family: Arial, sans-serif; font-size: 7pt; line-height: 115%;"><o:p></o:p></span></span></div>
<div class="MsoNormal">
<span style="background-color: black; font-family: Arial, sans-serif;"><br /></span></div>
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<span style="background-color: black; font-family: Arial, sans-serif;"><br /></span></div>
<div class="MsoNormal">
</div>
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<td style="border-bottom: dotted #006666 1.0pt; border: none; mso-border-bottom-alt: dotted #006666 .5pt; padding: 0cm 3.0pt 0cm 9.0pt;"><div class="MsoNormal" style="line-height: 10.8pt; margin-bottom: .0001pt; margin-bottom: 0cm; text-align: justify;">
<span style="background-color: black;"><b><span style="color: #5795cc; font-family: Arial, sans-serif; font-size: 9pt;"> </span></b><b><span style="color: #943634; font-family: Arial, sans-serif;"><span style="font-size: x-large;">Conclusion</span><span style="font-size: medium;"><o:p></o:p></span></span></b></span></div>
</td>
<td style="padding: 0cm 3.0pt 0cm 0cm;"><div align="right" class="MsoNormal" style="line-height: 10.8pt; margin-bottom: .0001pt; margin-bottom: 0cm; text-align: right;">
<span style="background-color: black;"><br /></span></div>
</td>
<td style="padding: 0cm 3.0pt 0cm 0cm; width: 15.0%;" width="15%"></td>
</tr>
</tbody></table>
<span style="background-color: black;"><br /></span><br />
<div class="MsoNormal">
<span style="background-color: black;"><span style="font-family: Arial, sans-serif; font-size: 7pt; line-height: 115%;"><br />
<br />
</span><span style="font-family: Arial, sans-serif;">Gorlin-Goltz
syndrome is an entity that often involves the maxillofacial region. Multiple
cyst of jaw may be an indicator of this pathology and may occur as early as 7-8
years of age. It is important to make an early diagnosis and proper management
of Gorlin-Goltz syndrome mainly due to its malignant predisposition. The
guideline for diagnosis includes a family history, careful oral and skin
examination, chest and skull radiographs, panoramic radiographs of the jaws,
and pelvic ultrasonography in women. This entity shares its differential
diagnosis with cherubism.</span><span style="font-family: Arial, sans-serif;"><br />
<br />
Diagnosis and therapy of this syndrome requires
a multidisciplinary approach (oral surgeons, dermatologists, surgeons, and
neurologists and geneticists). It consists of surgical removal of tumors and
adequate treatment of keratocyst. Patients with Gorlin-Goltz syndrome require
consistent sun protection. Genetic counseling that considers the genetic risks
is advisable for all patients with this syndrome, both familial and sporadic.<o:p></o:p></span></span></div>
<div class="MsoNormal">
<span style="font-family: Arial, sans-serif;"><span style="background-color: white;"><br /></span></span></div>
<div class="MsoNormal">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black;"><br /></span></span></div>
<div class="MsoNormal">
</div>
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<td style="border-bottom: dotted #006666 1.0pt; border: none; mso-border-bottom-alt: dotted #006666 .5pt; padding: 0cm 3.0pt 0cm 9.0pt;"><div class="MsoNormal" style="line-height: 10.8pt; margin-bottom: .0001pt; margin-bottom: 0cm; text-align: justify;">
<span style="background-color: black;"><b><span style="color: #5795cc; font-family: Arial, sans-serif;"><span style="font-size: x-large;"> </span></span></b><b><span style="color: #943634; font-family: Arial, sans-serif;"><span style="font-size: x-large;">References</span><span style="font-size: medium;"><o:p></o:p></span></span></b></span></div>
</td>
<td style="padding: 0cm 3.0pt 0cm 0cm;"><div align="right" class="MsoNormal" style="line-height: 10.8pt; margin-bottom: .0001pt; margin-bottom: 0cm; text-align: right;">
<span style="background-color: black;"><br /></span></div>
</td>
<td style="padding: 0cm 3.0pt 0cm 0cm; width: 15.0%;" width="15%"></td>
</tr>
</tbody></table>
<span style="background-color: black;"><br /></span><br />
<div class="MsoNormal" style="margin-bottom: 0.0001pt;">
<span style="background-color: black;"><br /></span></div>
<table border="0" cellpadding="0" cellspacing="0" class="MsoNormalTable" style="background-position: initial initial; background-repeat: initial initial; width: 100%;">
<tbody>
<tr>
<td style="padding: 0cm 0cm 0cm 0cm; width: 1.58%;" valign="top" width="1%"><div class="MsoNormal" style="line-height: 9.6pt; margin-bottom: .0001pt; margin-bottom: 0cm; text-align: justify;">
<span style="font-family: Arial, sans-serif; font-size: 7pt;"><span style="background-color: black; color: #cc0000;">1.<o:p></o:p></span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.42%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Manfredi M, Vescovi P, Bonanini M, Porter S. Nevoid basal cell
carcinoma syndrome: A review of the literature. Int J Oral Maxillofac Surg
2004;33:117-24.</span></span></div>
<div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;"> </span></span></div>
</td></tr>
<tr><td style="padding: 0cm 0cm 0cm 0cm; width: 1.58%;" valign="top" width="1%"><div class="MsoNormal" style="line-height: 9.6pt; margin-bottom: .0001pt; margin-bottom: 0cm; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; font-size: 9px;">2.</span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.42%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Ljubenoviζ M, Ljubenoviζ D, Biniζ I, Jovanoviζ D, Stanojeviζ M.
Gorlin-Goltz syndrome. Acta Dermatovenerol Alp Panonica Adriat 2007;16:166-9. </span></span></div>
<div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;"> <o:p></o:p></span></span></div>
</td>
</tr>
<tr>
<td style="padding: 0cm 0cm 0cm 0cm; width: 1.58%;" valign="top" width="1%"><div class="MsoNormal" style="line-height: 9.6pt; margin-bottom: .0001pt; margin-bottom: 0cm; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; font-size: 9px;">3.</span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.42%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Rai S, Gauba K. Jaw cyst-basal cell nevus-bifid rib syndrome: A case
report. J Indian Soc Pedod Prev Dent 2007;25:137-9. </span></span></div>
<div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;"> <o:p></o:p></span></span></div>
</td>
</tr>
<tr>
<td style="padding: 0cm 0cm 0cm 0cm; width: 1.58%;" valign="top" width="1%"><div class="MsoNormal" style="line-height: 9.6pt; margin-bottom: .0001pt; margin-bottom: 0cm; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; font-size: 9px;">4.</span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.42%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Esposito SJ, Kast G, Bradrick JP. Basal cell nevus syndrome: A
clinical report<i>.</i> J Prosthet Dent 1995;73:405-10. </span></span></div>
<div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;"> <o:p></o:p></span></span></div>
</td>
</tr>
<tr>
<td style="padding: 0cm 0cm 0cm 0cm; width: 1.58%;" valign="top" width="1%"><div class="MsoNormal" style="line-height: 9.6pt; margin-bottom: .0001pt; margin-bottom: 0cm; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; font-size: 9px;">5.</span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.42%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Ahmed N, Salman M, Mansoor MA. Gorlin-Goltz syndrome. J Coll
Physicians Surg Pak
2007;17:568-9. <o:p></o:p></span></span></div>
</td>
</tr>
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<br />
<br /></div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com2tag:blogger.com,1999:blog-3393509504180156297.post-38063751738902522262012-07-28T12:16:00.001-07:002012-07-29T01:46:18.209-07:00Ectodermal dysplasia with true anodontia<div dir="ltr" style="text-align: left;" trbidi="on">
<span style="background-color: black;"><br /></span><br />
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<td style="border-bottom: solid #C19BFF 1.5pt; border: none; height: 18.0pt; padding: 0cm 0cm 0cm 0cm; width: 85.0%;" width="85%"><span style="background-color: black;"><b><span style="color: #cf9aff; font-family: Arial, sans-serif; font-size: 10pt;"> </span></b><b><span style="color: #cf9aff; font-family: Arial, sans-serif;"><span style="font-size: x-large;">Abstract</span><span style="font-size: medium;"><o:p></o:p></span></span></b></span></td>
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<span style="background-color: black; font-family: Arial, sans-serif;"><br /></span></div>
<div class="MsoNormal" style="background-position: initial initial; background-repeat: initial initial;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black;">The hereditary condition known as ectodermal dysplasia is characterized</span><span style="background-color: black;">
by the absence or defect of two or more ectodermally derived structures. The
most commonly observed forms of ectodermal dysplasia are the hidrotic and
hypohidrotic types; discrimination is based on the absence or presence of sweat
glands. A case of 8-year-old male child with hypohidrotic ectodermal dysplasia
with complete anodontia of primary as well as secondary dentitions is
presented. The child had a short stature, low intelligent quotient (I.Q.,), and
was underweight. The patient experienced episodes of high fever, </span><span style="background-color: black;">was intolerant
to heat, and did not sweat. He exhibited smooth and dry skin, sparse
light-colored eyebrows. Dental clinicians can be the first to diagnose
ectodermal dysplasia due to the absence of teeth.<o:p></o:p></span></span></div>
<div class="MsoNormal" style="background-position: initial initial; background-repeat: initial initial;">
<span style="background-color: black; font-family: Arial, sans-serif;"><br /></span></div>
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<span style="background-color: black; font-family: Arial, sans-serif;"><br /></span></div>
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<td style="padding: 0cm 0cm 0cm 0cm;"><h2>
<span style="font-family: 'Times New Roman', serif;"><span style="background-color: black; color: magenta; font-size: x-large;">Introduction</span></span></h2>
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<span style="font-family: Arial, sans-serif; font-size: 7pt; line-height: 115%;"><br />
<br />
</span><span style="background-color: black;"><span style="font-family: Arial, sans-serif;">Ectodermal
dysplasia is a rare congenital hereditary entity.</span><span style="font-family: Arial, sans-serif; font-size: 11pt; line-height: 115%;">The ectodermal dysplasia represents a group of
inherited conditions in which two or more ectodermally derived anatomic
structures fail to develop. Ectodermal dysplasias' represent a large and
complex group of diseases comprising of more than 170 clinical conditions.</span><span style="font-family: Arial, sans-serif; font-size: 11pt; line-height: 115%;"> </span><span style="font-family: Arial, sans-serif;"><br />
</span><span style="font-family: Arial, sans-serif; font-size: 11pt; line-height: 115%;"><br /></span></span><br />
<span style="background-color: black; font-family: Arial, sans-serif; font-size: 11pt; line-height: 115%;"><br /></span><br />
<span style="background-color: black; font-family: Arial, sans-serif; font-size: 11pt; line-height: 115%;">Depending upon the presence or absence of sweat
glands, it is divided into the hidrotic (Clouston syndrome)</span><span style="font-family: Arial, sans-serif; font-size: 11pt; line-height: 115%;"><span style="background-color: black;"> and anhidrotic types. Latter variety is characterized
by anhidrosis, hypodontia, and hypotrichosis.(CST-syndrome i.e. Christ-
Siemen-Touraine syndrome and anhidrotic/hypohidrotic, ectodermal dysplasia
being synonymous.) </span>
<br />
</span><br />
<span style="background-color: black; font-family: Arial, sans-serif;">
<br />
In most cases, this disorder seems to show an
X-linked pattern, with gene mapping to Xq12-q13.1; therefore, a male predominance
is usually seen. Female patients may show partial expression of this abnormal
gene.</span><span style="background-color: black; font-family: Arial, sans-serif;"> Individuals
affected by it show the triad comprising anhydrosis/hypohydrosis,
hypotrichosis, and dental hypoplasia.</span><span style="background-color: black;"><a href="http://www.jomfp.in/article.asp?issn=0973-029X;year=2011;volume=15;issue=2;spage=244;epage=246;aulast=Bala#ref4"></a></span><span style="background-color: black; font-family: Arial, sans-serif;"> The patients present a soft, smooth,
thin dry skin. <o:p></o:p></span></div>
<div class="MsoNormal">
<span style="background-color: black; font-family: Arial, sans-serif;"><br />
Hypodontia has been considered to be a
multifactorial condition with genetic and environmental influences, and
published opinions differ on the importance of each factor. Larmour <i>et al.,</i> state
that recent developments in molecular genetics are revealing the roles of the
homeobox genes in the control of the complex epithelial/mesenchymal
interactions that occur during dental development. Those of particular interest
for dental development are the muscle-specific homeobox genes, Msx1 and Msx2.</span></div>
<div class="MsoNormal">
<span style="background-color: black; font-family: Arial, sans-serif;"><br /></span></div>
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<b><span style="background-color: black; font-family: Arial, sans-serif;"><span style="color: magenta; font-size: x-large;">Case Report</span><span style="font-size: medium;"><o:p></o:p></span></span></b></div>
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<span style="background-color: black;"><br /></span></div>
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<span style="background-color: black; font-family: Arial, sans-serif; font-size: 7pt; line-height: 115%;"><br />
<br />
</span><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Here
is the case report of a 8-year-old male child with ectodermal dys</span><span style="background-color: black;">plasia. The
chief complaint of the patient was difficulty in mastication due to absence of
maxillary and mandibular teeth. His personal history revealed that teeth never
erupted. His mother told that his birth was normal and family history was
negative. The patient experienced episodes of high fever, was intolerant to
heat, and did not sweat. He was unable to directly look towards a light source.
Physically, the child had a short stature and was underweight. His I.Q., level
was low, and it was evident when asked about schooling. The child had sparse
light-colored eyebrows</span></span><span style="background-color: black; font-family: Arial, sans-serif;">(Figure 1). Nails were thin and brittle </span><span style="background-color: black;">(Figure
2)</span><span style="background-color: black; font-family: Arial, sans-serif;"> and </span><span style="background-color: black; font-family: 'Times New Roman', serif;">(Figure 3)</span><span style="background-color: black; font-family: Arial, sans-serif;">. Skin was dry and rough</span><span style="background-color: black; font-family: Arial, sans-serif;"> </span><span style="background-color: black;">(Figure 1)</span><span style="background-color: black; font-family: Arial, sans-serif;">,</span><span style="background-color: black; font-family: Arial, sans-serif;"> </span><span style="background-color: black;">(Figure 2)</span><span style="background-color: black; font-family: Arial, sans-serif;"> and </span><span style="background-color: black;">(Figure
3)</span><span style="background-color: black; font-family: Arial, sans-serif;">. Other
characteristics of ectodermal dysplasia, such as frontal bossing, saddle nose,
reduced vertical dimension of face due to total anodontia were also noticed.</span><span style="background-color: black; font-family: Arial, sans-serif;"><br /></span></div>
<div class="MsoNormal">
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<span style="background-color: black;"><span style="font-family: Arial, sans-serif;">Intraoral
examination revealed absence of teeth with thin alveolar crests</span><span style="font-family: Arial, sans-serif;"> </span>(Figure 4)<span style="font-family: Arial, sans-serif;"> and </span>(Figure
5)<span style="font-family: Arial, sans-serif;">. Oral mucosa appeared
dry; otherwise, no mucosal defects were seen. The tongue and palate appeared
normal.<o:p></o:p></span></span></div>
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<b><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Figure 1:
Child showing dry skin, sparse eyebrows, eyelashes, and scalp hair</span><span style="background-color: white;"><o:p></o:p></span></span></b></div>
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<b><span style="background-color: black; font-family: Arial, sans-serif; font-size: 11pt; line-height: 115%;">Figure 2: Hands showing dystrophic (thin and brittle)
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<b><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Figure 3: Feet showing dry skin and dystrophic nails</span><span style="background-color: white;"><o:p></o:p></span></span></b></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh9baz-vJqqVQqIAFw68fHP2BEIZUH75D2oEn6Lm2Lo8-D_mmVeqCNC8EyrMi9ruKXtJRf-aNIJvOPKcRtyfz6lXg5qNGwNqZExdLCxIzm8QhM-n7aBQumM2Pqx_Zb5oiDbmYfCXS35z5fe/s1600/JOralMaxillofacPathol_2011_15_2_244_84515_u4.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="224" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh9baz-vJqqVQqIAFw68fHP2BEIZUH75D2oEn6Lm2Lo8-D_mmVeqCNC8EyrMi9ruKXtJRf-aNIJvOPKcRtyfz6lXg5qNGwNqZExdLCxIzm8QhM-n7aBQumM2Pqx_Zb5oiDbmYfCXS35z5fe/s320/JOralMaxillofacPathol_2011_15_2_244_84515_u4.jpg" width="320" /></a></div>
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<b><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Figure 4: Complete anodontia of maxillary arch</span><span style="background-color: white;"><o:p></o:p></span></span></b></div>
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<b><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Figure 5: Complete anodontia of mandibular arch</span><span style="background-color: white;"><o:p></o:p></span></span></b></div>
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<span style="background-color: black;"><span style="font-family: Arial, sans-serif;">Occlusal and panoramic radiographs revealed no primary and
permanent teeth<span class="apple-converted-space"> </span></span>(Figure 6)<span style="font-family: Arial, sans-serif;">,<span class="apple-converted-space"> </span></span>(Figure 7)<span class="apple-converted-space"><span style="font-family: Arial, sans-serif;"> </span></span><span style="font-family: Arial, sans-serif;">and<span class="apple-converted-space"> </span></span>(Figure 8)<span style="font-family: Arial, sans-serif;">. In
order to improve mastication and aesthetics, both upper and lower complete
dentures were fabricated<span class="apple-converted-space"> </span></span>(Figure
9)</span><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">.</span><span style="background-color: white;"><o:p></o:p></span></span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiH1P0HMg8lddAFxTTbJaxegWgNU4uOlZifega9uV7TTgNPGbm87s5Hm8CNMCVXSQU-1gJX-AI5zBI631Z89VvkGA_lcNtgTRIQv0gEYl1hyM73hObkNLWYc1y93C01EAkQ1aUPVpCguX1c/s1600/JOralMaxillofacPathol_2011_15_2_244_84515_u6.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiH1P0HMg8lddAFxTTbJaxegWgNU4uOlZifega9uV7TTgNPGbm87s5Hm8CNMCVXSQU-1gJX-AI5zBI631Z89VvkGA_lcNtgTRIQv0gEYl1hyM73hObkNLWYc1y93C01EAkQ1aUPVpCguX1c/s320/JOralMaxillofacPathol_2011_15_2_244_84515_u6.jpg" width="238" /></a></div>
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<b><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Figure 6: Occlusal view of maxilla</span><span style="background-color: white;"><o:p></o:p></span></span></b></div>
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<b><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Figure 7: Occlusal view of mandible</span><span style="background-color: white;"><o:p></o:p></span></span></b></div>
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<b><span style="font-family: Arial, sans-serif;"><span style="background-color: black;">Figure 8: Orthopantomogram (OPG) showing complete anodontia</span><span style="background-color: white;"><o:p></o:p></span></span></b></div>
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<b><span style="background-color: black; font-family: Arial, sans-serif;">Figure 9: Post treatment photograph</span></b><b><span style="background-color: white; font-family: Arial, sans-serif; font-size: 7pt; line-height: 115%;"><o:p></o:p></span></b></div>
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<b><span style="background-color: black; color: #cf9aff; font-family: Arial, sans-serif; font-size: x-large;">Discussion<o:p></o:p></span></b></div>
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<span style="background-color: black; font-family: Arial, sans-serif;">Hypohidrotic
ectodermal dysplasia is characterized by hypohidrosis, hypotrichosis, and
hypodontia.</span><span style="font-family: Arial, sans-serif;"><span style="background-color: black;"> Ectodermal dysplasia is one of the most important
anomalies of interest to dental clinicians because of the absent or misshapen
teeth.<br />
<br />
Hypodontia is known as one of the major factors
of ectodermal dysplasia and is almost always present. In severe cases, no teeth
form. The absence of primary teeth (true anodontia) is a rare phenomenon. In this case, the patient's history and clinical and
radiographic examination revealed the absence of primary teeth. Acikgoz <i>et al.</i>, and Vieira <i>et al.</i>, also reported true anodontia of primary teeth. Total
anodontia denoted by complete developmental absence of teeth in both primary
and secondary dentitions was reported Pirgon <i>et al.,</i> and
Pannu and Singh. Radiographs showed no signs of formation of tooth
buds. It is claimed that primary teeth must be present for the development of
their permanent successors. There are no permanent teeth in the oral cavity of
the patient, similar finding reported by Vieira<i>et al</i>.<br />
<br />
The patient experienced episodes of high fever,
was intolerant to heat, and did not sweat. The patient had sparse eyebrows.
Child's inability to perspire, more comfortable during cold weather, and
absence of hair from the eyebrows with scanty eyelashes were also reported by
Gupta <i>et al.,</i> and Pannu and Singh (2002). <br />
<br />
Short stature, underweight in relation to age
and mental retardation were reported in accordance to case reported by Gupta.<br />
<br />
Management: To improve the appearance,
mastication, and speech, the child was provided with maxillary and mandibular
complete dentures similar to treatment provided by Vierra <i>et al.,</i> Pannu and Singh. </span><span style="background-color: black;">The
dental team should be aware of the clinical presentation of ectodermal
dysplasia in order to provide the correct guidance for functional, social, and
psychological needs of the patients.</span><span style="background-color: white;"><o:p></o:p></span></span></div>
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<b><span style="background-color: black; color: #cf9aff; font-family: Arial, sans-serif;"><span style="font-size: large;">References</span><span style="font-size: medium;"><o:p></o:p></span></span></b></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">1.<o:p></o:p></span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Acikgoz A, Kademoglu O, Elekdag-Turk S, Karagoz F. Hypohidrotic
ectodermal dysplasia with true anodontia of the primary dentition.
Quintessence Int 2007;28:17-23.<br />
<o:p></o:p></span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">2.<o:p></o:p></span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Neville BW, Damm DD, Allen CM, Bouquot JE. Dermatologic diseases. Oral
and Maxillofacial pathology, 3 <sup>rd</sup> ed. Noida: Elsevier
Publications; 2009. p. 741-3.<br />
<o:p></o:p></span></span></div>
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<td style="padding: 0cm 0cm 0cm 0cm; width: 2.0%;" valign="top" width="2%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">3.<o:p></o:p></span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="background-color: black; color: #cc0000;"><span style="font-family: Arial, sans-serif;">Yavuz I, Kiralp S, Baskan Z. Hypohidrotic ectodermal dysplasia: A case
report. Quintessence Int 2008;39:81-6. </span><span style="font-family: Arial, sans-serif;"><o:p></o:p></span></span></div>
<div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;"> <o:p></o:p></span></span></div>
</td>
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<td style="padding: 0cm 0cm 0cm 0cm; width: 2.0%;" valign="top" width="2%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">4.<o:p></o:p></span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Suprabha BS. Hereditary ectodermal dysplasia: A case report. J Indian
Soc Pedo Prev Dent2002;20:37-40.<br />
<o:p></o:p></span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">5.<o:p></o:p></span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Gupta S. Christ-siemen-touraine syndrome-A case report. Journal of
Indian dental association2003;74:533-7.<br />
<o:p></o:p></span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">6.<o:p></o:p></span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Rajendran R. Diseases of the skin. In: Shafer WG, Hine MK, Levy BM,
Rajendran Rand Sivapathasundharam editors. A text book of oral pathology. 5 <sup>th</sup> ed.
New Delhi: Elsevier Publications;2006.p.1099-102.<br />
<o:p></o:p></span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">7.<o:p></o:p></span></span></div>
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<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="background-color: black; color: #cc0000;"><span style="font-family: Arial, sans-serif;">Larmour CJ, Mossey PA, Thind BS, Forgie AH, Stirrups DR. Hypodontia-A
retrospective review of prevalence and etiology, Part 1. Quintessence Int
2005;36:263-70. </span><span style="font-family: Arial, sans-serif;"><o:p></o:p></span></span></div>
<div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;"> <o:p></o:p></span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">8.<o:p></o:p></span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Vieira KA, Teixeira MS, Guirado CG, Gaviao MB. Prosthodontic treatment
of hypohidrotic ectodermal dysplasia with complete anodontia: Case report.
Quintessence Int 2007;38:75-80.<br />
<o:p></o:p></span></span></div>
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<td style="padding: 0cm 0cm 0cm 0cm; width: 2.0%;" valign="top" width="2%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">9.<o:p></o:p></span></span></div>
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<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="background-color: black; color: #cc0000;"><span style="font-family: Arial, sans-serif;">Pirgon O, Atabek ME, Tanju IA. Congenital anodontia in ectodermal
dysplasia. J Pediatr Endocrinol Metab 2008;21:1111-2. </span><span style="font-family: Arial, sans-serif;"><o:p></o:p></span></span></div>
<div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;"> <o:p></o:p></span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">10. <o:p></o:p></span></span></div>
</td>
<td style="padding: 0cm 0cm 0cm 0cm; width: 98.0%;" width="98%"><div class="MsoNormal" style="margin-bottom: .0001pt; margin-bottom: 0cm; mso-line-height-alt: 9.6pt; text-align: justify;">
<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Pannu K, Singh BD. Ectodermal dysplasia with total anodontia:
Rehabilitation of a seven year old child. J Indian Soc Pedo Prev Dent
2002;20:114-7.<br />
<o:p></o:p></span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">11. <o:p></o:p></span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="background-color: black; color: #cc0000;">Gupta HL, Singh H, Prabhakar BR. Anhidrotic hereditary ectodermal
dysplasia. Indian J Pediat 1965;32:173-5. <o:p></o:p></span></span></div>
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<br /></div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com0tag:blogger.com,1999:blog-3393509504180156297.post-65592748021483762902012-07-24T01:03:00.000-07:002012-07-24T01:08:01.642-07:00Four-Rooted Mandibular First Molar with an Unusual Developmental Root Fusion Line: A Case Report<div dir="ltr" style="text-align: left;" trbidi="on">
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<h2 style="text-align: left;">
<span style="color: orange; font-size: x-large;">Abstract</span></h2>
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The paper describes the anatomical variation of four roots in a mandibular permanent first molar diagnosed using multiple angulated preoperative radiographs and its successful nonsurgical endodontic management. Careful observation and exploration of the pulpal floor using a dental operating microscope revealed a peculiar developmental root fusion line on the pulp chamber floor. Based on the above observation, a correlation between this unusual line and the existence of additional roots has been proposed and discussed.</div>
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<h2>
<span style="color: orange; font-size: x-large;">1. Introduction</span></h2>
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One of the most important aspects in contemporary endodontics is a thorough knowledge of the internal and external root anatomy. Additional roots and root canals if not detected could lead to endododontic failure. Thus, a thorough knowledge of the root and root canal morphology and a good anticipation of their possible morphological variations will help reduce endodontic failure caused by incomplete debridement and obturation. Anatomical variation is prevalent in many teeth, with some teeth having as many as 5 separate roots or even seven or eight separate root canals. The mandibular first molar, or the “6-year molar,” which is the largest tooth in volume and most complex in root and canal anatomy, is possibly the most treated and least understood posterior tooth.The purpose of the present paper is to report the successful nonsurgical endodontic management of a four-rooted permanent mandibular first molar with each root containing its own independent root canal and additionally to discuss a peculiar observation of the pulpal floor.</div>
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<span style="color: orange; font-size: x-large;">2. Case Report</span></h2>
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A 27-year-old female reported with the chief complaint of a “fractured filling” in her left lower back tooth. History revealed intermittent pain localized to the same tooth during mastication. The tooth was previously restored with a silver amalgam restoration 7 years back. Clinical examination revealed a silver amalgam restoration with secondary caries in the left mandibular first molar (tooth 19) which was tender to percussion. Vitality tests elicited no response. Preoperative radiographs showed widening of periodontal ligament space in relation to the mesial root apex. In addition, radiographic apical contour of the tooth suggested that there might be two distal and two mesial roots (Figure 1(a)). From the clinical and radiographic findings a diagnosis of pulpal necrosis with symptomatic apical periodontitis was made and endodontic treatment was initiated.</div>
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<span style="background-color: black;"><b>Figure 1: </b>(a) Preoperative radiograph of tooth 19.</span>
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<span style="background-color: black;"><b>Figure 1: </b>(b) Access opening showing four canals (MBR: Mesiobuccal; MLR: Mesiolingual; DBR: Distobuccal; DLR: Distolingual). </span></div>
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<span style="background-color: black;"><b>Figure 1: </b>(c) Working length radiograph of tooth 19 in eccentric angulation.</span></div>
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<span style="background-color: black;"><b>Figure 1: </b>(d) Postobturation radiograph.</span></div>
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Following endodontic access cavity preparation, two mesial and one buccally placed distal canal orifice was identified. Upon visual inspection of the floor of the pulp chamber using a dental operating microscope, a dark line was observed extending from the distal canal orifice towards the distolingual corner. At this corner, the overlying dentin was removed and a second distal canal orifice was detected. The conventional access was modified to improve access to the additional canals (Figure 1(b)). Root canal orifices were named as per the nomenclature proposed by Albuquerque et al. Working length was confirmed (Figure 1(c)) and the canals were instrumented. Calcium hydroxide was placed as an intracanal medicament with a lentulospiral and the access cavity was sealed with Cavit G. The patient was asymptomatic at the next appointment, a week later, which allowed for root canal obturation and a coronal composite restoration (Figure 1(d)).
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<span style="color: orange; font-size: x-large;">3. Discussion</span></h2>
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A number of anatomical variations have been described in the mandibular first molar. Kottoor et al. reported the presence of three distal canals, while Ghoddusi et al. noted the presence of four distal canals. Presence of three and four mesial root canals has also been reported. Like the number of root canals, the number of roots may also vary. The major variant in this tooth type is the presence of an additional third root; a supernumerary distolingual root called radix entomolaris. Its prevalence varies in different populations ranging from 3% of the African population to more than 30% of the Mongoloid population. An extremely rare variation of an additional mesiobuccal root is called the radix paramolaris (RP).</div>
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Morita in a laboratory study examined 2,164 extracted mandibular first molars. He reported only a single four-rooted first molar, in a male patient, which formed 0.04% of the total sampled Japanese population (Mongoloid race). Various other extensive laboratory studies in different population and ethnic groups have not reported a single four-rooted mandibular first molar. Only two case reports have previously described the presence of four-rooted mandibular first molar. However, both have reported three distal and one mesial root. The present report describes a four-rooted mandibular first molar with two mesial and two distal roots in which each of the four roots have an independent root canal.</div>
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In mandibular first molars with two roots and each root having two distinct canals (for instance, mesiobuccal and mesiolingual canals in the mesial root), the angle formed between the developmental root fusion lines (DRFLs) joining these canal orifices is more obtuse. This can be visualized in both the mesial and distal DRFLs of such two-rooted mandibular first molars (Figure 2(a)). In the case presented here, the angle formed between the DRFLs joining both the mesial and distal orifices was more acute; presenting in the form of a letter “X” (Figure 1(b)). This could signify that when an additional root is present both mesially and distally, the angle between the DRFLs which connect the orifices changes to a more acute angle (Figure 2(b)). Thus, the relationships of the DRFLs joining the canal orifices could provide an insight into the root anatomy of mandibular first molars. Further clarification of these observations would be required by individual laboratory studies or other case reports to allow their use as diagnostic criteria in cases of four-rooted mandibular first molars wherein each root presents with a single canal.</div>
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<b>Figure 2: </b>Diagrammatic representations illustrating the correlation between the developmental root fusion lines (DRFL) on the pulpal floor with the canal orifices in permanent mandibular first molars with varying root and root canal anatomy. (a) A more obtuse angle (<i>α</i>) between the connecting DRFL in teeth with 2 roots, 4 canals. (b) A more acute angle (<i>α </i><sup>1</sup>) between the connecting DRFL in teeth with 4 roots, 4 canals.
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<span style="color: orange; font-size: x-large;">4. Conclusion</span></h2>
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Successful endodontic treatment begins with proper clinical and radiographic examinations. A practitioner must be vigilant, as variations of root and canal anatomy might be encountered at any time during treatment. This paper may intensify the complexity of mandibular first molar variation and is intended to reinforce clinicians’ awareness of the variable morphology of root canals.</div>
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<span style="color: orange; font-size: x-large;">References</span></h2>
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<li id="B1" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">L. R. G. Fava, “Root canal treatment in an unusual maxillary first molar: a case report,”<i>International Endodontic Journal</i>, vol. 34, no. 8, pp. 649–653, 2001.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B2" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">R. R. Slowey, “Radiographic aids in the detection of extra root canals,” <i>Oral Surgery Oral Medicine and Oral Pathology</i>, vol. 37, no. 5, pp. 762–772, 1974.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B3" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">R. C. Burns and E. J. Herbranson, “Tooth morphology and access cavity preparation,” in <i>Pathways of the Pulp</i>, S. Cohen and R. C. Burns, Eds., pp. 173–229, Mosby, St Louis, Mo, USA, 8th edition, 2002.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"></span></span></li>
<li id="B4" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">J. Kottoor, S. Hemamalathi, R. Sudha, and N. Velmurugan, “Maxillary second molar with 5 roots and 5 canals evaluated using cone beam computerized tomography: a case report,” <i>Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology</i>, vol. 109, no. 2, pp. e162–e165, 2010.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B5" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">E. S. Reeh, “Seven canals in a lower first molar,” <i>Journal of Endodontics</i>, vol. 24, no. 7, pp. 497–499, 1998.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B6" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">J. Kottoor, N. Velmurugan, R. Sudha, and S. Hemamalathi, “Maxillary first molar with seven root canals diagnosed with cone-beam computed tomography scanning: a case report,” <i>Journal of Endodontics</i>, vol. 36, no. 5, pp. 915–921, 2010.</span></li>
<li id="B7" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">J. Kottoor, N. Velmurugan, and S. Surendran, “Endodontic management of a maxillary first molar with eight root canal systems evaluated using cone-beam computed tomography scanning: a case report,” <i>Journal of Endodontics</i>, vol. 37, no. 5, pp. 715–719,2010.</span></li>
<li id="B8" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">D. V. Albuquerque, J. Kottoor, and N. Velmurugan, “A new anatomically based nomenclature for the roots and root canals-part 2: mandibular molars,” <i>International Journal of Dentistry</i>, vol. 2012, Article ID 814789, 2012.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"></span></span></li>
<li id="B9" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">J. Kottoor, R. Sudha, and N. Velmurugan, “Middle distal canal of the mandibular first molar: a case report and literature review,” <i>International Endodontic Journal</i>, vol. 43, no. 8, pp. 714–722, 2010.</span></li>
<li id="B10" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">J. Ghoddusi, N. Naghavi, M. Zarei, and E. Rohani, “Mandibular first molar with four distal canals,”<i>Journal of Endodontics</i>, vol. 33, no. 12, pp. 1481–1483, 2007.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B11" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">H. Fabra-Campos, “Unusual root anatomy of mandibular first molars,” <i>Journal of Endodontics</i>, vol. 11, no. 12, pp. 568–572, 1985.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B12" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">G. H. Sperber and J. L. Moreau, “Study of the number of roots and canals in Senegalese first permanent mandibular molars,” <i>International Endodontic Journal</i>, vol. 31, no. 2, pp. 117–122, 1998.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B13" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">R. T. Walker and L. E. Quackenbush, “Three-rooted lower first permanent molars in Hong Kong Chinese,” <i>British Dental Journal</i>, vol. 159, no. 9, pp. 298–299, 1985.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B14" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">F. L. Calberson, R. J. De Moor, and C. A. Deroose, “The radix entomolaris and paramolaris: clinical approach in endodontics,” <i>Journal of Endodontics</i>, vol. 33, no. 1, pp. 58–63, 2007.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B15" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">M. Morita, “Morphological studies on the roots of lower first molars in Japanese,” <i>Shika Gakuho</i>, vol. 90, no. 6, pp. 837–854, 1990 (Japanese).<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B16" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">H. A. Ahmed, N. H. Abu-Bakr, N. A. Yahia, and Y. E. Ibrahim, “Root and canal morphology of permanent mandibular molars in a Sudanese population,” <i>International Endodontic Journal</i>, vol. 40, no. 10, pp. 766–771, 2007.</span></li>
<li id="B17" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">R. Peiris, M. Takahashi, K. Sasaki, and E. Kanazawa, “Root and canal morphology of permanent mandibular molars in a Sri Lankan population,” <i>Odontology</i>, vol. 95, no. 1, pp. 16–23, 2007.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B18" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">A. A. Al-Qudah and L. A. Awawdeh, “Root and canal morphology of mandibular first and second molar teeth in a Jordanian population,” <i>International Endodontic Journal</i>, vol. 42, no. 9, pp. 775–784, 2009.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
<li id="B19" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">S. Friedman, J. Moshonov, and A. Stabholz, “Five root canals in a mandibular first molar,”<i>Endodontics and Dental Traumatology</i>, vol. 2, no. 5, pp. 226–228, 1986.</span></li>
<li id="B20" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px 0px 12px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">S. J. Lee, K. H. Jang, L. S. W. Spangberg et al., “Three-dimensional visualization of a mandibular first molar with three distal roots using computer-aided rapid prototyping,” <i>Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology</i>, vol. 101, no. 5, pp. 668–674, 2006.</span></li>
<li id="B21" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; text-align: justify; vertical-align: baseline;"><span style="color: #cc0000;">P. Krasner and H. J. Rankow, “Anatomy of the pulp-chamber floor,” <i>Journal of Endodontics</i>, vol. 30, no. 1, pp. 5–16, 2004.<span class="reflinks" style="border: 0px none; font-family: inherit; font-style: inherit; margin: 0px; outline: none 0px; padding: 0px; vertical-align: baseline;"> </span></span></li>
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<br /></div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com0tag:blogger.com,1999:blog-3393509504180156297.post-59882790784541026102012-07-23T18:43:00.001-07:002012-07-23T19:23:45.844-07:00Lasers used in Operative Dentistry - A presentation<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="http://www.slideshare.net/slideshow/embed_code/2567967">Lasers used in Operative Dentistry</a></div>
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<span style="background-color: black; color: orange; font-size: large;"><span class="notranslate">LASERS USED IN OPERATIVE DENTISTRY</span> — Presentation Transcript</span></h2>
<ul class="transcripts h-transcripts" style="color: #3b3835; font-family: 'Helvetica Neue', Helvetica, Arial, sans-serif; list-style: none; margin: 0px 180px 0px 0px; padding: 0px; text-align: -webkit-auto;">
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">1. GOOD AFTERNOON</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">2. LASERS USED IN OPERATIVE DENTISTRY GUIDED BY: Prof. H.D.Adhikary Dept. of Conservative DentistryDr.R.Ahmed Dental College & Hospital</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">3. CONTENTSIntroductionHistory of lasersComponents of lasersTypes of lasersApplication of lasers in operative dentistrySummary</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">4. INTRODUCTIONDentistry has advanced a lot.Among various advances, one which have good scope of improvement is the use oflasersin dentistry.Recent advances in laser technology will bring revolution in dentistry.Laser is an acronym forlightamplification by stimulatedemission ofradiation.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">5. DISCOVERY OF LASERS:It was discovered by Shallow & Towns in 1958. First working laser was built by Mailman ofHughesresearch laboratories in 1960.HISTORY OF LASERS IN DENTISTRY:Vain used a ruby laser & reported extensive deep destruction of carious tissue along with melting of dentin.Paghdiwala[U.S.A] in 1988,first time tested the ability of Er:yag laser on dental hard tissue. In 1997,Er:yag laser was cleared for marketing by Food & drug administration of U.S.A.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">6. COMPONENTS OF LASERThere are 3 main parts of laser delivery system.(1).LASING OR ACTIVE MEDIUMIt is the material which is capable of absorbing the energy produced by the external sourcethrough subatomic configuration of its component molecules & subsequently giving theexcess energy as photons of light.It can be solid, liquid or gas.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">7. (2).ENERGY OR PUMPING SOURCEIt is used to excite or pump the atoms inlasing medium to their higher energy levels that are essential for laser production.It can be electrical,thermal,chemical oroptical.(3).OPTICAL OR RESONATING CHAMBERThe lasing medium is located within theoptical chamber.It is a cylindrical structure with fullyreflecting mirror on one side & partially reflecting mirror on other side--parallel to each other.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">8. This arrangement allows reflection of photonsof light, back & across the chamber.It will result in production of intense photo resonance within the medium.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">9. TYPES OF LASERS2 categories of lasers are used in medicine & dentistry(1).HARD LESARS -Longer wavelength- Cuts the tissue by ablation.- Used for tooth & bone applications.(2).SOFT LASERS OR LOW LEVEL LASERS- Low energy wavelengths - Cuts tissues by coagulation,vapourisation & carbonisation.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">10. - They are believed to stimulate circulation & cellular activity & causes various effectssuch as anti-inflammatory,vascular,musclerelaxant,analgesia& tissue healing.There are many types of lasers used in dentistry, depending upon their active medium(1).CARBONDIOXIDE LASER- WAVELENGTH:10.6um - USES: SOFT TISSUES , DENTIN DESENSITIZATION(2).ARGON LASERS- WAVELENGTH:488,514.5um - USES: CURING , SOFT TISSUE DESENSITIZATION</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">11. (3).Nd:YAG[NEODYMIUM:YTTRIUM-ALLUMINIUM GARNET] LASER- WAVELENGTH:1.064um - USES: SOFT TISSUE DESENSITIZATION , ANALGESIATOOTH WHITENING , PERIODONTICS, ENDODONTICS(4).KTP[POTASIUM-TITANYL PHOSPHATE] LASER(5).HELIUM-NEON[He-Ne](6).RUBY LASER(7).EXCIMER LASER</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">12. (8).HOLMIUM[Ho]:YAGLASER(9).ERBIUM[Er]:YAG LASER- WAVELENGTH:2.94um - USES: HARD TISSUE(10).ERBIUM-CHROMIUM[Er-Cr]:YSGG LASER- WAVELENGTH: 2.79um - USES: HARD TISSUE(11).DIODE- WAVELENGTH: 800-830um - USES:SOFT TISSUE , PERIODONTICS</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">13. Effects of lasers</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">14. Effects on tissues on certain temperatures60`100`200`</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">15. APPLICATION OF LASERS IN OPERATIVEDENTISTRYDIAGNOSIS OF DENTAL CARIES(A).INFRARED LASER FLUORESCENCE[DIAGNODENT]- Diagnodent is an instrument, recently designed to facilitate the detection of dental caries. - Used for detection of caries on occlusal & smooth surface.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">16. (B).LASER INDUCED FLUORESCENCE -Kutsch in 1992,illuminated carious & non carious tissue with argon laser along with dark field photography. - He reported that while illuminating, carious lesionhas clinical appearance of dark,fiery,orange-red colour.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">17. CARIES DETECTION</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">18. CAVITY PREPARATION WITH LASER- NUMBER OF STUDIES HAVE BEEN PERFORMED FOR THE USE OF Er:yag LASER FOR CAVITY PREPARATION. - Results of studies says that little or no noticeable pulp reaction is produced while preparing the cavity with Er:yag laser. - It is safe & can be used for cavity preparation.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">19. CAVITY PREPARATIONWITH LASERS</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">20. Effect on carious lesions</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">21. ADDITIONAL BENEFITSA.)minimises patient fear of the drill.B.)no irritating sound like traditional drills.C.)the cavity with laser preparation appears open,patent,fresh & devoid of all debris.D.)mono-infection with Enterococcusfaecalis is avoided - hence sterile cavity.E.)melts the dentin & blocks the tubules,thus hydrodynamic theory of dentin sensitivity is ruled out.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">22. PREVENTION OF DENTAL CARIES WITHLASERSLaser can be used for prevention of dental caries.Different types of lasers increases the resistance to dental caries by reducing the rate of demineralization of substance of enamel & dentin.Argon laser alters the surface characteristics of enamel to make it caries resistant.----</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">23. MECHANISM OF ACTIONCarbonate is lost from carbonated appetite mineral of tooth during laser irradiationPulsed co2 laser irradiation interacts with the phosphate group in dental materialsIt gets preferentially absorbed & transformedefficiently to heatCarbonated hydroxyapetite in the surface & in the immediate subsurface of enamel is heated at temp.greater than 400`cCarbonate is decomposed, leaving behind the a hydroxyapetitelike mineral that is less soluble</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">24. BLEACHING WITH LASERS- Power bleaching is the term used for acceleratedin-office tooth whitening procedures, using laser or Xenon plasma arc-curing light.(A).ARGON LASER- A true laser light is delivered to chemical agent. - The action is to stimulate crystals in the chemical. - No thermal effect, so less dehydration of enamel. - The treatment time is 10sec. per application per tooth.It is the advantageous for clinician & patient.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">25. (B).DIODE LASER- A true laser light produced from a solid statesource. - It is ultra fast, taking 3 to 5 sec. to activatebleaching agent. - This type of lasers produce no heat.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">26. PHOTOPOLYMERIZATION OF COMPOSITE RESIN WITH LASER - ARGON LASERS ARE USED FOR THIS PURPOSE. - FOR POLYMERIZATION OF CAMPHORQUINONE ACTIVATED COMPOSITE RESIN,THE ARGON LASERINCREASES;~ THE DEPTH OF CURE ~ THE DIAMETRIC TENSILE STRENGTH ~ ADHESIVE BOND STRENGTH ~ DEGREE OF POLYMERIZATION OF MATERIELS.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">27. REDUCES;~ Acid solubility of surrounding enamel Decreases the time of activation Significantly.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">28. ADVANTAGES OF LASERS(1).Minimal damage to surrounding tissues.(2).Haemostatic effect by sealing blood vessels.(3).Reduction of postoperative inflammation & edema.(4).Little postoperative scarring.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">29. (5).Reduction in postoperative pain sensationsince nerve endings are blocked.(6).Dressing & suturing is not required forwound closer.(7).Operating time is reduced.(8).Sterilization of wound due to reduction inin amount of microorg. exposed to laserirradiation.(10).Excellentwound healing.(11).Laser exposure to tooth enamel causes reduction in caries activity.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">30. (12).Patient becomes free of fear & anxiety. (13).Advantageous for medically compromised patients,since no medication is required like antibiotics or pain-killers.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">31. DISADVANTAGES OF LASERS(1).Laser beam could injure the patient or operator By direct beam or reflected light, causing retinalburns.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">32. (2).It available only at big hospital & treatment is very expensive.(3).Specially trained person is needed.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">33. SUMMARYAs the research on use of laser in dentistry isgiving bright results, lasers are getting more & more famous among dentists.</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">34. Special thanks goes to:a.) Dr. Soumen Palb.) Mr.AbhisekChatterjeec.) Mr.NurulHasanMollahd.)Mr.Tousif Ahmed</span></li>
<li style="line-height: 18px; margin: 0px 0px 15px;"><span style="background-color: black;">35. Thank you….</span></li>
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com4tag:blogger.com,1999:blog-3393509504180156297.post-74743507711316061942012-07-23T18:15:00.002-07:002012-07-23T18:23:28.976-07:00A novel wavelet neural network based pathological stage detection technique for an oral precancerous condition<div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: x-large;">Abstract</span></h2>
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<strong style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><b>Aim</b>:</strong> To describe a novel neural network based oral precancer (oral submucous fibrosis; OSF) stage detection method.</div>
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<strong style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><b>Method</b>:</strong> The wavelet coefficients of transmission electron microscopy images of collagen fibres from normal oral submucosa and OSF tissues were used to choose the feature vector which, in turn, was used to train the artificial neural network.</div>
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<strong style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><b>Results</b>:</strong> The trained network was able to classify normal and oral precancer stages (less advanced and advanced) after obtaining the image as an input.</div>
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<strong style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><b>Conclusions</b>:</strong> The results obtained from this proposed technique were promising and suggest that with further optimisation this method could be used to detect and stage OSF, and could be adapted for other conditions.</div>
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<span style="color: #783f04; font-size: x-large;">Introduction</span></h2>
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Cancers of the oral cavity are increasing at an alarming rate and have been reported to account for approximately 220 000 new cases each year for men (5% of all cancers) and about 90 000 for women (2% of all cancers). Two third of these cases are recorded in developing countries. A high incidence of oral cancer is seen in the Indian subcontinent as a result of the late diagnosis of potential precancerous lesions and conditions. Oral submucous fibrosis (OSF) is an insidious chronic progressive precancerous condition of the oral cavity and oropharynx with a high degree of malignant potential. A large proportion of these precancerous lesions convert to squamous cell carcinoma, the malignant transformation rate being in the order of 7.6%. OSF is prevalent in the Indian subcontinent in all age groups and across all socioeconomic strata, but the incidence exhibits regional and interregional variations (0.2–4.57%), being highest in Southern India. This disease is now a public health issue in many parts of the world including the UK, South Africa, and many southeast Asian countries.</div>
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“The simple pathological evaluation procedure currently used for oral submucous fibrosis does not provide a quantitative analysis of the vital changes in the tissues”</div>
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The aetiology of OSF is not well understood, but maximum importance has been given to the chewing of areca nut in isolation or in combination with betel leaf or other tobacco products. Arecoline, an active alkaloid found in betel nuts, stimulates fibroblasts to increase collagen production by 150%.However, available data suggest that a multifactorial mechanism is involved in the pathogenesis of OSF, including areca nut chewing, the ingestion of chillies, and deficiencies of nutrients, trace metals, and vitamins, in addition to hypersensitivity to various dietary constituents and genetic and immunological predisposition. </div>
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Presently, no specific diagnostic test is available for OSF except for histopathological studies. The pathological status of OSF is mainly assessed by light microscopic studies of oral biopsies and clinical evaluation. Microscopically, the main features of OSF are less vascularised collagenous connective tissue with occasional progressive atrophy of the muscle fibres, a minimal to moderate degree of chronic inflammatory infiltration, and atrophic overlying epithelium with a variable degree of dysplastic changes.</div>
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The main histopathological characteristic of OSF is the deposition of collagen in the subepithelial connective tissue leading to epithelial atrophy. It has been found that exposure of buccal mucosal fibroblasts to alkaloid may result in the accumulation of collagen. Reduced degradation of the α1(I) collagen trimer synthesised by OSF fibroblasts may induce alteration of the ratio of α1(I) to α2(I) chains.<span style="line-height: 0px;"> </span>Collagenase activity has been found to be lower in OSF than in normal oral mucosa. These findings suggest that OSF should be considered as a collagen metabolic disorder resulting from alkaloid exposure and individual variations in collagen metabolism.</div>
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The simple pathological evaluation procedure currently used does not provide a quantitative analysis of the vital changes in the tissues—that is, epithelial dysplastic changes, subepithelial fibrosis, etc. Accordingly, histopathological grading of the disease state is also empirical. Ultrastructural studies on collagen in oral submucous fibrosis qualitatively noted variations in the width and periodicity of fibrillar collagen between diseased and normal tissue specimens. Therefore, our present study analyses transmission electron micrography (TEM) images of subepithelial fibrillar collagen in early and advanced stages of OSF and compares them with those obtained from normal oral mucosa by applying a novel computer aided technique. In this computer aided diagnostic (CAD) approach, a specific attempt is made to grade OSF stages in a quantitative manner, to minimise the ambiguity in the presently accepted empirical (clinical and histopathological) diagnostic procedure of OSF. This quantitative approach may finally lead to the identification of suitable biomarkers for the more specific grading of OSF.</div>
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CAD refers to a diagnostic process during which a radiologist uses computer analysis as a diagnostic aid to achieve a more accurate interpretation of the disease state. The precancer diagnostic importance of the CAD system coupled with wavelet ANN (artificial neural network) is studied by analysing collagen in OSF and normal oral mucosa. The wavelet transformation technique is ideal for obtaining information from signals that are aperiodic, noisy, intermittent, or transient. ANN is an important statistical tool that can improve the characterisation of pathological images especially of precancer and cancers. There are only a few reports on the successful applications of machine learning to precancer diagnosis.<span style="line-height: 0px;"> </span>Thus, our study could strengthen the foundation of ANN in CAD applications.</div>
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<b><span style="font-size: x-large;">MATERIALS AND METHODS</span></b></h2>
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<span style="font-size: large;">Selection of patients</span></h3>
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Clinically diagnosed patients with OSF were subjected to incisional biopsy with their previous consent at the department of oral and maxillofacial pathology, R Ahmed Dental College and Hospital, Kolkata, India for histopathological evaluation. Portions of each oral mucosal biopsy from the clinically and histologically confirmed cases of early (n <img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" />=<img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /> 52) and advanced (n <img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" />=<img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /> 58) stages of OSF were taken for the analysis of fibrillar collagen ultrastructure by TEM. Normal healthy volunteers (n <img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" />=<img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /> 35) of similar age and food habits, but without the oral habit, were also included in our study.</div>
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<span style="font-size: large;">Clinical classification of OSF stages</span></h3>
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The classification/grading of OSF was carried out according to the degree of trismus, which directly correlates with the degree of fibrosis, progression of the disease, and location of the OSF lesion in the oral mucosa. Trismus, or reduction in the overall mouth opening, is one of the most reliable manifestations of OSF, and it has been a cardinal clinical feature for grading patients into different groups. The gradation of trismus and in turn the gradation of the disease process was assessed by measuring the distance between the incisal edges of the upper and lower central incisal teeth—the interincisal distance (IID)—using vernier calipers as follows: mild or moderate grade (IID, <img alt="[gt-or-equal, slanted]" border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/ges.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /> 1.5 but < 3.5 cm) and severe grade (IID, < 1.5 cm), considering IID <img alt="[gt-or-equal, slanted]" border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/ges.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /> 3.5 as normal.</div>
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<span style="font-size: large;">TEM study</span></h3>
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Biopsy samples (1 × 2 mm) were fixed in primary fixative (2.5% glutaraldehyde in 0.12M phosphate buffer) for 48 hours at 4°C. The tissues were then washed in 0.12M phosphate buffer and postfixed in 2% osmium tetroxide for two hours at room temperature with constant shaking. After postfixation, tissues were dehydrated in graded alcohol and processed for spur embedding. Ultrathin sections were cut on the Nova Ultratome (LKB, Sweden), collected on copper grids, and stained with uranyl acetate and lead citrate. Sections were observed under TEM (JEOL, Japan; 100CX TEM) at 60 kV.</div>
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<span style="font-size: large;">Wavelet ANN based analysis of TEM collagen images</span></h3>
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We have devised a novel wavelet ANN based scheme to detect and grade the stages of OSF (advanced and less advanced) by analysing TEM images of subepithelial collagen fibres from normal healthy volunteers and patients with OSF. Figure 1A<a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f1/" rid-figpopup="f1" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -1em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">1A–F</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a>–F shows representative images at a magnification of ×64 000.</div>
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Figure 1</div>
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<span style="font-size: 15px;">Transmission electron microscopy images of collagen. (A) Normal transverse section (TS); (B) TS of less advanced oral submucous fibrosis (OSF); (C) TS of advanced OSF; (D) normal longitudinal section (LS); (E) LS of less advanced OSF; (F) LS of advanced OSF.</span>
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Accordingly, a set of 145 random samples (64 × 64 pixels) of subepithelial collagen image data was used to make a large training set. The depth of all the images was 8. Two hundred and fifty six different shades were needed to represent all the colours from complete black to absolute white. This 64 × 64 pixel image was decomposed into four levels using the “HAAR” wavelet. Both the approximate and detail coefficients were extracted for each level. The feature vector was chosen judiciously with the combination of these approximate and detail coefficients. These feature vectors were used to train the ANN. During the test, the images were decomposed into 64 × 64 non-overlapping pixel blocks. The approximate and detail coefficients were extracted for each block. These data were then fed into the network. The output can be of three different types: advanced and less advanced stage of OSF and normal. Based on the number of blocks in each of these three classes, a decision will have been taken for the test image.</div>
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<span style="line-height: 1.2857;">Wavelet and sub-band decomposition and feature vector extraction</span><span style="line-height: 0px;"> </span><span style="line-height: 1.2857;">(</span><a href="http://www.mathworks.com/access/helpdesk/toolbox/wavelet/wavelet.shtml" ref="reftype=extlink&article-id=1770817&issue-id=141132&journal-id=162&FROM=Article%7CBody&TO=External%7CLink%7CURI&rendering-type=normal" style="border: 0px; color: #642a8f; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;" target="pmc_ext">http://www.mathworks.com/access/helpdesk/toolbox/wavelet/wavelet.shtml</a><span style="line-height: 1.2857;">)</span></h3>
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In continuous signal analysis, a signal <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">g(t)</em> is often represented by a weighted sum of basis functions:</div>
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where <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">ψ<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub>(t)</em> is the basis function and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">c<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em> is the coefficient.</div>
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Multiresolution analysis can be done using continuous and discrete wavelet transforms (CWT and DWT). To define CWT, a scaled and translated version of the basis function, called the mother wavelet, is used to achieve the constant Q requirement. Considering a real band pass filter with impulse response<em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">ψ(t)</em> of zero mean:</div>
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<span style="font-size: 15px;">The CWT is defined as:</span>
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where <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">ψ*(t)</em> is the complex conjugate of <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">ψ(t)</em>, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">aɛR+</em>, and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">bɛR</em>.</div>
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Equation 3 can be rewritten as:</div>
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<span style="font-size: 15px;">where:</span></div>
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<span style="font-size: 15px;">In the case of discrete signals the theory of filter banks and their application to sub-band signal decomposition must be briefly discussed. For example, a simple two channel filter bank structure (fig 2</span><a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f2/" rid-figpopup="f2" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -0.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">2)</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a><span style="font-size: 15px;">) is used to explain the decomposition and reconstruction of a signal using DWTs.</span>
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<span style="font-size: 15px;">Figure 2 </span><span style="background-color: black;"><span style="font-size: 15px;">Wavelet decomposition and reconstruction of a discrete signal</span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">x</em><span style="font-size: 15px;">(</span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">n)</em><span style="font-size: 15px;">.</span></span></div>
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<span style="font-size: 15px;">A discrete time signal </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">x(n)</em><span style="font-size: 15px;"> is applied to a pair of filters. A lower resolution signal is obtained by convoluting </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">x(n)</em><span style="font-size: 15px;"> with a half band low pass filter having an impulse response </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">h<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">2</sub>(n)</em><span style="font-size: 15px;">. The half band signal can be made full band by down sampling with a factor of two (doubling the scale by a factor of two in the analysis). The z-transform </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Y<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">2</sub>(z)</em><span style="font-size: 15px;"> of the resulting signal </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">y<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">2</sub>(n)</em><span style="font-size: 15px;"> can be expressed as:</span>
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where <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">H<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">2</sub>(z)</em> and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">X<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">2</sub>(z)</em> are the z-transform of <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">h<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">2</sub>(n)</em> and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">x(n)</em>. Compared with the original signal <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">x(n)</em>, the filtered signal <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">y<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">2</sub>(n)</em> is reduced in resolution by a factor of two as a result of low pass filtering and doubled in scale as a result of down sampling. In a similar manner, it is possible to compute the added details of a signal as a high pass version of <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">x(n)</em> using a filter with impulse response <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">h<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">1</sub>(n)</em> followed by down sampling. Wavelet analysis became popular in the multiresolution analysis of biomedical images because of its ability to obtain smooth approximation at different levels.</div>
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The same sub-band decomposition can be carried out in the case of two dimensional signals. As mentioned in the previous section, large numbers of 64 × 64 pixel image templates were taken to extract the feature vector for training the ANN. Figure 3A<a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f3/" rid-figpopup="f3" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -1em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">3A–D</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a>–D shows four such training samples, two images of normal samples and two of advanced stage OSF. These sample images have been decomposed by HAAR wavelets into four levels. In each level, there are three sets of detail coefficients: horizontal (<em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">H<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>), vertical (<em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">V<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>), and diagonal (<em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">D<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>); <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">i</em> <img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" />=<img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /> 1, 2, 3, 4, as shown in fig 4<a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f4/" rid-figpopup="f4" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -0.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">4.</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a>. The dimensions of <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Hi</em>, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">V<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>, and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">D<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em> are 64*2<sup style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">−i</sup> × 64*2<sup style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">−i</sup> pixels. <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">H<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">V<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>, and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">D<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em> were extracted using the “detcoef2” function of MATLAB 5.1. The four approximation coefficients, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">A<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>, were extracted from the four levels using “appcoef2”. The frobenious norm was computed for <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">H<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">V<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">D<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em>, and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">A<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em> and denoted as:</div>
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<span style="font-size: 15px;">Figure 3 Training 64 ×64 pixel sample transmission electron microscopy image of oral subepithelial collagen. (A) Normal transverse section (TS); (B) normal longitudinal section (LS); TS of advanced stage oral submucous fibrosis (OSF); LS of advanced stage OSF.</span>
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<span style="font-size: 15px;">Wavelet decomposition of 64 × 64 pixel training image sample.</span>
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<span style="font-size: 15px;">The element of the feature vector (</span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">FV</em><span style="font-size: 15px;">) is the frobenious norm of </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">H<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em><span style="font-size: 15px;">, </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">V<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em><span style="font-size: 15px;">, </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">D<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em><span style="font-size: 15px;">, and </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">A<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em><span style="font-size: 15px;">.</span>
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i <img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" />=<img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font-size: 15px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /> 1,2,3,4 where <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">κ</em> is set at 0.001.</div>
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Multilayered perceptron feed forward neural network</h3>
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Figure 5<a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f5/" rid-figpopup="f5" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -0.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">5</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a> shows a representative multilayered perceptron feed forward network. Each node represented by the box is called a perceptron.</div>
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Figure 5</div>
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<span style="font-size: 15px;">Multilayered perceptron model.</span>
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It has been proved that a three layered network can represent a non-linear function of any order.<span style="line-height: 0px;"> </span>The numbers of layers and numbers of nodes in the hidden layer are guided by many practical aspects, such as redundancy, number of input training sets, spurious oscillations, etc. However, the most crucial part of an ANN based model is to train the network. The most widely studied and used training algorithm is the so called back propagation technique, which is robust and reliable. The main problem with neural network training is to devise a method of updating the representative weights that minimises the error. However, the updating of the weights has been done here by the Levenberg-Marquardt algorithm. The Levenberg-Marquardt algorithm performs much better with some knowledge of the process, so that quick convergence is obtained with a very small error.</div>
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Figure 6<a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f6/" rid-figpopup="f6" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -0.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">6</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a> shows the structure of the network. In this figure, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">v<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">ij</sub></em> and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">w<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">pq</sub></em> denote the weights for the successive layers. The basic purpose of training a network is to optimise <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">v<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">ij</sub></em> and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">w<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">pq</sub></em> with respect to a particular set of input–output training patterns.</div>
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<span style="font-size: 15px;">Figure 6</span></div>
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<span style="font-size: 15px;">Weight vectors in the multilayered perceptron feed forward network.</span>
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<span style="font-size: 15px;">The responses at the hidden nodes </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">b<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">j</sub></em><span style="font-size: 15px;"> </span><img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /><span style="font-size: 15px;">=</span><img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /><span style="font-size: 15px;"> 1,2…</span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">p</em><span style="font-size: 15px;"> are calculated by evaluating the contributions from all the input nodes through a non-linear mapping function:</span>
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where the function <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">f(•)</em> chosen is the “tansig” function of MATLAB 5.1.</div>
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The tansig function is given by:</div>
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<em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">θ<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">j</sub></em><span style="font-size: 15px;"> is the bias at the </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">j<sup style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">th</sup></em><span style="font-size: 15px;"> hidden layer node and </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">a<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">i</sub></em><span style="font-size: 15px;"> is the input vector. Similarly, </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">c<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">k</sub></em><span style="font-size: 15px;">, </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">k</em><span style="font-size: 15px;"> </span><img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /><span style="font-size: 15px;">=</span><img alt=" " border="0" src="http://www.ncbi.nlm.nih.gov/corehtml/pmc/pmcents/thinsp.gif" style="border: 0px; font: inherit; margin: 0px; max-width: 100%; padding: 0px; vertical-align: baseline;" title="" /><span style="font-size: 15px;"> 1,2,…</span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">q</em><span style="font-size: 15px;"> is calculated using:</span>
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where <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">τ<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">k</sub></em> is the bias at the <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">k<sup style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">th</sup></em> output layer node.</div>
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The function “trainlm” in the neural network toolbox in MATLAB 5.1 was used to train the network. It uses a mixture of the Gauss-Newton method and a gradient descent technique for optimisation of the weights, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">w<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">jk</sub></em> and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">v<sub style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">ij</sub></em>.</div>
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The Levenberg-Marquardt weight update rule is:</div>
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where <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">J</em> is the Jacobian matrix of derivatives of each error to each weight, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">μ</em> is a scalar, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">I</em> is the identity matrix, and <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">e</em> is an error vector. Training continues until the error goal is met and the minimum error gradient occurs.</div>
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Training/testing by ANN</h3>
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In our present study, a three layer ANN was used. A single hidden layer with four neurones was found to be sufficient for training (fig 7<a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f7/" rid-figpopup="f7" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -0.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">7).</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a>). The maximum number of epochs was fixed at 400 and the sum squared error goal was kept at 10<sup style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">−5</sup>. The learning rate and minimum feasible gradient were chosen as 0.01 and 0.05, respectively. Detailed discussions of these parameters are available in Demuth and Beale.</div>
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<span style="font-size: 15px;">Figure 7</span></div>
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<span style="font-size: 15px;">Convergence of artificial neural network training.</span>
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<b><span style="font-size: x-large;">RESULTS</span></b></h2>
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After successful training, several images from different patients were tested. The feature vector was extracted from each of the contiguous 64 × 64 pixel blocks by wavelet decomposition. These test feature vectors were fed into the ANN. Figs 8<a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f8/" rid-figpopup="f8" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -0.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">8</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a>–10<a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f10/" rid-figpopup="f10" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a> show the ANN outputs for three different test images. The target output has three different states, denoted as −1, 0, and +1, which represent normal, less advanced stage, and advanced stage OSF, respectively. In the case of untrained test samples, the ANN output for a particular 64 × 64 pixel block may not map exactly to one of the three states—for example, a sample of advanced state OSF may produce an output of +0.9 instead of +1.0—so that bands need to be defined around these three states. These bands corresponding to normal, less advanced, and advanced stages have been designated as follows: if the output of a 64 × 64 pixel block is less than −0.5, the block is categorised as “normal”; if the output is between −0.5 and +0.5 is categorised as “less advanced”; and if the output is greater than +0.5 it is categorised as “advanced”.</div>
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Figure 8</div>
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<span style="font-size: 15px;">Artificial neural network (ANN) output for an image of normal cells.</span>
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<span style="font-size: 15px;">Figure 9</span></div>
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<span style="font-size: 15px;">Artificial neural network (ANN) output for an image of less advanced stage of oral submucous fibrosis.</span>
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<span style="font-size: 15px;">Figure 10</span></div>
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<span style="font-size: 15px;">Artificial neural network (ANN) output for an image of advanced stage oral submucous fibrosis.</span>
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<span style="font-size: 15px;">In fig 8</span><a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f8/" rid-figpopup="f8" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -0.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">8</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a><span style="font-size: 15px;"> a normal image has been tested and the target output of each 64 × 64 pixel block is set as −1. There are 60 blocks of 64 × 64 pixels. Of these 60 blocks, only nine are misclassified. Similarly, in fig 9</span><a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f9/" rid-figpopup="f9" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -0.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">9</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a><span style="font-size: 15px;">the test image is a less advanced stage of disease and the target output is set at 0. Of the total number of 297 blocks, 26 blocks are wrongly classified, whereas in fig 10</span><a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f10/" rid-figpopup="f10" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -1em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">10,</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a><span style="font-size: 15px;">, the test image is advanced stage of the disease and the target output is set as +1. Of 60 blocks only six do not show the correct signature.</span>
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<span style="font-size: 15px;">To provide a measure of the efficiency of the proposed ANN technique, the properly classified block index (PCBI) has been computed for all the test images. PCBI has been defined as follows:</span>
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<span style="font-size: 15px;">where </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">N<sup style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">p</sup></em><span style="font-size: 15px;"> and </span><em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">N<sup style="border: 0px; font-size: 0.8461em; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">T</sup></em><span style="font-size: 15px;"> are the total number of properly classified blocks and the total number of 64 × 64 pixel blocks in the test image. After classifying the blocks into three states −1, 0, and +1, the number of blocks in each state has been computed. If N</span><sup style="border: 0px; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">P</sup><sub style="border: 0px; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">−1</sub><span style="font-size: 15px;">, N</span><sup style="border: 0px; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">P</sup><sub style="border: 0px; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">0</sub><span style="font-size: 15px;">, and N</span><sup style="border: 0px; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: -0.5em; vertical-align: baseline;">P</sup><sub style="border: 0px; font: inherit; line-height: 0; margin: 0px; padding: 0px; position: relative; top: 0.25em; vertical-align: baseline;">1</sub><span style="font-size: 15px;"> are the number of 64 × 64 pixel blocks classified as normal, less advanced, and advanced, respectively, the number of properly classified blocks is:</span>
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<span style="font-size: 15px;">Based on the magnitude of the PCBI, the final diagnosis is performed on the nature of the test images. A binary decision is taken based on the PCBI. If the PCBI is greater than 50% (fig 11</span><a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/figure/f11/" rid-figpopup="f11" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -1em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">11),</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a><span style="font-size: 15px;">), the wavelet ANN based system can identify the correct diagnosis. In table 1</span><a class="fig-table-link table figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770817/table/t1/" rid-figpopup="t1" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -0.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">1,</span></span><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span></a><span style="font-size: 15px;">, 16 test images were used to check the diagnostic ability of the proposed wavelet ANN based system: all test images were diagnosed properly by the proposed system.</span>
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<span style="background-color: black;"><span style="font-size: 15px;">Figure 11 </span><span style="font-size: 15px;">Binary decision for oral submucous fibrosis stage detection. PCBI, properly classified block index.</span></span></div>
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<span style="font-size: x-large;"><b>DISCUSSION</b></span></h2>
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Our study proposes a novel ANN based CAD technique to identify the progressive stages of the oral precancerous condition OSF. TEM images of oral subepithelial collagen fibres (test images) are subdivided into 64 × 64 pixel contiguous blocks and these blocks undergo wavelet decomposition. The wavelet coefficients are used as feature vectors. In the less advanced stage of the disease, some of the blocks show the signature of the normal collagen image, whereas others have the signature of advanced stage OSF. As a result, the false detection rate is high in the less advanced stage of the disease but the PCBI is always greater than 50%. Because the final decision is taken based on the magnitude of the PCBI, it always leads to the correct diagnosis.</div>
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It should be mentioned that from these sample images 16 features were extracted using wavelet transformation. However, all 16 features may not contribute equally to classifying the image characteristics. There are some common features and some unwanted features resulting from noise that can mislead both the training process and the decision making process. Therefore, in future studies the feature set could be selectively weighted or restricted using a suitable technique,<span style="line-height: 0px;"> </span>so that unwanted or misleading features could be deactivated or isolated.</div>
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Take home messages</span></h5>
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<li style="border: 0px; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">
<span style="color: cyan;">We have developed a novel neural network based method for detecting and staging oral precancer (oral submucous fibrosis; OSF)</span></div>
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<li style="border: 0px; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">
<span style="color: cyan;">The wavelet coefficients of transmission electron microscopy images of collagen fibres from normal oral submucosa and OSF tissues were used to choose the feature vector which, in turn, was used to train the artificial neural network</span></div>
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<span style="color: cyan;">The trained network was able to classify normal and oral precancer stages (less advanced and advanced) after obtaining the image as an input</span></div>
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<span style="color: #783f04; font-size: large;">Abbreviations</span></h3>
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ANN, artificial neural network</div>
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CAD, computer aided diagnosis</div>
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CWT, continuous wavelet transform</div>
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DWT, discrete wavelet transform</div>
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IID, interincisal distance</div>
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OSF, oral submucous fibrosis</div>
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PCBI, properly classified block index</div>
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TEM, transmission electron microscopy</div>
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<h2>
<span style="background-color: white; color: #985735; font-family: arial, helvetica, clean, sans-serif; line-height: 1.125;"><span style="font-size: x-large;">REFERENCES</span></span></h2>
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<span class="ref-label" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">10.</span> <span class="ref-cit" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="citation" id="__citation10" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><strong style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">van Wyk CW</strong>, Grobler-Rabie AF, Martell RW, <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">et al.</em> HLA-antigens in oral submucous fibrosis. <span class="ref-journal" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">J Oral Pathol Med</span> 1994;<span class="ref-vol" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">23</span>:23–7. </span></span></div>
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<span class="ref-label" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">29.</span> <span class="ref-cit" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><strong style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Mishra A</strong>, Dutta PK, Ghosh MK. Non-rigid cardiac motion quantification from 2-D image sequences based on wavelet synthesis. <span class="ref-journal" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Image and Vision Computing</span> 2001;<span class="ref-vol" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">19</span>:929–39.</span></div>
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<span class="ref-label" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">33.</span> <span class="ref-cit" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><strong style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Fiori S</strong>, Grimani F, Burrascano P. Novel neural network feature selection procedure by generalization maximization with application to automatic robot guidance. <span class="ref-journal" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">International Journal of Smart Engineering and System Design</span> 2002;<span class="ref-vol" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">4</span>:91–106.</span></div>
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com0tag:blogger.com,1999:blog-3393509504180156297.post-82985122354220695112012-07-22T02:18:00.003-07:002012-07-22T18:37:13.047-07:00A case of dyskeratosis congenita with primary amenorrhea and adenocarcinoma of stomach<div dir="ltr" style="text-align: left;" trbidi="on">
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Dyskeratosis congenita (DC) is a rare disease characterized by hyperpigmentation, nail dystrophy and mucous membrane abnormality. Commonly occurring in males, the patients die young usually due to bone marrow suppression. Malignancies of various descriptions have been reported in this disease, the commonest being solid tumors of head/neck (squamous cell carcinoma). We report the case of a female patient with DC, who presented to us with severe wasting and primary amenorrhea and died of carcinoma stomach in our hospital 3 weeks later.</div>
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Introduction</span></h2>
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">Dyskeratosis congenita (DC) is a rare inherited disorder characterized by premature aging, bone marrow failure and predisposition to malignancies.</span><br />
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">In its classical form, there is skin pigmentation, nail dystrophy and mucous membrane leukoplakia. The major form of DC is X-linked and, therefore, there is an abundance of male patients. However, carrier females may have complete clinical manifestation.</span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;"> We report the case of a female patient, who presented to us with hyperpigmentation, significant weight loss and primary amenorrhea. She expired within 3 weeks of hospital admission.</span><br />
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<span style="font-size: x-large;">Case Report</span></h2>
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">Our patient was a 21-year-old woman with progressive weight loss, loss of appetite and extreme weakness for the last 6 months. She also had history of gradually increasing pigmentation in various parts of the body along with marked hair loss for the last 8 years. The patient had not experienced menarche till then. There was no history of fever, diarrhea, sexual exposure, polyuria/polyphagia or palpitations.</span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">On examination, the patient was 140 cm tall, with a weight of 20 kg [body mass index (BMI) 10.8 kg/m </span><sup style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">2</sup><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;"> ] and had an emaciated build. She had moderate pallor with normal pulse rate and rhythm. Her BP was 100/60 mm of Hg without any significant postural drop. Secondary sexual characters were infantile. There was no edema, clubbing, icterus, lymphadenopathy or sternal tenderness. Thyroid gland was normal. Skin examination revealed reticulate hyperpigmentation, telangiectasia and some depigmented macules on neck, chest as well as all the flexural surfaces (Figure 1)</span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">. Examination of the oral cavity revealed swollen gums, white patches over the tongue<span style="background-color: black;"> </span></span><span style="background-color: black;"><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">(Figure 2)</span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">, hard palate </span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">(Figure 3)</span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;"> and buccal mucosa. The patient had diffuse alopecia over the scalp. The nails were brittle with vertical ridges </span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">(Figure 4)</span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">. There was no abdominal organomegaly or free fluid. Respiratory, central nervous system and cardiovascular system examination was noncontributory.</span></span></div>
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<b style="font-family: Verdana, Arial, sans-serif; font-size: 13px; line-height: 17px; text-align: -webkit-center;">Figure 1: Reticulate hyperpigmentation, telangiectasia and depigmented macule on neck and periorbital areas</b>
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<b style="font-family: Verdana, Arial, sans-serif; font-size: 13px; line-height: 17px; text-align: -webkit-center;">Figure 2: Leukoplakia of tongue and dental malalignment</b>
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<b style="font-family: Verdana, Arial, sans-serif; font-size: 13px; line-height: 17px; text-align: -webkit-center;">Figure 3: Network of leukoplakia on hard palate</b>
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<b style="font-family: Verdana, Arial, sans-serif; font-size: 13px; line-height: 17px; text-align: -webkit-center;">Figure 4: Finger nails showing vertical ridges and broken edges</b>
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">Blood examination showed 7.5 g/dl of hemoglobin, WBC count of 3500/mm </span><sup style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">3</sup><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;"> and platelet count of 100,000/mm </span><sup style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">3</sup><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;"> . Blood biochemistry was essentially normal, including electrolytes and albumin. Chest X-ray was noncontributory. USG abdomen revealed hypoplastic uterus with infantile ovaries. Anti nuclear antibody was negative and test for HIV was nonreactive. In view of the weight loss, hypotension and pigmentation, a cosyntropin test was done and 1 hour serum cortisol was normal. Thyroid profile was noncontributory. Other hormones like luteinizing hormone (LH), follicle stimulating hormone (FSH) as well as estrogen and progestogen gave low values depicting a hypogonadotropic hypogonadism. A skin biopsy was taken for characterization of the pigmentation.</span><br />
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">Meanwhile, the patient started going downhill with onset of melena, poor intake and increasing pallor. Blood transfusions were given and upper GI endoscopy was done. The endoscopy revealed a proliferative growth at the antral region of stomach. Biopsy proclaimed an adenocarcinoma of stomach. The skin biopsy was consistent with DC. Unfortunately, we lost the patient before further evaluation was possible.</span><br />
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<span style="font-size: x-large;">Discussion</span></h2>
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">The differential diagnosis, when the patient was first encountered, included Addison's disease, polyglandular autoimmune syndromes, internal malignancy, malabsorption syndrome with pellagra and even anorexia nervosa. However, as the preliminary reports arrived, most of these were excluded.</span><br />
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">Characteristic reticulate pigmentation interspersed with areas of depigmentation in the flexural zones was suggestive of disorders of reticulate pigmentation like Dowling Degos disease, reticulate acropigmentation of Kitamura, Revescz Syndrome and DC.</span><br />
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">Apart from pigmentation, this patient had alopecia, nail dystrophy and leukoplakia of the tongue. She had moderate anemia and mild leukopenia and suffered an untimely death due to carcinoma stomach at the age of 22 years. The conglomeration of features pointed toward DC.</span><br />
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">DC is a rare disease with around 500 cases reported from 1910 to 2008.</span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">The number of male cases is three times that of female ones. This is because of an X-linked transmission in most cases. In 1995, a DC Registry was established, which showed 76 out of 83 patients as males. Heterozygous females show variable expression depending on tissue-specific patterns of random X-inactivation. However, autosomal dominant and autosomal recessive inheritances have been reported. The gene responsible for X-linked DC encodes for a protein "dyskerin" that is essential for ribosomal biosynthesis and telomerase RNP assembly. Autosomal dominant form has mutations in the RNA component of the telomerase human telomerase RNA component (hTERC). Defects in these mechanisms lead to diminished telomere lengths.</span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;"> </span><br />
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">The clinical manifestations start appearing at the second decade of life. Apart from skin and appendicular abnormalities, the patient eventually develops bone marrow depression, which is the commonest cause of mortality. Some atypical features include pulmonary fibrosis and renal agenesis.</span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">These patients are also predisposed to various types of malignancies like squamous cell carcinomas of skin and mucous membranes, adenocarcinomas of anorectum, esophagus, stomach, CA pancreas, Hodgkin's disease and many more. The exact incidence of CA stomach in DC is not known. Available literature is in the form of anecdotal case reports, one from India as well. </span><span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;"> </span><br />
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">This patient had another interesting aspect, i.e., primary amenorrhea. Hormonal assay revealed hypogonadotrophic hypogonadism. This patient may not have attained the critical body weight required for menarche. She had always been frail in comparison to her siblings.</span><br />
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<span style="font-family: Verdana, Arial, sans-serif; line-height: 17px; text-align: -webkit-auto;">Hypogonadism and hyposthenic build have been documented in DC but no specific data are available regarding primary amenorrhea for females. </span><br />
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References</span></h2>
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<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">1.</span></td><td><span style="color: #cc0000; font-size: small;">Knight S, Vulliamy T, Copplestone A, Gluckman E, Mason P, Dokal I. Dyskeratosis Congenita (DC) Registry: Identification of new features of DC. Br J Haematol 1998;103:990-6.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">2.</span></td><td><span style="color: #cc0000; font-size: small;">Alter BP, Giri N, Savage SA, Rosenburg PS. Cancer in dyskeratosis congenita. Blood 2009;113:6502-3.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">3.</span></td><td><span style="color: #cc0000; font-size: small;">Bessler M, Wilson DB, Mason PJ. Dyskeratosis congenita and telomerase. Curr Opin Pediatr 2004;16:23-8.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">4.</span></td><td><span style="color: #cc0000; font-size: small;">Balci S, Engiz O, Erekul A, Gozdasoglu S, Vulliamy T. An atypical form of dyskeratosis congenita with renal agenesis and no mutation in DKC1, TERC and TERT genes. J Eur Acad Dermatol Venereol 2009;23:607-8.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">5.</span></td><td><span style="color: #cc0000; font-size: small;">Hermann M. Idiopathic pulmonary fibrosis - telomerase mutation in familial form. Pneumologie 2008;62:121.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">6.</span></td><td><span style="color: #cc0000; font-size: small;">Chatura KR, Nadar S, Pulimood S, Mathai D, Mathan MM. Gastric carcinoma as a complication of dyskeratosis congenita in an adolescent boy. Digest Dis Sci 1996;41:2340-2.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">7.</span></td><td><span style="color: #cc0000; font-size: small;">Baykal C, Kavak A, Gukan P, Buyukbabani N. Dyskeratosis congenita associated with three malignancies. J Eur Acad Dermatol Venereol 2003;17:216-8.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">8.</span></td><td><span style="color: #cc0000; font-size: small;">Sorrow JM Jr, Hitch JM. Dyskeratosis congenita. First report of its occurrence in a female and a review of literature. Arch Dermatol 1963;88:340-7.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">9.</span></td><td><span style="color: #cc0000; font-size: small;">Kalb ER, Grossman ME, Hutt C. Avascular necrosis of bone in dyskeratosis congenita. Am J Med 1986;80:511-3.<br /> </span></td></tr>
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<br class="Apple-interchange-newline" /></div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com0tag:blogger.com,1999:blog-3393509504180156297.post-86126215624149017822012-07-22T01:50:00.002-07:002012-07-28T03:51:02.254-07:00Non-Hodgkins lymphoma of maxilla: A rare entity<div dir="ltr" style="text-align: left;" trbidi="on">
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Non-Hodgkin's lymphomas are a group of neoplasms that originate from the cells of the lymphoreticular system. Forty percent of non-Hodgkin's lymphomas arise from extra nodal sites. Non-Hodgkin's lymphomas detected primarily in the bone are quite rare, but among jaw lesions, they are more frequently present in the maxilla than in the mandible. There are no classical characteristic clinical features of lymphomas involving the jaw bones. Swelling, ulcer or discomfort may be present in the region of the lymphoma, or it may mimic a periapical pathology or a benign condition. Extranodal non-Hodgkins lymphoma of the maxilla could present as one of the early manifestation of detrimental diseases. Clinically these types of lymphoma can mimic an inflammatory endo-periodontal lesion with symptoms of pain and local discomfort. The greater the delay in diagnosis subsequently worsens the prognosis. A case of maxillary non-Hodgkin's lymphoma with an unusual presentation is discussed.</div>
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<span style="color: #5795cc; font-size: large;"> </span><span style="color: blue; font-size: x-large;">Introduction</span></h2>
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Lymphomas are a diverse group of neoplasm's affecting the lympho reticular system. Most of them originate from B lymphocyte. Lymphoma is the second common malignancy of head and neck. Primary non-Hodgkin's lymphoma (NHL) of the bone is rare, accounting for <5%. In 1963, the term primary lymphoma of bone was introduced by Ivins and Dahlin. The etiology is unknown even though virus and immuno-suppression are associated. The most common manifestations are pain and swelling in the jaw bone, but it is often clinically diagnosed as a dental infection. Hence, the diagnosis of lymphoma in jaw bone is often delayed. Biopsy is considered when there is a nonhealing extraction wound and if any oral wound is not resolving for a prolong period. We present a case with a chief compliant of mobile teeth, which was later diagnosed as primary NHL of the maxilla.
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<span style="color: blue; font-size: x-large;">Case Report</span></h2>
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A 30-year-old female patient reported to the department of oral and maxillofacial surgery of Dr. R. Ahmed Dental College & Hospital with complains of growth in the left upper jaw at the site of extraction wound. History revealed she was apparently alright 15 days back; she visited a local dentist for pain in the left upper back teeth, which were found to be mobile and were extracted. Following extraction she noticed a small growth which was insidious in onset and gradually increased to the present size at the site of extraction after 15 days of teeth removal. She revisited the same dentist who referred to our institution. Her medical and family history was not contributory. She was happily housewife with two children. She did not have any abusive habits.</div>
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On examination a single, lobulated, sessile pink in color, nonpulsatile lesion was found to be present in 25, 26, 27 regions which extended beyond the occlusal<span style="background-color: black;"> surfaces of teeth both buccally and palatally of approximately 4 cm × 3cm in size (Figure 1). On palpation, the swelling was fibrous and edematous which was interfering with the occlusion (Figure 2). There were indentations of the lower teeth on the swelling. There was no regional lymphadenopathy. Differential diagnosis of squamous cell carcinoma and benign tumors were considered. Orthopantomogram (OPG) and PNS view revealed haziness in the left maxillary antrum with radiolucency extending in the alveolus of 25, 26, and 27 regions. Otherwise, her skeletal survey was normal. The CT scan of maxilla (Figure 3), (Figure 4) and (Figure 5) revealed break in continuity of buccal, palatal walls, and inferior wall of maxillary antrum. An incisional biopsy was carried out after doing routine blood investigations. Western blot test revealed that patient was HIV positive. The biopsy specimen revealed sheets of abnormally large lymphoid cells with high nucleus: cytoplasmic ratio, coarse chromatin, and inconspicuous nucleoli with abnormal mitotic (Figure 6). The features were suggestive of large cell lymphoma of B-cell type. Immuno-histochemistry revealed positive CD20, LCA, and CD3, CK were negative, which proved conclusively the lesion to be as a NLM, diffuse large B-cell type. The HIV status was in the fourth stage which superseded non-Hodgkin's lymphoma as per WHO classification. History regarding the HIV-positive status did not reveal any mode of transmission of HIV infection.</span></div>
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<b style="text-align: -webkit-center;">Figure 1: Intra-oral growth extending from 25 to 27 with extension on buccal and palatal side</b>
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<b style="text-align: -webkit-center;">Figure 2: Sagittal section of CT showing the extent into the antrum</b>
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<b style="text-align: -webkit-center;">Figure 3: Lateral skull radiographic view of maxilla in CT showing destruction of maxillary alveolus</b>
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<b style="text-align: -webkit-center;">Figure 4: Coronal CT showing extent of lesion</b>
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<b style="text-align: -webkit-center;">Figure 6: Histopathological examination</b>
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She was referred to the oncologist. The patient was started on anti-retroviral treatment. Chemotherapy was advised by the oncologist and a total of three cycles were suggested at the gap of every 3 weeks. The treatment regimen followed was that of classical CHOP therapy which comprised of using cyclophosphamide, doxorubicin (hydrodoxorubicin), vincristine (oncovin), and prednisolone. At the end of two cycles the swelling started regressing in size and totally disappeared after three cycles. The growth completely disappeared after chemotherapy <span style="background-color: white;"> </span><span style="background-color: black;">(Figure 7). The patient died 6 months after chemotherapy.</span></div>
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<b style="text-align: -webkit-center;">Figure 7: Regression of the lesion</b>
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<span style="color: #5795cc; font-size: large;"> </span><span style="color: blue; font-size: x-large;">Discussion</span></h2>
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Lymphomas are a diverse group of neoplasms affecting the lympho reticular system. Lymphomas have been traditionally divided into Hodgkin's disease and non-Hodgkin's disease. Hodgkin's disease often presents as nodal disease, commonly involving cervical, axillary, and inguinal nodes, whereas non-Hodgkin's disease may develop extra-nodally, outside the lymphoid system and can occur in stomach, salivary glands, and rarely in oral cavity and jaws.</div>
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Lymphomas are second only to squamous cell carcinoma in the frequency of malignant neoplasms involving the soft tissues of head and neck region, which usually affects the lymph nodes. NHL are a group of highly diverse malignancies and have great tendency to affect organs and tissues that do not ordinarily contain lymphoid cells. Twenty-thirty percentage of NHL arise from extra-nodal sites.</div>
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The head and neck is the second most common region for the extra-nodal lymphoma, the first being the gastro intestinal tract. NHL rarely manifests as a primary malignancy in the head and neck region of >1% and may give an important clue for undiagnosed HIV infection, which accounts for 2% of oral neoplasms in patients with AIDS. Among various head and neck sites, Waldeyers ring, which is the area encompassed by the nasopharynx, tonsil, and base of the tongue, is the most often involved by malignant lymphoma. The nose, para-nasal sinuses, orbit(s), and salivary glands are the other sites affected in head and neck region. Involvement of the oral cavity is not common. The maxilla is affected more commonly than the mandible. Palate and gingiva account for almost 70% of lesions in maxilla as seen in our case.</div>
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It more commonly affects the middle aged and the elderly (40-80 yrs) with slight male predilection with a male to female ratio of 3:2. There is reversal of the incidence of NHL among young HIV-positive patients. HIV patients are 60 times at risk than the general population and around 3% of HIV-infected people develop lymphomas. In our case, patient was only 30 years old with good health. The gingival and palate regions are commonly affected, while involvement of the alveolus and buccal vestibule, as seen in our patient, is rare. Secondary organ involvement along with the primary in the oral cavity is generally observed.</div>
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Primary lymphoma of the bone was first described by Parker and Jackson as primary reticular cell sarcoma of bone. Clinical features of lymphoma of the oral region are not characteristic. They occur as local bony swelling, tooth mobility, painless inflammation of the mucosa with or without ulcerations, and rarely facial or dental pain. Additional observations include trismus, otalgia, gingival ulceration, sinusitis, or cervical lymphadenopathy. The oral NHL is more common benign oral and dental pathological conditions. In our case, the patient was aware of the slow growing swelling that was not painful and of short duration which was 15 days following extraction of mobile teeth. Specific and evident radiological signs of bone involvement may be absent in 10-20% of cases. The radiographic findings usually are those of periapical inflammatory processes or osteitis. Diffuse trabecular honeycomb images are occasionally observed. Those may be the images of cortical destruction and invasion of the maxillary sinus. Differential diagnosis includes infectious process such as systemic or deep mycosis, dento-alveolar abscess, Wegener's granulomas, midline lethal granulomas, squamous cell carcinomas, metastatic tumors, neoplastic process, wherein very rapid growth is a feature of sarcomas and lympho proliferative disorders.</div>
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NHL can be managed by chemotherapy, radiotherapy, and surgery in various combinations. NHL arising in bone is best treated by chemotherapy and may not require radiotherapy. Generally, a combination of chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) and field radiation is recommended for treatment. Monoclonal antibodies directed against antigens or within the lymphoma and injection of interferon have also been used. Survival is excellent in localized disease, whereas disseminated disease seems less favorable.</div>
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The prognosis of the disease is good with a maximum of 5-year survival rate in 30% of cases after therapy. The disease may occasionally progress into a diffuse pattern with cutaneous nodules and plaques which undergo blast transformation or rarely turn into leukemia. Currently, the median survival rate of patients with AIDS related to lymphomas after treatment is 5-11 months, as was in our case. In contrast, the response of the non-HIV-positive population to aggressive chemotherapy in the absense of immuno-suppression has highly been effective; 65% to 85% experienced a complete survival response and 50% to 75% attained long-term survival.</div>
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<span style="color: blue; font-size: x-large;">Conclusion</span></h2>
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The main purpose of this article is to develop awareness among dentists as there is an increased risk of oral NHL in the HIV-positive population and to emphasize the importance of including NHL in the differential diagnosis of intra oral soft tissues or ulcerations. This is to stress the importance of early diagnosis to ensure appropriate treatment, to improve prognosis, and quality of life. Prognosis is excellent in localized disease, whereas in disseminated disease, it is less favorable. Lymphomas arising in bone may be effectively managed by chemotherapy alone. Thus, with the rising incidence of extra-nodal lymphomas it has become very important for present age dentists not to take any swellings of the orofacial region at face value but to properly investigate its pathology and treat it judiciously.
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<span style="color: blue; font-size: x-large;">References</span></h2>
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">1.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Boulaadas M, Benazzou S, Sefiani S, Nazih N, Essakalli L, Kzadri M. Primary extranodal non-Hodgkin's lymphoma of the oral cavity. J Craniofac Surg 2008;19:1183-5.</span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">2.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Dinakar J, Priya L, Reddy S. Primary non-Hodgkin's lymphoma of the mandible. J Oral Maxillopath 2010;14:73-6.</span></td></tr>
<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">3.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Frei M, Dubach P, Reichart PA, Schmitt AM, Mueller-Garamvölgyi E, Bornstein MM. Diffuse swelling of the buccal mucosa and palate as first and only manifestation of an extranodal non-Hodgkin 'double-hit' lymphoma: report of a case. Oral Maxillofac Surg 2012;16:69-74. </span></td></tr>
<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">4.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Kini R, Saha A, Naik V. Diffuse Large B cell lymphoma of mandible: A case report. Med Oral Patol Oral Cir Bucal 2009;14:e421-4.</span></td></tr>
<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">5.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Sankaranarayanan S, Chandrasekar T, Srinivasa Rao P, Rooban T, Ranganathan K. Maxillary Non-Hodgkins lymphoma. J Oral Maxillofac Pathol 2005;9:34-6.</span></td></tr>
<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">6.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Pratibha R, Ahmed S, Janaki VR. Primary extranodal non-Hodgkin's lymphoma- A case report. Indian J Dermatol Venereol Leprol 2004;70:172-4.</span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">7.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Eisenbud L, Scinbba J, Mir R, Sachs SA. Oral presentations in nonHodgkin's Vs lymphoma: A review of thirty one cases. Part I. Data analysis. Oral Surg Oral Pathol 1984;57:272-80.</span></td></tr>
<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">8.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Slootweg PJ, Wittkampf AR, Kluin PM, de Wilde PC, van Unnik JA. Extranodal nodal non-Hodgkin's Vs lymphoma of the oral tissues. An analysis of 20 cases. J Maxillofac Surg 1985;13:85-92. </span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">9.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Lozada-Nur F, de Sanz S, Silverman S Jr, Miranda C, Regezi JA. Intra oral non-Hodgkin's lymphoma in seven patients with acquired immunodeficiency syndrome. Oral Surg Oral Med Oral Pathpl Oral Radiol Endod 1996;82:173-8. </span></td></tr>
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<br /></div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com3tag:blogger.com,1999:blog-3393509504180156297.post-47594888539666072742012-07-20T23:56:00.002-07:002012-07-22T19:13:46.463-07:00Evaluation of DNA damage in oral precancerous and squamous cell carcinoma patients by single cell gel electrophoresis<div dir="ltr" style="text-align: left;" trbidi="on">
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<b>Context:</b> Single cell gel electrophoresis (SCGE) or "comet assay" is a rapid and very sensitive fluorescent microscopic method for detecting various forms of DNA damage at individual cell level.<br />
<b>Aims:</b> The aim of the present study was to detect the extent of DNA damage in oral cancer, oral submucous fibrosis (OSMF) and leukoplakia in comparison to normal individual.<br />
Settings and Design: A total of 44 consecutive patients with oral cancer (<i>n</i>=26), leukoplakia (<i>n</i>=12) and OSMF (<i>n</i>=6) and 10 healthy normal volunteers with normal oral epithelia (controls) were recruited from Dr. R. Ahmed Dental College and Hospital and were assessed for the extent of DNA damage using SCGE following clinical diagnosis.<i><br /></i><b>Materials and Methods:</b> Peripheral blood was collected by venepuncture and comet assay was performed using SCGE. Mean tail length was compared between diagnostic groups and between different oral habit groups using <i>t</i>-tests and analysis of variance (ANOVA). Pearson's product moment correlation was used to examine the linear association between the extent of DNA damage and oral habit pack-years. Scheffe's pair-wise test was employed to adjust for multiple comparisons.<br />
<b>Results:</b> None of the controls were associated with any oral habits. Mean (±SD) tail lengths (in mm) for cancer (24.95 ± 5.09) and leukoplakia (12.96 ± 2.68) were significantly greater than in controls (8.54 ± 2.55, <i>P</i><0.05). After adjustment, well-, moderately, and poorly differentiated carcinomas had significantly greater tail length than controls. Whereas the extent of DNA damage in cancer cases was significantly greater in leukoplakia than in compared to OSMF (11.03 ± 5.92), the DNA damage in latter was not different from controls. DNA damage for people with any oral habit (19.78 ± 7.77) was significantly greater than those with no habits (8.54 ± 2.55; <i>P</i><0.0001).<br />
<b>Conclusions:</b> DNA damage measured by SCGE is greater in leukoplakia and squamous cell carcinoma, but not in OSMF. Deleterious oral habits are also associated with greater DNA damage.</div>
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Introduction</span></h2>
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Oral squamous cell carcinoma has a multifactor etiology. Factors such as genetic, environmental and gene-environment interactions, viral, and behavioral (smoking, alcohol) have been implicated in the etio-pathologic continuum of oral cancer including recent population-based studies.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> One of the important hallmarks for cancer progression is DNA damage, resulting either from various carcinogens accumulating from etiologic influences or due to genetic errors.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> If detectable and quantifiable, these may contribute toward an easy detection and prediction system for oral cancer development and prognosis. Molecular and genetic techniques have enabled us to unravel some of the critical events associated with development of oral cancer and precancer.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> Examining associations of DNA damage with environmental factors and factors related to personal habits is an important challenge for molecular epidemiology, especially to develop better early detection tests and provide better prediction tests for oral cancer occurrence and progression.</span><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">The "comet assay", also called single cell gel electrophoresis (SCGE), is a sensitive and rapid technique for quantifying and analyzing DNA damage in individual cells, originally developed by Östling and Johansson in 1984.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> Singh </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">, later modified this technique in 1988, when it became popular as the alkaline SCGE.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> The name of the assay comes from the image of the electrophoresis gel which resembles a "comet" with a distinct head and tail. The cell with DNA damage appears in the form of "comet" while undamaged cell appears as a halo. The head is composed of intact DNA, while the tail consists of damaged (single-strand or double-strand breaks) or broken pieces of DNA.</span><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">The SCGE has been used for evaluating DNA lesions and is used to detect DNA damage caused by double-strand breaks, single-strand breaks (SSB), alkali labile sites, oxidative base damage, and DNA cross-linking with DNA or protein.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">The SCGE is also used to monitor DNA repair by living cells and is applicable to any eukaryotic organism and cell type.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">The extent of DNA liberated from the head of the comet is directly proportional to the amount of DNA damage.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> The comet assay is inexpensive once the laboratory infrastructure has been set in place, and gives results within a few hours and it is an appropriate tool for environmental monitoring, </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">though handling of samples, for example, proper protection from light and less shearing of blood samples are some essential criteria that should be taken care of.</span><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Although cellular changes in peripheral blood in a diverse range of malignancies have been reported in megakaryocytes, monocytes and in polymorphonuclear leukocytes, the DNA SSB have not been studied in detail.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> Similarly, although there is evidence that deleterious oral habits such as smoking, alcohol consumption and betel quid chewing are associated with oral cancer, </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> no study has examined the association of these habits with demonstrable DNA damage. In conducting this study, our aims were to: a) assess DNA damage in whole blood of subjects with oral squamous cell carcinoma and its comparison with some progressive precancerous conditions such as leukoplakia and oral submucous fibrosis (OSMF) using SCGE compared to normal subjects and b) to examine the association of DNA damage with deleterious oral habits such as smoking, pan chewing, and chewing tobacco.</span></div>
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</span><span style="color: blue;">Materials and Methods</span></span></h2>
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">0Study subjects were recruited from Dr. R. Ahmed Dental College and Hospital in Kolkata, India, following standard clinical diagnostic criteria and under their informed consent. The study was approved by an ethics review committee of the institute. A total of 44 consecutive patients with oral cancer (n=26), leukoplakia (n=12) and OSMF (n=6) and 10 healthy normal volunteers with normal oral epithelia (controls) were assessed for the extent of DNA damage using SCGE. Complete medical history was taken and oral habits were recorded in detail using a detailed questionnaire administered to all subjects. Detailed oral examination was carried out by a trained clinical oral pathologist. The lesion diagnoses were confirmed histopathologically. Whole blood was collected from antecubital vein, labeled and stored in tubes [with ethylenediaminetetraacetic acid (EDTA)], which were kept in a flask with ice and protected from light until processed in the laboratory.</span><br />
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<b style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">SCGE of DNA</b><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Phosphate buffered saline (PBS) suspended peripheral blood cells were embedded in a thin agarose gel (1% low melting) on a microscope slide. All cellular proteins were then removed from the cells by lysing with a lysis buffer [2.5 M NaCl, 0.1 M Na2 EDTA and 10 mM Trizma base, 1% TritonX and 10% dimethyl sulfoxide (DMSO)] and refrigerated overnight. DNA was allowed to unwind under alkaline conditions. Electrophoresis was performed for 20 minutes under alkaline condition (300 mM NaOH, and 1 mM EDTA, pH>13) at 280 mA and 24 V (~0.74 V/cm). The broken DNA fragments or damaged DNA undergoing electrophoresis migrate away from the nucleus. In this process, the smallest fragments travel the farthest. Following electrophoresis, the slides were neutralized using neutralizing buffer (0.4 M Tris, pH 7.5). Thereafter, following staining with a fluorescent dye (ethidium bromide 2 mg/ml), the DNA "comet" was easily visualized using a fluorescent microscope (Leica DM 3000) and the head and tail lengths were measured in 50 randomly selected cells per slide using Leica QWinPlus digital image processing and analysis software, Leica Microsystems, Switzerland. The DNA damage was evaluated by the length of the comet's tail for each cell.</span><br />
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<b style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Statistical analysis</b><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">This cross-sectional study was analyzed as a traditional case-control study with the extent of DNA damage as the main outcome. Oral habits were dichotomized as present/absent and a second variable of oral habit pack-years of exposure was also examined. Mean tail length was compared between diagnostic groups and between different oral habit groups using t-tests and analysis of variance (ANOVA). Pearson's product moment correlation was used to examine the linear association between the extent of DNA damage and oral habit pack-years. Scheffe's pair-wise test was employed to adjust for multiple comparisons. All statistical analyses were done using SAS</span><sup style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">®</sup><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> V8.2 statistical software package (PC-SAS) (Cary, NC, USA).</span></div>
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Results</span></h2>
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Mean (±SD in years) age of controls (36 ± 16.4) was greater than OSMF (30.0 ± 11.2) although lesser than leukoplakia (44.0 ± 8.6) and oral cancer (54.3 ± 8.5) patients. Overall, 85% of the subjects in the study sample were men; 82% had at least one deleterious oral habit (43% smoked bidi, 17% smoked cigarette, 15% chewed pan, and 15% chewed tobacco); 48% had oral cancer; 22% leukoplakia, 11% OSMF and 19% were controls with no oral lesions and having normal oral epithelium. Overall, 46.4% had office-based jobs; 37% were farmers or laborers and the rest (17%) either stayed at home or were students attending university.</span><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">(Figure 1)<span style="background-color: black;">, </span></span><span style="background-color: black;"><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">(Figure 2)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">, </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">(Figure 3)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> and </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">(Figure 4)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> show the representative "comets" in normal epithelium, leukoplakia, OSMF and oral cancer. (Table 1)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> provides a composite description of DNA damage and extent of oral habits (in pack-years) in different lesion diagnostic groups. The mean (±SD) tail lengths (in mm) for oral cancer (24.95 ± 5.09) and leukoplakia (12.96 ± 2.68) were statistically significantly more than that of controls (8.54 ± 2.55, </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">P</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"><0.05) in bivariate analysis. Mean tail length in OSMF, although higher than controls (11.03 ± 5.92), was not significantly different. Extent of bidi smoking and pan chewing (measured in pack-years) were substantially greater in oral cancer subjects compared to others. Substantial pack-years of bidi and cigarette smoking exposure were evident among leukoplakia subjects. None of the OSMF subjects in this study reported chewing pan although they reported substantial exposure to chewing tobacco.</span></span></div>
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<b style="font-family: Arial, Verdana, Helvetica, sans-serif; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 1: Non-fragmented and undamaged DNA in normal healthy adults</b>
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<b style="font-family: Arial, Verdana, Helvetica, sans-serif; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 2: DNA fragmentation in oral leukoplakia</b>
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<b style="font-family: Arial, Verdana, Helvetica, sans-serif; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 3: DNA fragmentation in oral submucous fibrosis</b>
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<span style="background-color: black;"><span style="font-family: Arial, Verdana, Helvetica, sans-serif; font-size: 12px; line-height: 18px; text-align: justify;"><b>Figure 4: DNA fragmentation in oral cancer</b></span>
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; font-size: 12px; line-height: 18px; text-align: justify;"><b style="background-color: black;">Table 1: Mean (standard deviation) comet length (DNA damage - tail length) and oral habits in pack-years in oral cancer and precancer groups</b></span>
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Table 2 describes the extent of DNA damage among subjects with different deleterious oral habits. Extent of DNA damage for people with any oral habit (19.78 ± 7.77) was significantly greater than those with no habits at all (8.54 ± 2.55; </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">P</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"><0.0001). Similarly, those smoking bidi, cigarette, or pan had significantly greater DNA damage compared to subjects not having those habits in the respective habit groups. Pearson's correlation between tail length and oral habits suggests moderate positive linear correlation between bidi smoking exposure in pack-years and tail length (r=0.52), and between pan chewing (in pack-years) and tail length (r=0.41).</span></div>
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Table 3 shows the ANOVA source table for modeling tail length differences between controls, leukoplakia, OSMF and leukoplakia after adjusting for deleterious oral habits such as bidi smoking, tobacco chewing, pan chewing and cigarette smoking. The overall model was better than an intercept-only model (</span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">P</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"><0.0001). This ANOVA model had good explanatory power explaining 76% of the variability in the data (R </span><sup style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">2</sup><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> =0.757). After adjustment for oral habits, oral cancer subjects had significantly greater tail length than that of controls. Extent of DNA damage of cancer cases was also significantly greater than in leukoplakia. However, tail length in OSMF (11.03 ± 5.92) or leukoplakia (12.96 ± 2.69) patients was not significantly different from that of controls. Upon removing OSMF from the diagnostic lesion groups and the non-contributing exposure factors (cigarette smoking and tobacco chewing), the difference in tail length between leukoplakia and controls came close to the statistical significance level.</span>
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<b style="font-family: Arial, Verdana, Helvetica, sans-serif; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 3: ANOVA source table for tail length (μ m) in cancer and precancer after adjusting for oral habits, Scheffe's pair-wise test was used to control for multiple comparison</b>
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Discussion</span></h2>
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Several studies have demonstrated an independent association of deleterious oral habits such as smoking, betel quid chewing and chewing tobacco with occurrence of oral cancer.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> The precancerous conditions such as leukoplakia, characterized by a white patch, mainly associated with tobacco smokers, and OSMF, characterized by deposition of collagen and marked blanching of oral cavity, leading to inability to open mouth, mainly associated with smokeless tobacco and betel quid chewers, have a greater prevalence in our country. Both of these conditions have high cancer turnover potentiality and if detected early can be prevented and treated successfully. With present advances in genotoxicologic studies, extent of DNA damage provides a platform to determine the cancer progression.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> The association of these oral habits with DNA damage has never been clearly established. Moreover, comet assay provides a generalized picture of a population that shows whether it is under environmental carcinogenic stress, and may become an epidemiologic asset. We have been able to demonstrate in this study that DNA damage is associated with oral cancer and leukoplakia, and also that DNA damage is associated with deleterious oral habits. Bidi smoking and pan chewing or presence of any deleterious oral habit led to DNA with greater tail length.</span><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Exploring these relationships a little further, we found moderate linear relationship between smoking and pan chewing, and comet tail length, providing general evidence that greater the exposure to these habits, greater would be the extent of DNA damage and vice versa. However, the difference in comet tail length between those chewing and not chewing tobacco did not achieve statistical significance in this study just as the Pearson's coefficient showed a negative, but strong correlation. But comparing the extent of DNA damage of tobacco chewers with those with no oral habits presented a somewhat different scenario. We attribute these discrepancies to the composition of comparison groups because those reporting not chewing tobacco had several other habits that confounded the relationship between tobacco chewing and extent of DNA damage. We did not have enough mutually exclusive oral habit groups to allow a meaningful comparison of independent effect of each oral habit. Similar explanation also holds for the association of cigarette smoking with the extent of DNA damage.</span><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">In multivariable analyses, ANOVA models suggested that comet tail length was significantly greater in oral cancer compared to other groups even after adjusting for all oral habits that were included in the models. This model was better than an intercept-only model and also explained about 76% of the variation. Although we demonstrated significantly greater tail length in leukoplakia compared to controls in bivariate analysis, this was not obvious in multivariable analyses after adjusting for multiple comparison. However, upon further modeling, we found that by removing oral habits that did not contribute much to the model (i.e. keeping only the main contributor-bidi smoking), the R </span><sup style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">2</sup><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> value increased to 78% and comet tail length difference between leukoplakia and controls came very close to becoming statistically significant. Although we could not specifically demonstrate that extent of DNA damage was greater in leukoplakia compared to controls after adjusting for oral habits, we attribute this to the low power in this study.</span><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">The present study has some limitations that include its small sample size, and because of this we observed a peculiar problem in data analysis as none of the controls reported any deleterious oral habits that we measured. This observation did not allow for certain comparisons to be carried out. However, we noticed that extent of oral habits measured as pack-years of exposure were substantially greater for oral cancer and leukoplakia patients compared to those not exposed to the corresponding oral habit. Bivariate analyses demonstrated that extent of DNA damage in oral cancer and leukoplakia were greater than in controls and pack-year of exposure were generally greater in oral cancer. Despite the limitations, we have been able to demonstrate that DNA damage in blood cells measured by SCGE is greater in oral cancer and leukoplakia, but not in OSMF. Deleterious oral habits are also associated with greater DNA damage.</span><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Although none of the evidence in this cross-sectional and small study per se provides an opportunity to consider temporal associations and infer causality, there is preponderance of evidence in published literature to discuss potentially causal associations in the context of this study.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> One of the key factors to consider is that the DNA damage demonstrated in our study is in T-cells in the blood which belongs to a distinctly different biological compartment than the site of the lesion. From a potentially etiological mechanism explanation standpoint, the biological effect(s) of oral habits on oral tissues would take place through direct interaction between the exposure agent and/or a subsequent exposure through systemic absorption and release through subepithelial capillaries in the submucosa or through secretion into either saliva or gingival crevicular fluid. Therefore, it is intuitive to consider that substantial DNA damage demonstrated in the blood compartment is an indirect evidence of potentially greater damage in local tissue (oral epithelium). Measuring the extent of DNA damage directly in oral epithelium would provide direct evidence of association of DNA damage in oral epithelium with these deleterious oral habits to develop an etiological explanation. However, measuring the extent of DNA damage in blood cells could provide for the possibility of developing an easy detection test because blood is collected in all routine investigations and no extra invasion would need to be performed for such a test, should it become available in the future.</span><br />
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Studies have demonstrated direct lesion tissue genetic damage in leukoplakia with increased frequency of loss of heterozygosity.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">Therefore, demonstration of DNA damage using SCGE in oral epithelium will expand the possibility of developing early detection tests using exfoliative cytology techniques. Suitability of comet assay performed on white blood cells as a rapid test in biomonitoring occupational exposure to DNA-damaging agents across several industries has been extensively reviewed by Møller </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> The authors concluded that in general, the comet assay is considered a suitable and fast test for DNA-damaging potential in biomonitoring studies. Genetic changes in margins of resections of cancer/precancer </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px; text-align: justify;"> may also be an important determinant of success of intervention in these cases. These are some of the potential situations where demonstrating DNA damage using SCGE may lead to further advancement in our understanding of the biology of oral cancer and precancer for developing possible worthy early detection tests.</span></div>
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References</span></h2>
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<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">1.</span></td><td><span style="color: #cc0000; font-size: small;">Warnakulasuriya S. Significant oral cancer risk associated with low socioeconomic status. Evid Based Dent 2009;10:4-5.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">2.</span></td><td><span style="color: #cc0000; font-size: small;">Weinberg RA. Biology of cancer. London: Taylor and Francis Inc; 2006.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">3.</span></td><td><span style="color: #cc0000; font-size: small;">Zhang L, Cheung KJ Jr, Lam WL, Cheng X, Poh C, Priddy R, <i>et al.</i> Increased genetic damage in oral leukoplakia from high risk sites: Potential impact on staging and clinical management. Cancer 2001;91:2148-55.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">4.</span></td><td><span style="color: #cc0000; font-size: small;">Zhang L, Cheng X, Li Y, Poh C, Zeng T, Priddy R, <i>et al.</i> High frequency of allelic loss in dysplastic lichenoid lesions. Lab Invest 2000;80:233-7.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">5.</span></td><td><span style="color: #cc0000; font-size: small;">Östling O, Johanson KJ. Microelectrophoretic study of radiation-induced DNA damages in individual mammalian cells. Biochem Biophys Res Commun 1984;123:291-8.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">6.</span></td><td><span style="color: #cc0000; font-size: small;">Singh NP, McCoy MT, Tice RR, Schneider EL. A simple technique for quantitation of low levels of DNA damage in individual cells. Exp Cell Res 1988;175:184-91.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">7.</span></td><td><span style="color: #cc0000; font-size: small;">Fairbairn DW, Olive PL, O'Neill KL. The Comet assay: A comprehensive review (Review). Mutat Res 1995;339:37-59.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">8.</span></td><td><span style="color: #cc0000; font-size: small;">Collins AR. The comet assay for DNA damage and repair (Review). Mole Biotechnol 2004;26:249-61.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">9.</span></td><td><span style="color: #cc0000; font-size: small;">Rojas E, Lopez MC, Valverde M. Single cell gel electrophoresis: Methodology and applications (Review) J Chromatogr B Biomed Sci Appl 1999;722:225-54.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">10.</span></td><td><span style="color: #cc0000; font-size: small;">Anderson D, Yu TW, McGregor DB. Comet assay responses as indicators of carcinogen exposure (Review). Mutagenesis 1998;13:539-55.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">11.</span></td><td><span style="color: #cc0000; font-size: small;">Moller P, Knudsen LE, Loft S, Wallin H. The comet assay as a rapid test in biomonitoring occupational exposure to DNA-damaging agents and effect of confounding factors. Cancer Epidemiol Biomarkers Prev 2000;9:1005-15.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">12.</span></td><td><span style="color: #cc0000; font-size: small;">Korabiowska M, Voltmann J, Honig JF, Bortkiewicz P, Konig F, Cordon-Cardo C, <i>et al.</i> Altered expression of DNA double-strand repair genes Ku70 and Ku80 in carcinomas of the oral cavity. Anticancer Res 2006;26:2101-5.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">13.</span></td><td><span style="color: #cc0000; font-size: small;">Proia NK, Paszkiewicz GM, Nasca MA, Franke GE, Pauly JL. Smoking and smokeless tobacco-associated human buccal cell mutations and their association with oral cancer: A review. Cancer Epidemiol Biomarkers Prev 2006;15:1061-77.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">14.</span></td><td><span style="color: #cc0000; font-size: small;">Ribeiro DA. Single-cell gel (comet) assay as a promising tool for the detection of DNA damage induced by compounds used in dental practice: The oral cancer risk assessment. Crit Rev Oncog 2008;14:165-75.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">15.</span></td><td><span style="color: #cc0000; font-size: small;">Avasn Maruthit Y, Rao RS, Palivela H, Thakre S. Impact of gutkha chewing and smoking on microbial environment of oral cavity: A case study on slum dwellers of selected areas in Visakhapatnam. J Environ Sci Eng 2004;46:268-73.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">16.</span></td><td><span style="color: #cc0000; font-size: small;">Zhang L, Rosin MP. Loss of heterozygosity: A potential tool in management of oral premalignant lesions? J Oral Pathol Med 2001;30:513-20.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">17.</span></td><td><span style="color: #cc0000; font-size: small;">Zhang L, Poh CF, Lam WL, Epstein JB, Cheng X, Zhang X, <i>et al.</i> Impact of localized treatment in reducing risk of progression of low-grade oral dysplasia: Molecular evidence of incomplete resection. Oral Oncol 2001;37:505-12. </span></td></tr>
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com0tag:blogger.com,1999:blog-3393509504180156297.post-33800001208630681572012-07-20T22:45:00.002-07:002012-07-22T19:21:42.566-07:00Erupted maxillary conical mesiodens in deciduous dentition in a Bengali girl - A case report<div dir="ltr" style="text-align: left;" trbidi="on">
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Abstract</span></h2>
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Mesiodens is a midline supernumerary tooth commonly seen in the maxillary arch. It is the most significant dental anomaly affecting permanent dentition mainly and primary dentition rarely. It may occur as an isolated dental anomalous condition or may be associated with a syndrome. Many theories have been promulgated to explain its etiology. But an exact etiology is still obscure. Incidence of mesiodens in children varies from 0.15 to 3.8%. Boys are affected more (2 : 1) than Girls. Morphologically, mesiodens may be of three types: the most commonly seen is conical, while tuberculate and supplementary types.</div>
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<span style="color: magenta; font-size: x-large;">Introduction</span></h2>
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Numerical superiority in a dentition when compared to normal is known as Hyperdonua. The tooth or teeth causing this numerical excess is/are called the supernumerary tooth or teeth.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">The supernumerary tooth present in the midline of the maxilla between the two central incisors is referred to as 'mesiodens.' The plural number of mesiodens is mesiodentes. The incidence of mesiodens in permanent dentition ranges from 0.15 to 3.8%, whereas in primary dentition it ranges from 0 to 1.9%.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">They are twice more common in boys, while no significant sex distribution is noted in primary supernumerary teeth.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Mesiodens may erupt normally, stay impacted, appear inverted, take an ectopic position, or follow an abnormal path of eruption. It is seen that the frequency of erupted primary supernumerary teeth is much higher than that of the permanent supernumerary teeth (73 </span><i style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">vs</i><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">25%). </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Mesiodens or mesiodentes may precipitate a variety of complications, for example, crowding, delayed eruption, diastema, rotations, cystic lesions, and resorptions of adjacent teeth, etc., to the developing dentition/occlusion of a child. Supernumerary teeth may occur as a single isolated dental anomaly or in association with other developmental anomalies, or syndromes such as cleft palate and cleft lip, cleido-cranial dysostosis, Down's syndrome, and Gardner's Syndromes. The incidence of supernumerary teeth in cleft lip and cleft palate case may be as high as 28%.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Supernumerary teeth of the premaxillary region may appear in a variety of shapes though the most common type is conical or peg shaped (61%).</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">The other two commonly present are tuberculate and supplemental (adjacent tooth like).</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Over the years, suggestions or theories have been put forward to explain the etiology of supernumerary teeth, which includes phylogenetic reversion (atavistic theory), split in tooth bud (dichotomy theory), locally conditioned hyperactivity of the dental lamina (dental lamina theory), and a combination of genetic and environmental factors (unified etiologic explanation).</span>
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<span style="color: magenta; font-size: x-large;"> Case Report</span></h2>
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">The parents of a 4-year-old girl reported to the Department of Pedodontics and Preventive Dentistry of Dr. R. Ahmed Dental College and Hospital, Kolkata with the chief complaint of a gradual development of an odd appearance of teeth. The girl was following childhood immunization schedule strictly. The medical and family history was noncontributory. No significant abnormality was noted in the extra-oral examination (Figure 1)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Intra-oral examination revealed a complement of the primary dentition in a well-maintained oral health. A conical mesiodens was noted between the central incisors<span style="background-color: black;"> </span></span><span style="background-color: black;"><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> (Figure 2)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">. Intra-oral periapical radiograph of the maxillary anterior region showed a completely formed mesiodens with a conical crown and a root </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> (Figure 3)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">. Orthopantomogram also revealed the mesiodens </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> (Figure 4)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">.</span></span></div>
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">The mesiodens was extracted under local anesthesia, after making a preoperative impression for record<span style="background-color: black;"> </span></span><span style="background-color: black;"><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> (Figure 5)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">, </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> (Figure 6)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">, </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> (Figure 7)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">.</span></span></div>
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<span style="color: #555555; font-size: 15px;">
</span><span style="color: magenta; font-size: x-large;">Discussion</span></h2>
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">The first report of supernumerary teeth appeared between 23 and 79 ad.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Mesiodens account for a 45-67% of all super numerary teeth.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Balk (1917) defined mesiodens as the most common of supernumerary teeth located mesial to both centrals, appearing peg shaped in a normal position or inverted position.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Regezi and Sciubba mentioned that the anterior midline of maxilla is the most common site of supernumerary tooth in which case the supernumerary tooth is known as mesiodens.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Very few supernumerary teeth have been reported for the primary dentition.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> The present case is quite unusual as this reports a mesiodens in primary dentition and that too in a girl.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Supernumerary teeth are classified according to their shape and size (morphology) and location. The present case, reports of a conical mesiodens.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Conical mesiodens has certain characteristics, which are as follows:</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">· They are usually located between the permanent maxillary central incisors but rarely erupt labially.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">· They erupt during childhood.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">· They usually have complete root formation ahead of the adjacent teeth.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">· They rarely cause delay in eruption of central incisors, but may cause alteration of path of eruption of these teeth.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">A labially positioned mesiodens may cause palatal deflection of an incisor that may erupt with a rotation or in reverse bite rotationship. Other clinical problems associated with mesiodens are the development of malocclusion, ectopic eruption of adjacent teeth, cystic changes in the follicle, etc. Detection of mesiodens or supernumerary teeth is best achieved by clinical examination and radiography (IOPA, Occlusal, Orthopantomogram).</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">If there is no concomitant hypodontia, the choice of treatment of mesiodens is removal. In case of unerupted mesiodens, before surgical extraction is attempted, the location of the tooth/teeth and the state of root formation of adjacent teeth must be ascertained.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">In the present case, the erupted conical mesiodens in the four-year-old girl was a great aesthetic concern to the parents. And an immediate extraction of the mesiodens was undertaken under local anesthesia to pervert the development of psychological trauma in the child, to minimize complications, and to achieve a good prognosis.</span></div>
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<span style="color: magenta; font-size: x-large;">
References</span></h2>
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<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">1.</span></td><td><span style="color: #cc0000; font-size: small;">Sharma A, Gupta S, Madam M. Uncommon mesiodens - a. report of two cases. J. Indian Soc. Pedo Prev. Dent 1999;17:69-71.</span><br />
<span style="color: #cc0000; font-size: small;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">2.</span></td><td><span style="color: #cc0000; font-size: small;">Gallas MM, Garcia A. Retention of Permanent Incisors by mesiodens: A family affair. BDJ 2000;188:63-4.</span><br />
<span style="color: #cc0000; font-size: small;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">3.</span></td><td><span style="color: #cc0000; font-size: small;">Prabhu NT, Rebeca J, Munshi AK. Mesiodens in the primary dentition - A case report. J Indian Soc Pedo Prev Dent 1998;16:935.</span><br />
<span style="color: #cc0000; font-size: small;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">4.</span></td><td><span style="color: #cc0000; font-size: small;">Jeng-fen Liu, Characteristics of Premaxillary Supernumerary teeth: A survey of 112 cases. J Dent Child 1995;262-5. </span><br />
<span style="color: #cc0000; font-size: small;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">5.</span></td><td><span style="color: #cc0000; font-size: small;">Zilberman Y, Marlon M, Shteyer A. Assessment of 100 children in Jerusalem with supernumerary teeth in the premaxillary region. J Dent Child 1992;44-7. </span><br />
<span style="color: #cc0000; font-size: small;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">6.</span></td><td><span style="color: #cc0000; font-size: small;">Weinberger BW. An introduction to history of Dentistry. St. Louis CV Mosby Co 1948. </span><br />
<span style="color: #cc0000; font-size: small;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">7.</span></td><td><span style="color: #cc0000; font-size: small;">Jiau Fu Z, Mauricio M, David LK, Robert JH. Supernumerary and congenitally absent teeth: a literature review. J Clin Pediatr Dent 1996;20:87-95. </span><br />
<span style="color: #cc0000; font-size: small;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">8.</span></td><td><span style="color: #cc0000; font-size: small;">J Randle Luten, Jr. The Prevalence of supernumerary teeth in primary and mixed dentition. J Dent Child 1967;34:346-53.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">9.</span></td><td><span style="color: #cc0000; font-size: small;">JA Ragezi, JJ Sciubba. Oral Pathology - Clinical Pathologic Correlation. 3rd edn. W. B. Saunder Co., Philadelphia: Lonndorn, New York.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">10.</span></td><td><span style="font-size: small;"><span style="color: #cc0000;">Laura Castillo Kalen. The incidence of mesiodens in children of Hispanic descent. The Journal of Pedodontics 1986;10:164-8. </span> </span></td></tr>
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com1tag:blogger.com,1999:blog-3393509504180156297.post-72486008313643732592012-07-12T00:44:00.000-07:002012-07-22T19:39:40.748-07:00Study of neutrophils isolated from peripheral blood of patients suffering from aggressive periodontitis at the cellular level: Receptors and cytoskeletal reorganization<div dir="ltr" style="text-align: left;" trbidi="on">
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Abstract</span></h2>
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<b>Background:</b> Aggressive periodontitis (AgP) has been associated with polymorphonuclear leukocyte's (PMNL) dysfunction and periodontal pathogens possess variety of virulence factors that can impair PMNL's function. This study investigated the possible association between defective neutrophil adhesion and β<sub>2</sub> -integrin expression and defective neutrophil migration and actin polymerization level in the peripheral blood of neutrophils from the patients with AgP. <b>Materials and Methods:</b> A total of 30 individuals both male and female, age ranges between 13 - 48 years, were included in the study. Healthy controls (group I, <i>n</i>=10), chronic periodontitis (ChP) (group II, <i>n</i>=10), and AgP (group III,<i>n</i>=10), all without any systemic diseases and non-smokers, were recruited. Peripheral blood samples were taken and β<sub>2</sub> -integrin expression and actin polymerization levels were estimated by using fluorescence activated cell sorter analysis. <b>Results:</b> In AgP cases, both average values (β<sub>2</sub> -integrin and actin level) were significantly less than that of normal subjects (<0.001). But for ChP cases, only the average value of actin level is significantly lower than that of normal subjects (<0.025). <b>Conclusion:</b> Lower β<sub>2</sub> -integrin expression in the AgP cases signifies lower neutrophil adhesion in AgP cases than normal, and the lower average value of actin polymerization for the AgP cases suggest lower migration capacity of neutrophils in AgP cases than normal.</div>
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Introduction</span></h2>
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<span style="line-height: 18px;">The oral cavity acts as one of the most important gates for pathogens to enter into the host, and despite the high prevalence of individuals harboring bacterial pathogens, only limited group of otherwise healthy individuals exhibit severe form of aggressive periodontitis (AgP), while other do not suffer from any progressing forms of periodontal disease.</span><br />
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<span style="line-height: 18px;">Thus, microbial factors alone always are not able to explain inter-individual differences in the outcome and course of periodontal disease.</span><br />
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<span style="line-height: 18px;">AgP encompasses a distinct type of periodontitis that affect people who, in most cases, otherwise appear healthy. It tends to have a familial aggregation and there is a rapid rate of disease progression. </span><span style="line-height: 18px;"> </span><br />
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<span style="line-height: 18px;">Neutrophils (PMNs) are the key components of this host response and are responsible for neutralizing periodontopathic bacteria in both the gingival crevice and the underlying connective tissue. Neutrophil to function effectively, require their fully functional motility. Proinflammatory cytokine-induced shedding of the L-selectin, followed by increased expression of the β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrin at the PMN surface, is one of the main mechanisms underlying transendothelial migration. </span><br />
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<span style="line-height: 18px;">Motile function of neutrophil is directly and/or indirectly dependent upon the proper polymerization and depolymerization of the actin cytoskeleton, from a more fluid globular actin form (g-actin) to a more rigid filamentous network of actin (f-actin). </span><br />
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<span style="line-height: 18px;">The directed migration (chemotaxis) of PMNLs to the sites of infection or inflammation is essential for the host's defense against bacterial invasion. </span><i style="line-height: 18px;">In vivo</i><span style="line-height: 18px;">, PMNLs rapidly migrate from the blood stream through the vascular-endothelium and through the connective tissue to the site of infection where they destroy the invading microorganisms. </span><br />
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<span style="line-height: 18px;">The present study was undertaken to find out the possible association between defective PMN adhesion and β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrin expression and defective PMN migration and actin polymerization level in the peripheral blood neutrophils of AgP patients and the same were compared with that of normal subjects and patients suffering from chronic periodontitis. Since no report of such type of study is available in the literature and it seems to be the first of its kind in the Indian scenario.</span><br />
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<span style="font-size: x-large;">Materials and Methods</span></h2>
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<span style="line-height: 18px;">The subjects were selected from:</span><br />
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<li>Case group: Out patients Department of Oral Diagnosis, Dr. R. Ahmed Dental College and Hospital, Kolkata</li>
<li>Control group: The subjects were selected from the students and staff of Dr. R. Ahmed Dental College and Hospital, Kolkata.</li>
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<span style="line-height: 18px;">The study was carried out in the:</span><br />
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<li>Department of Periodontics, Dr. R. Ahmed Dental College and Hospital, Kolkata</li>
<li>Department of Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology. Ballygunge Science College, Kolkata.</li>
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<b style="line-height: 18px;">Criteria for case selection</b><br />
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<li>All cases were free of any past history of systemic diseases</li>
<li>No cases had received antibiotics, systemic steroid therapy, or anti-inflammatory drugs within the preceding three months.</li>
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<span style="line-height: 18px;">Cases engaged in tobacco smoking were excluded.</span><br />
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<b style="line-height: 18px;">Criteria for group division</b><br />
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<span style="line-height: 18px;">Total thirty subjects were equally divided into following three groups:</span><br />
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<i style="line-height: 18px;">Group I (normal healthy control)</i><br />
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<li>For group I, the "healthy periodontium" describe a subject with no clinical or radiographic evidence of current or previous loss of connective tissue attachment or supporting bone, no bleeding on probing, and no signs of gingival inflammation or other signs of disease activity </li>
<li>Age group was taken between 13-48 years.</li>
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<i style="line-height: 18px;">Group II (chronic periodontitis)</i><br />
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<li>Age group was taken between 30-48 years as chronic periodontitis (ChP) is prevalent in adults, but may be found in younger patients also</li>
<li>There was attachment loss and amount of tissue destruction was found to consistent with local etiologic factors of plaque and calculus </li>
<li>Subgingival calculus and radiographically, horizontal and/or vertical bone loss was found.</li>
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<i style="line-height: 18px;">Group III (aggressive periodontitis)</i><br />
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<li>Either showed circumpubertal onset with periodontal damage being localized to permanent first molars and incisors or showed generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors around the age of 30 years </li>
<li>Non-contributory medical history, rapid attachment loss and bone destruction, familial aggregation of cases, and amount of deposit were inconsistent with severity of periodontal tissue destruction </li>
<li>Radiographically, either showed "arc-shaped loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar" or severe bone loss associated with the minimal number of teeth.</li>
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<b style="line-height: 18px;">Periodontal examination</b><br />
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<span style="line-height: 18px;">The clinical periodontal parameters used were the plaque index (PlI),</span><span style="line-height: 18px;"> gingival index, </span><span style="line-height: 18px;"> calculas index - simplified (CI-S),</span><span style="line-height: 18px;"> mobility index (Lindhe, 1983).</span><span style="line-height: 18px;"> Probing depth and attachment levels were recorded at four points around each tooth in millimeter. Full mouth radiographic assessments were made by Orthopantomogram.</span>
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<b style="line-height: 18px;">Hematological examination</b><br />
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<i style="line-height: 18px;">Isolation of neutrophil</i><span style="line-height: 18px;"> </span><br />
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<span style="line-height: 18px;">Twenty milliliters of peripheral blood was collected from Antecubital vein of Healthy Control, ChP and AgP subjects. The whole blood was heparinized (25 units/ml of blood). Six milliliters of six percent dextran (Amersham Biosciences, Uppsala Sweden) was added to precipitate RBC. After half an hour, plasma was separated from Red Blood Cell (RBC) precipitate and was added with 12 ml Ficoll - Paque plus solution (Amersham Biosciences, Uppsala Sweden) to precipitate neutrophil. Then the sample was centrifuged (Biofuge Stratus, Porton-Down, Great Britain) for 30 minutes at 2000 RPM at 4°C temperature. Supernatant was decanted. For hypotonic lysis of contaminating RBC, 6 ml distilled water was added and simultaneously shake for 45 seconds. To stop the hypotonic lysis, 2 ml of 3.6% sodium chloride solution was added and centrifuged for half an hour and then decanted. The resulting neutrophil precipitate was resuspended in 2 ml neutrophil buffer.</span><br />
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<i style="line-height: 18px;">Detection of β<sub>2</sub> integrin</i><span style="line-height: 18px;"> </span><br />
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<span style="line-height: 18px;">Three hundred and fifty microliters of the above solution was taken and fifteen microliters integrin β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> mouse monoclonal antibody (Santa Cruz Biosciences, Santa Cruz, California) was added as primary antibody. Mixture was rotated in a "CELL MIXTURE" at 4°C for 45 minutes. It was then centrifuged for 1 minute at 2000 RPM. The precipitate was then washed with Phosphate Buffer Saline (PBS) and 300 μl PBS buffer was added. Again, it was centrifuged for 1 minute at 2000 RPM. Twenty microliters of Rabbit Antimouse IgG - TRITC Conjugate (Bangalore Genei) was added as secondary antibody and it was then rotated in a "CELL MIXTURE" at 4°C in dark room. The mixture was again centrifuged and prepared for fluorescence activated cell sorter (FACS) analysis by adding neutrophil buffer to make the sample 1000 μl. All antibodies were diluted in PBS and used at saturating concentrations, as determined in preliminary experiments.</span><br />
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<i style="line-height: 18px;">Detection of actin polymerization</i><span style="line-height: 18px;"> </span><br />
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<span style="line-height: 18px;">Three hundred and fifty microliters of neutrophil suspension was again taken from main sample and ten microliters of glutamic acid (3 mg/ml) was mixed as a ligand for one and half minutes. A total of 4.6% paraformaldehyde was mixed for fixing the reaction. After 15-20 minutes, it was centrifuged for 1 minute at 2000 RPM and supernatant was removed. 0.5% Triton X 100 (MERCK, Bombay, India) was mixed with the sample to facilitate entry of dye (Alexa 488 phalloidin) within the neutrophil and better visualization of actin polymerization. After 5-6 minutes, 2λ Alexa 488 phalloidin (Molecular Probes) was mixed. By adding neutrophil buffer, the sample was prepared for FACS analysis.</span><br />
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<b style="line-height: 18px;">FACS analysis</b><br />
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<span style="line-height: 18px;">The β-2 integrin expression on the cell surface and actin polymerization level was measured by using Flowcytometry and analyzed by using</span><i style="line-height: 18px;">Cell Quest Pro software</i><span style="line-height: 18px;">. Ten thousand events were counted per sample and the fluorescence was measured.</span></div>
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Results</span></h2>
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<span style="line-height: 18px;">(Table 1)<span style="background-color: black;">,</span></span><span style="background-color: black;">(Table 2)<span style="line-height: 18px;"> and </span>(Table 3)<span style="line-height: 18px;"> show the β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrin expression in normal subjects, AgP, and ChP patients, respectively. </span>(Table 4)<span style="line-height: 18px;">,</span>(Table 5)<span style="line-height: 18px;"> and </span>(Table 6)<span style="line-height: 18px;"> show the actin polymerization level in normal subjects, AgP, and ChP patients, respectively. </span>(Table 7)<span style="line-height: 18px;"> shows statistical indices for each group (Average (AV), standard deviation (S.D.), standard error of the averages (S.E.), coefficient of variation (C.V. in percentages) and range and correlation coefficient).</span></span><br />
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<b style="background-color: black; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 1: β2 integrin levels in neutrophils of normal healthy subjects</b>
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<b style="background-color: black; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 2: β2 integrin levels in neutrophils of aggressive periodontitis cases</b>
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<b style="background-color: black; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 3: β2 integrin levels in neutrophils of chronic periodontitis cases</b>
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<b style="background-color: black; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 4: Actin polymerization levels in neutrophils of normal subjects</b>
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<b style="background-color: black; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 5: Actin polymerization levels in periodontitis cases</b>
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<b style="background-color: black; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 6: Actin polymerization level in neutrophils of aggressive neutrophils of chronic periodontitis cases</b>
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<b style="background-color: black;">Table 7: Statistical indices AV, SD, SE, CV, R and r for β2 integrin level and actin polymerization level of normal subjects, aggressive periodontitis cases, and chronic periodontitis cases</b></div>
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<span style="line-height: 18px;">The coefficient of variation is a measure of the extent of variation in relation to average (S.D./average in percentage). It could be seen that highest C.V. is for ChP cases (28.086) for β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> - integrin expression, followed by actin of ChP (18.084), and 11.808, in respect of β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> - integrin of AgP. For the normal subjects, both for β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> - integrin and actin the C.V. values are very small (4.037 or 3.69, respectively). Also for actin in AgP patients, the C.V. is small (5.603). Small C.V. values denote consistent sample values, whereas high C.V. values signify inconsistent sample values. It will also be corroborated from the S.D. values or the ranges.</span><br />
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<span style="line-height: 18px;">Correlation analysis of the data showed negative correlation between the β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> - integrin and actin groups for each of normal, ChP, and AgP cases. In the last row <span style="background-color: black;">of the </span></span><span style="background-color: black;">(Table 7)<span style="line-height: 18px;">, the 'r' values have been shown. All the three 'r' values are negative indicating negative association between the β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> - integrin and actin for all the three groups (normal, ChP, and AgP). The correlation coefficients are however not significant at 5% level of significance.</span></span></div>
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<span style="line-height: 18px;">For both β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrin and actin, the average values for AgP cases are significantly less than that of normal values. The critical value of 't' at 18 degrees of freedom is 3.922 at </span><i style="line-height: 18px;">P</i><span style="line-height: 18px;">=0.001. As both the 't' values with degree of freedom (d.f) 18 exceeds the critical value of 't' at 0.1% level, they are significant at P=0.001. </span><br />
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<span style="line-height: 18px;">Unlike the previous comparison<span style="background-color: black;"> </span></span><span style="background-color: black;">(Table 8)<span style="line-height: 18px;">, in </span>(Table 9)<span style="line-height: 18px;"> for β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrin the ChP cases do not differ significantly from the control cases. The difference between the two average values (74.896 for normal and 70.791 for ChP) do not reach the significant level (t=0.645, d.f=18, </span><i style="line-height: 18px;">P</i><span style="line-height: 18px;">>0.05). However, for actin, the average value for the ChP case (75.793) is significantly lower than that of normal cases (88.205). The differences between these averages exceed the critical value of 't' at 2.5% level (t=2.786, dif=18, </span><i style="line-height: 18px;">P</i><span style="line-height: 18px;"><0.025).</span></span></div>
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<b style="background-color: black; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 8: Aggressive periodontitis cases compared with normal subjects</b>
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<b style="background-color: black; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 9: Chronic periodontitis cases compared with normal subjects</b>
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<span style="line-height: 18px;">For β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrin, the ChP cases have significantly higher average value (70.791) than the average value (55.693) of AgP cases (t=2.40, d.f=18,</span><i style="line-height: 18px;">P</i><span style="line-height: 18px;"><0.05) </span><span style="background-color: white;">(Table 10)</span><span style="background-color: white; line-height: 18px;">.</span></div>
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<b style="background-color: black; font-size: 12px; line-height: 18px; text-align: -webkit-center;">Table 10: Comparison between chronic periodontitis and aggressive periodontitis</b>
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<span style="line-height: 18px;">For actin, the two average value (70.019 and 75.793, respectively, for AgP and ChP cases) do not differ significantly (t=1.281, d.f=18, </span><i style="line-height: 18px;">P</i><span style="line-height: 18px;">>0.05).</span></div>
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</span><span style="font-size: x-large;">Discussion</span></h2>
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<br />
<span style="line-height: 18px;">In the present study, statistical analysis reveals<span style="background-color: black;"> </span></span><span style="background-color: black;">(Table 7)<span style="line-height: 18px;"> the average values of β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> - integrin expression (55.69) for AgP patients were significantly lower than that of normal subjects (74.896) and ChP patients (70.79) </span>(Table 10)<span style="line-height: 18px;">, but in case of actin polymerization level for AgP (70.02), the value was significantly lower when compared with normal subjects (88.21) only. The result signifies that there might be functional defect (adhesion and migration) in neutrophil isolated from AgP patients. In the ChP group, as both values were comparable to those of a healthy control group, it signifies that neutrophil defect was not a characteristic feature for ChP cases.</span></span><br />
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<span style="line-height: 18px;">It is well established that neutrophil adhesion to the vascular endothelium is directly proportional to the β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> - integrin expression on the neutrophil surfaces.</span><span style="line-height: 18px;">There have been conflicting reports on the expression of β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrins at the surface of PMN from patients with periodontitis.</span><span style="line-height: 18px;"> Agarwal et al.</span><span style="line-height: 18px;"> reported that the increased adherence of neutrophils from juvenile periodontitis (JP) patients was attributed to unregulated plasma membrane expression of β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrins in PMNs.</span><br />
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<span style="line-height: 18px;">In the earlier studies, Van Dyke</span><span style="line-height: 18px;"> and Suzuki et al.</span><span style="line-height: 18px;"> reported that >60% of Localized Juvenile Periodontitis (LJP) patients showed depressed PMN chemotaxis. Champagne et al.</span><span style="line-height: 18px;"> in a study with LJP reported 43% cases with depressed chemotaxis, but statistical analysis revealed no significant difference in f-actin polymerization. This could be due to the fact that directional movement of LJP neutrophil is altered by abnormalities in signaling, but the machinery of movement (change in actin polymerization) is intact in these cells.</span><br />
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<span style="line-height: 18px;">It is also reported that actin polymerization is essential for neutrophil migration and increased polymerization is related with increased migration of neutrophil and vice versa.</span><span style="line-height: 18px;"> </span><span style="background-color: black;">(Table 7)<span style="line-height: 18px;">showed higher coefficient of variation (18.084) in ChP cases, and lower coefficient of variation (5.603) in AgP cases. The higher variation of result in chronic periodontitis cases from normal subjects might be due to proposed hyper-responsive neutrophil phenotype in ChP (an innate property of neutrophils, i.e., constitutive), or involve a functional sensitization or priming by cytokines or bacterial components (peripheral priming may also have a constitutive element). On the contrary, slight variation of result in AgP cases might be due to heterogenous nature of neutrophils. It is generally accepted that the population of peripheral blood PMNs is functionally heterogenous. This heterogenesity could be due to different proportions of immature or senescent PMNs in the circulating pool,</span><span style="line-height: 18px;"> modulation of PMN function by different inflammatory mediators,</span><span style="line-height: 18px;"> race or geographical (ethnic) origin (since a genetic component has been suggested to be involved in early-onset periodontitis). </span></span></div>
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<span style="line-height: 18px;">The major limitations of the present study are the small sample size (n=10 in each group). Though age is no more a criteria for periodontal case diagnosis,</span><span style="line-height: 18px;"> the age considerations were taken here because in elderly patients, the affect due to endogenous risk factors may be 'diluted' by the presence of cumulated exogenous risk factors. The methodological differences, in particular, PMN isolation procedures have been shown to modify the surface expression of molecules that are not detectable in whole blood and that may be markers of PMN activation.</span><span style="line-height: 18px;"> In contrast to the study of Agarwal et al.,</span><span style="line-height: 18px;"> the test with 10 AgP patients in the present study were performed after the periodontal treatment, when the patients were in the maintenance phase of therapy and free of acute or chronic infections. Therefore, the infection-associated serum factors (tumor necrosis factor α, interleukin 1β) are not interfered with the β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> - integrin expression and actin polymerization level in the present study. Another drawback of the present study is that due to lower prevalence of AgP cases the study was not performed separately for Localized Aggressive Periodontitis (LAgP) cases and for Generalized Aggressive Periodontitis (GAgP) cases. Another drawback of the present study is all cases and subjects were selected clinically and radiographically, but microbial testing which is the more confirmatory for both AgP and ChP cases was not performed.</span></div>
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Conclusion</span></h2>
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<span style="line-height: 18px;">It is still possible that AgP neutrophils present with a functional defect so minor, that it does not lead to any systemic pathology, but important enough to allow for the development of a periodontal lesion. Depressed PMN migration could lead to delayed host response. Elevated PMNs migration could also be harmful due to excessive liberation of inflammatory mediators. </span><br />
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<span style="line-height: 18px;">Depolymerization of actin cytoskeleton stimulates β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrin mobility and activates β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -mediated cell adhesion. Furthermore, an intact actin cytoskeleton is needed to establish adhesion for cell spreading. Impaired neutrophil adhesion due to lack of β</span><sub style="line-height: 18px;">2</sub><span style="line-height: 18px;"> -integrins results in incompetent PMN mediated immunity and severe bacterial infections.</span><span style="line-height: 18px;">Neutrophil hyperadhesion inhibits migration of neutrophils to the site of infection which could hamper host resistance.</span><br />
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<span style="line-height: 18px;">Van Dyke et al.</span><span style="line-height: 18px;"> reported that depressed neutrophil chemotaxis can be a reliable marker for genetic studies. If the basic cytoskeletal defect in AgP cases is well established, the disease can be diagnosed at its early stage and can be treated accordingly.</span><br />
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<span style="line-height: 18px;">Further studies with larger sample size are necessary for definite conclusion regarding the role of cytoskeletal organization in controlling neutrophil function in AgP patients.</span>
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References</span></h2>
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">1.</span></td><td><span style="color: #cc0000;">Lang NP, Bartold PM, Cullinam M, Jeffcoat M, Mombelli A, Murakami S, <i>et al</i>. International classification workshop. Consensus report: Aggressive Periodontitis. Ann Periodontol 1999;4:53.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">2.</span></td><td><span style="color: #cc0000;">Anderson DA, Springer TA. Leukocyte adhesion deficiency: An inherited defect in the Mac-1, LFA-1, and p150-95 glycoproteins. Annu Rev Med 1987;38:175.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">3.</span></td><td><span style="color: #cc0000;">Stossel TP. The machinery of blood cell movements. Blood 1994;84:367-79.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">4.</span></td><td><span style="color: #cc0000;">Waterman CM, Salmon ED. Positive feedback interactions between microtubule and actin dynamics during cell motility. Curr Opin Cell Biol 1999;11:61-7.</span><br />
<span style="color: #cc0000;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000;">5.</span></td><td><span style="color: #cc0000;">Malech HL, Gallin JI. Neutrophils in human disease. N Engl J Med 1987;317:687-94.</span><br />
<span style="color: #cc0000;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000;">6.</span></td><td><span style="color: #cc0000;">Kornman SK, Wilson TG. Treatment planning for patients with inflammatory periodontal diseases: Advances in periodontics. Edited by Thomas G. Advances in periodontics, 3 <sup>rd</sup> ed. Lowa City, Lowa, USA uintessence Publishing Co; 1992. p. 87-97.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">7.</span></td><td><span style="color: #cc0000;">Flemmig TF. Periodontitis. Ann Periodontol 1999;4:32.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">8.</span></td><td><span style="color: #cc0000;">Parameter on aggressive periodontitis. American Academy of Periodontology. J Periodontol 2000;71:867-9.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">9.</span></td><td><span style="color: #cc0000;">Silness J, Löe H. Periodontal disease in pregnancy II. Correlation between oral hygiene and periodontal condition. Acta Odont Scand 1964;22:112-35.</span><br />
<span style="color: #cc0000;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000;">10.</span></td><td><span style="color: #cc0000;">Löe H, Silness J. Periodontal disease in pregnancy I. Prevalence and severity. Acta Odont Scand 1963;21:533-51.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">11.</span></td><td><span style="color: #cc0000;">Greene JC, Vermilion JR. The simplified oral hygiene index. J Am Dent Assoc 1964;68:7-13.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">12.</span></td><td><span style="color: #cc0000;">Tonetti MS, Mombelli A. Aggressive Periodontitis. Lindhe J. Clinical Periodontology and Implant Dentistry, 4 <sup>th</sup> Ed. New Delhi: Blackwell Munksgaard; 2003. p. 216-42.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">13.</span></td><td><span style="color: #cc0000;">Agarwal S, Suzuki JB, Piesco NP, Aichelmann-Reidy MB. Neutrophil function in juvenile periodontitis: Induction of adherence. Oral Microbiol Immunol 1994;9:262-71.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">14.</span></td><td><span style="color: #cc0000;">Gainet J, Dang PM, Chollet-Martin S, Brion M, Sixou M, Hakim J, <i>et al</i>. Neutrophil dysfunctions, IL-8 and soluble L-selectin plasma levels in rapidly progressive versus adult and localized juvenile periodontiotis: Variations according to disease severity and microbial flora. J Immunol 1999;163:5013-9.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">15.</span></td><td><span style="color: #cc0000;">Smith CW, Marlin SD, Rothlein R, Toman C, Anderson DC. Cooperative interactions of LFA-1 and Mac-1 with intercellular adhesion molecule-1 in facilitating adherence and transendothelial migration of human neutrophils <i>in vitro</i>. J Clin Invest 1989;83:2008-17.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">16.</span></td><td><span style="color: #cc0000;">Asman BA, Gustafsson K, Bergström K. Gingival crevicular neutro-phils: Membrane molecules do not distinguish between periodontitis and gingivitis. J Clin Periodontol 1998;24:927.</span><br />
<span style="color: #cc0000;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000;">17.</span></td><td><span style="color: #cc0000;">Van Dyke TE, Horoszewicz HU, Cianciola LJ, Genco RJ. Neutrophil chemotaxis dysfunction in human periodontitis. Infect Immun 1980;26:124-32.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">18.</span></td><td><span style="color: #cc0000;">Van Dyke TE, Schweinebraten LJ, Cianciola S, Offenbacher S, Genco RJ. Neutrophil chemotaxis in families with localized juvenile periodontitis. J Periodontal Res 1985;20:503-14.</span><br />
<span style="color: #cc0000;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000;">19.</span></td><td><span style="color: #cc0000;">Suzuki JB, Collison BC, Falkler WA, Nauman RK. Immunology profile of juvenile periodontitis. II. Neutrophil chemotaxis, phagocytosis and spore germination. J Periodontol 1984;55:461-7.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">20.</span></td><td><span style="color: #cc0000;">Champagne CM, Vaikuntam J, Warbington MI, Rose L, Daniel MA, Van Dyke TE. Cytoskeletal actin reorganization in neutrophils from patients with localized juvenile periodontitis. J Periodontol 1998;69:209-18.</span><br />
<span style="color: #cc0000;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000;">21.</span></td><td><span style="color: #cc0000;">Huttenlocher A, Ginsberg MH, Horwitz AF. Modulation of cell-migration by integrin-mediated cytoskeletal linkages and ligand-binding affinity. J Cell Biol 1996;134:1551-62.</span><br />
<span style="color: #cc0000;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000;">22.</span></td><td><span style="color: #cc0000;">Howard TH, Oresajo CO. The kinetics of chemotactic peptide-induced change in F-actin content, F-actin distribution, and the shape of neutrophils. J Cell Biol 1985;101:1078-85.</span><br />
<span style="color: #cc0000;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000;">23.</span></td><td><span style="color: #cc0000;">Hoffstein S, Goldstein IM, Weissman G. Role of microtubule assembly in lysosomal enzyme secretion from human polymorphonuclear leukocytes. A reevaluation. J Cell Biol 1977;73:242-56.</span><br />
<span style="color: #cc0000;"> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000;">24.</span></td><td><span style="color: #cc0000;">Pedersen MM. Chemotactic response of Neutrophil polymorphonuclear leukocytes in juvenile periodontitis measured by the leading front method. Scand J Dent Res 1988;96:421-7.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">25.</span></td><td><span style="color: #cc0000;">Repo H, Saxén L, Jäättelä M, Ristola M, Leirisalo-Repo M. Phagocyte function in juvenile periodontitis. Infect Immun 1990;58:1085-92.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">26.</span></td><td><span style="color: #cc0000;">Page RC, Vandesteen GE, Ebersole JL, Williams BL, Dixon IL, Altman LC. Clinical and laboratory studies of a family with a high prevalence of juvenile periodontitis. J Periodontol 1985;56:602-10.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">27.</span></td><td><span style="color: #cc0000;">Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">28.</span></td><td><span style="color: #cc0000;">Macey MG, McCarthy DA, Vordermeier S, Newland AC, Brown KA. Effects of cell purification methods on CD11b and L-selectin expression as well as the adherence and activation of leukocytes. J Immunol Methods 1995;181:211.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">29.</span></td><td><span style="color: #cc0000;">Arnaout AM. Leukocyte adhesion molecules deficiency: Its structural basis, pathophysiology and implications for modulating the inflammatory response. Immunol Rev 1990;145-80.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000;">30.</span></td><td><span style="color: #cc0000;">Dahinden C, Galanos C, Fehr J. Granulocyte activation by endotoxin. I. Correlation between adherence and other granulocyte functions and role of endotoxin structure on biologic activity. J Immunol 1983;130:857-62.</span><br />
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com0tag:blogger.com,1999:blog-3393509504180156297.post-72216209608580390582012-07-11T23:53:00.001-07:002012-07-22T19:46:46.830-07:00Oral submucous fibrosis: A report of two pediatric cases and a brief review<div dir="ltr" style="text-align: left;" trbidi="on">
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Oral submucous fibrosis is a chronic debilitating disorder which is usually seen in adults with areca nut chewing habit. A rapid upsurge in the popularity of commercial areca nut products, especially among the younger generation, is a cause of grave concern, as satisfactory management is still lacking. Hereby, two pediatric cases of oral submucous fibrosis are reported.</div>
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Oral submucous fibrosis (OSMF) is a chronic disorder characterized by progressive fibrosis of the lining mucosa of the upper digestive tract involving the oral cavity, oropharynx, and frequently the upper third of the esophagus, resulting in intolerance to spicy foods, a burning sensation in the mouth, xerostomia, and limitation of mouth opening, tongue mobility, swallowing, or phonation.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> </span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">It mostly occurs in Asian countries, where chewing betel quid (BQ; contains areca nut, tobacco, slaked lime, or other spices) and other commercial preparations of areca nut in attractive pouches is popular.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Epidemiologic surveys in India show the rate of prevalence to be about 0.5%. Persons between 20 and 40 years of age are most commonly affected, with a female: male ratio of 3:1.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Morbidity of OSMF among BQ users is about 3.2% </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> and it has a malignant transformation rate in the range of 7-13%. </span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Histologically, OSMF shows the characteristic features of juxta-epithelial fibrosis, mostly along with atrophy of the overlying epithelium, accumulation of hyalinized collagen beneath the basement membrane, and a progressive loss of vascularity. </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> </span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">The pathogenesis of the disease is not well established, but is believed to be multifactorial. Various mechanisms suggested include: 1) clonal selection of fibroblasts with a high amount of collagen production during long-term exposure to areca nut, </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> 2) stabilization of collagen structure by catechin and tannins from BQ, 3) production of stable collagen (type I) by OSF fibroblasts, 4) increase in collagen cross-linking by up-regulation of lysyl oxidase, 5) deficient collagen phagocytosis, and 6) micronutrient and vitamin deficiencies.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Mainly adults are affected and it is uncommon in the pediatric age group. Only limited number of pediatric cases have been reported in the literature.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> A youngest case of 4-year-old girl has been reported in the literature. </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Hereby, two cases of OSMF are reported, highlighting the potential danger of involvement of the pediatric age group from "Pouch Culture."</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">A 10-year-old local factory worker boy reported with difficulty in opening mouth and taking spicy food for the last 3 months. Both his parents were laborers. He was reportedly chewing gutkha two to three times a day for the last 1 year, as his colleagues at the local factory encouraged him to take the habit. On examination, reduced inter-incisal distance (IID=1.5 cm), and generalized blanched oral mucosa involving the soft palate and the anterior faucial pillars were observed (Figure 1)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> and (Figure 2)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">. On palpation, loss of normal resilience and pliability of the mucosa with dense fibrotic bands were observed in the buccal mucosa bilaterally. Routine hematological investigations were within the normal range except for the hemoglobin which was 9.1 gm%. A clinical diagnosis of OSMF was confirmed and the boy was prescribed oral iron supplementations, vitamin A, and zinc acetate after counseling to completely quit the habit, but unfortunately the patient failed to report for further follow-up.</span>
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<b>Figure 1: Intraoral view showing difficulty in mouth opening with blanching of oral mucosa, generalized stains</b></div>
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<b style="font-family: Arial, Verdana, sans-serif; font-size: 13px; line-height: 17px; text-align: -webkit-center;">Figure 2: Inter-incisal distance=1.5 mm</b>
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">A 12-year-old girl complained of burning sensation on having food for the last 3-4 years, which has aggravated recently. The girl's grandmother was a habitual pan masala chewer and unaware of the consequences, used to give her granddaughter a small amount of it almost daily since she was 5 years old. General physical examination revealed normal general condition.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">On oral examination, generalized blanched mucosa was observed with loss of elasticity and presence of vertical fibrous bands bilaterally in the buccal mucosa. The uvula was shrunken and the tongue was atrophic. Few retained deciduous root stumps and generalized tobacco stains were observed on dental hard tissue examination (Figure 3)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">. The IID was 1.9 cm (Figure 4)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">. Routine hematological examination revealed nothing significant. A diagnosis of OSMF was established. Following the conservative line of treatment, biopsy was considered unnecessary as it adds to the discomfort for patient. Rebound fibrosis has also been reported in certain cases. The girl and her guardians were motivated to completely stop the habit and avoid spicy food. Oral prophylaxis and extraction of the retained root stumps was advised.</span>
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<b style="font-family: Arial, Verdana, sans-serif; font-size: 13px; line-height: 17px; text-align: -webkit-center;">Figure 4: Pre-supplementation inter-incisal distance=1.9 mm</b>
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">The patient was administered vitamin A (25,000 IU OD) and zinc acetate syrup (5 ml bid) for 3 months. Warm saline rinses and mild mouth-opening exercises were advised along with regular check-up after 15 days followed by 1 month interval.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">A relief from burning sensation was reported on the first recall visit itself, i.e. after 15 days. Mouth opening also improved slowly, and after the 3 months regimen, the IID was reported to be 2.5 cm (Figure 5)</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">. Only mild improvement was noticed in the blanching of the oral mucosa. The patient was further advised vitamin B complex supplements every alternate day for the next one month along with warm saline rinses and is under regular follow-up.</span>
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<b style="font-family: Arial, Verdana, sans-serif; font-size: 13px; line-height: 17px; text-align: -webkit-center;">Figure 5: Post-supplementation inter-incisal distance=2.4 mm</b>
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</span><span style="font-size: x-large;">Discussion</span></span></h2>
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">OSMF is regarded as a collagen metabolic disorder with an overall increased collagen production and decreased collagen degradation resulting in increased collagen deposition in the oral tissues, and fibrosis due to alkaloid exposure. </span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">The list of treatment modalities is extensive and includes the use of micronutrients and minerals, CO2 laser, pentoxifylline, lycopene, interferon gamma, turmeric, hyalase, chymotrypsin, and placental extracts. As fibrosis cannot be reversed when mouth opening is severely reduced, surgical interventions such as myotomy, coronoidectomy, and excision of the fibrotic bands have also been reported in the literature. Alternatively, procedures such as insertion of stent, physiotherapy, local heat therapy, and mouth-opening exercises with acrylic carrots and ice-cream sticks have been tried with variable success rates. </span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Till today, no well-established treatment for OSMF exists and approaches using injections of steroids, chymotrypsin, hyaluronidase, or alcohol, and surgery using mucosal or non-vascularized split thickness grafts have not only been ineffective but have also often exacerbated the condition, with added scar tissue. </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> </span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">Copper plays a pivotal role in the pathogenesis of OSMF. Copper released in high amounts from areca nut has been reported to up-regulate the enzyme lysyl oxidase in OSMF cases as copper is a ligand for the enzyme. </span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Zinc is an essential component of a large number of enzymes participating in the synthesis of carbohydrates, lipids, proteins, and nucleic acids, and also plays a central role in humoral and cellular immune system.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Further, Di Silvestro </span><i style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">et al</i><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">. had reported that higher levels of dietary zinc reduce the bioavailability of copper at absorption stage.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Vitamin A is an essential nutrient needed in small amounts by humans for normal functioning of the visual systems, growth and development, maintenance of epithelial integrity, and immune functions.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> So, based on the previous studies and our own institutional experience, a 3-month regimen of vitamin A and zinc acetate was prescribed with cessation of the habit and regular check-up.</span><span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;"> Improvement in burning sensation and an increase in mouth opening were observed after 3 months.</span><br />
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<span style="font-family: Arial, Verdana, sans-serif; line-height: 17px; text-align: -webkit-auto;">To conclude, the present drug treatments are empirical and symptomatic in nature. A combination of several drugs may play an important role in the treatment because it is a multifactorial disease. In the near future, younger ones may be affected more and an active preventive approach is required to limit the morbidity associated with the modern pouch culture.</span><br />
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References</span></h2>
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<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">1.</span></td><td><span style="color: #cc0000; font-size: small;">Rajendran R. Oral submucous fibrosis-etiology, pathogenesis and future research. Bull World Health Organ 1994;72:985-96.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">2.</span></td><td><span style="color: #cc0000; font-size: small;">Trivedy CR, Craig G, Warnakulasuriya S. The oral health consequences of chewing areca nut. Addict Biol 2002;7:115-25.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">3.</span></td><td><span style="color: #cc0000; font-size: small;">Hayes PA. Oral submucous fibrosis in a 4- year -old girl. Oral Surg Oral Med Oral Pathol 1985;59:475-8.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">4.</span></td><td><span style="color: #cc0000; font-size: small;">Shah B, Lewis MA, Bedi R. Oral submucous fibrosis in a 11-year-old Bangladeshi girl living in the United Kingdom. Br Dent J 2001;191:130-2.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">5.</span></td><td><span style="color: #cc0000; font-size: small;">Mundra RK, Gupta SK, Gupta Y. Oral submucous fibrosis in Paediatric age group., lJO and HNS 1999;51:60-2.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">6.</span></td><td><span style="color: #cc0000; font-size: small;">Jiang X, Hu J. Drug treatment of oral submucous fibrosis: A review of the literature. J Oral Maxillofac Surg 2009;67:1510-5.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">7.</span></td><td><span style="color: #cc0000; font-size: small;">Pindborg JJ, Chawla TN, Srivastava AN. Epithelial changes in oral submucous fibrosis. Acta Odontol Scand 1965;23:277-86.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">8.</span></td><td><span style="color: #cc0000; font-size: small;">Tilakaratne WM, Klinikowski MF, Saku T. Oral submucous fibrosis: Review on aetiology and pathogenesis. Oral Oncol 2006;42:561.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">9.</span></td><td><span style="color: #cc0000; font-size: small;">Anil S, Beena VT. Oral submucous fibrosis in a 12-year-old girl: Case report. Pediatr Dent 1993;15:120-2.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">10.</span></td><td><span style="color: #cc0000; font-size: small;">Yusuf H, Yong SL. Oral submucous fibrosis in a 12-year-old Bangladeshi boy: A case report and review of literature. Int J Paediatr Dent 2002;12:271-6.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">11.</span></td><td><span style="color: #cc0000; font-size: small;">Dyavanagoudar SN. Oral Submucous Fibrosis: Review on Etiopathogenesis. J Cancer Sci and Ther 2009;1:72-7.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">12.</span></td><td><span style="color: #cc0000; font-size: small;">Jiang X, Hu. Drug treatment of oral submucous fibrosis: A review of literature. J Oral Maxillofac Surg 2009;67:1510-5.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">13.</span></td><td><span style="color: #cc0000; font-size: small;">Marx RE, Stern D. Oral and Maxillofacial Pathology. A rationale for diagnosis and treatment. 1 <sup>st</sup> ed. Quintessence Publishing, Illinois 2003. p. 317-9.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">14.</span></td><td><span style="color: #cc0000; font-size: small;">Fedorowicz Z, Chan Shh-Yen E, Dorri M, Nasser M, Newton T, Shi L. Lack of reliable evidence for oral submucous fibrosis treatments. Evid Based Dent 2009;10:8.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">15.</span></td><td><span style="color: #cc0000; font-size: small;">Trivedy C, Baldwin D, Warnakulasuria S, Johson N, Peters T. Copper content in areca nut products and oral submucous fibrosis. Lancet 1997;349:1447.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">16.</span></td><td><span style="color: #cc0000; font-size: small;">World health organisation. Vitamin and mineral requirements in human nutrition. 2 <sup>nd</sup> ed. WHO Press, Geneva 2004. p. 230-44.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">17.</span></td><td><span style="color: #cc0000; font-size: small;">Zinc and copper: Evidence for interdependence, not antagonism. Nutrition 2001;17:734-42.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">18.</span></td><td><span style="color: #cc0000; font-size: small;">World health organisation. Vitamin and mineral requirements in human nutrition. 2 <sup>nd</sup> ed. WHO Press, Geneva 2004. p. 17-37.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">19.</span></td><td><span style="color: #cc0000; font-size: small;">Kumar A, Sharma SC, Sharma P. Beneficial effect of oral zinc in the treatment of oral submucous fibrosis. Indian J Pharmacol 1991;23:236.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">20.</span></td><td><span style="color: #cc0000; font-size: small;">Dhariwal R, Mukherjee S, Pattanayak S, Chakraborty A, Ray JG, Chaudhuri K. Zinc and vitamin A can minimize the severity of Oral submucous fibrosis. Br Med J Case Rep 2010;doi:10.1136/bcr.10.2009.2348.<br /> </span></td></tr>
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com0tag:blogger.com,1999:blog-3393509504180156297.post-8394314114565692592012-07-11T23:14:00.002-07:002012-07-22T19:57:42.496-07:00Management of amlodipine-induced gingival enlargement: Series of three cases<div dir="ltr" style="text-align: left;" trbidi="on">
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Gingival enlargement is one of the side effects associated with certain drugs. Amlodipine, a calcium channel blocker, used as antihypertensive drug has been found associated with gingival hyperplasia. This case series presents diagnosis and management of amlodipine-induced gingival hyperplasia. Amlodipine-induced gingival enlargement was diagnosed and managed by thorough scaling and root planning. Drug substitution and surgical intervention was performed in first two cases. The pathogenesis of gingival enlargement is uncertain and the treatment is still largely limited to the maintenance of an improved level of oral hygiene and surgical removal of the overgrown tissue. Several factors may influence the relationship between the drugs and gingival tissues as discussed by Seymour <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">et al</em>. Meticulous oral hygiene maintenance, switchover to alternative drug, professional scaling and root planning and surgical excision of enlarged gingival tissue may help overcome the effect of these drugs.</div>
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<span style="font-size: x-large;">INTRODUCTION</span></h2>
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Gingival enlargement is one of the side effects associated with the administration of several drugs. Currently, more than 20 drugs are associated with gingival enlargement. Drugs having side effect of gingival enlargement can be broadly divided into three categories: anticonvulsants, calcium channel blockers and immunosuppressants. Many of the calcium channel blockers used as antihypertentive drugs have been implicated in causing gingival enlargement. Amlodipine is dihydropyridine derivative used as antihypertensive drug having longer action and comparatively lesser side effect than Nifedipine (calcium channel blocker). Amlodipine-induced gingival enlargement is comparatively less prevalent among calcium channel blockers. Since pathogenesis of gingival enlargement is not well-understood, it is still a challenge for the periodontists to diagnose and manage the case effectively.</div>
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<span style="font-size: large;">Prevalence</span></h2>
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Amlodipine-induced gingival enlargement is comparatively less prevalent than other calcium channel blocker. Jorgensen, 1997 had reported the prevalence of amlodipine-induced gingival enlargement as 3.3%.</div>
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<span style="font-size: x-large;">CASE REPORT</span></h2>
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Case 1</h2>
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A 47-year-old female was referred to the Department of Periodontia of Dr. R. Ahmed Dental College and Hospital, Kolkata with complaints of gingival enlargement with foul odor, bleeding and fetid discharge from gums since 1 year. General examination revealed normal built. Patient was hypertensive with history of taking amlodipine 5 mg once daily+losartan 50 mg once daily since last 7 years.</div>
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Intraoral examination revealed poor oral hygiene, generalized nodular enlargement of gingiva mainly on the facial aspect of teeth. Gingiva was inflammed and soft to firm in consistency [Figure 1a].</div>
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Figure 1</div>
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<span style="font-size: 15px; line-height: 21px;">Case 1 — (a) intraoral picture at first visit (b) three months after phase-1 therapy (c) after correction of maxillary gingival overgrowth by flap procedure (d) after correction of mandibular gingival overgrowth by external bevel gingivectomy (e) photomicrogragh showing hyperplastic squamous epithelium with few chronic inflammatory cells in connective tissue (f) twelve-month postoperative view</span>
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Investigation</h3>
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Routine blood and orthopantomographical examination were within normal limit.</div>
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Treatment</h3>
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Amlodipine was omitted as per advice of physician, switching over to monotherapy of losartan 50 mg once in a day. Patient was educated and motivated for maintenance of proper oral hygiene. Professional scaling and root planning was performed. After 3 months of phase-1 therapy, remaining excess gingival tissue was planned to correct by surgical intervention. [Figure 1b] Gingivectomy was instituted for maxillary gingival tissue flap procedure and for mandibular gingival tissue [Figure 1c and <a class="fig-table-link fig figpopup" href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3118083/figure/F1/" rid-figpopup="F1" style="border: 0px; color: #642a8f; cursor: pointer; display: inline-block !important; font-size: 15px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline; zoom: 1 !important;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; position: relative; text-decoration: none; vertical-align: baseline;"><span class="figpopup-sensitive-area" style="background-color: transparent; border: 0px; color: transparent; cursor: pointer; font: inherit; left: -1.5em; margin: 0px; opacity: 0; padding: 0px; position: absolute; text-decoration: none; top: 0px; vertical-align: baseline;">and</span></span></a>d].</div>
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Histopathological examination</h3>
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Excised tissue was sent for histopathological examination. Section stained with H and E revealed the presence of hyperplastic squamous epithelium without any dysplastic features. There was mild chronic inflammatory cells infiltrate in the connective tissue [Figure 1e].</div>
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Followup visit</h3>
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On seventh day of follow-up visit periodontal pack was removed. Healing procedure was uneventful. Clinical outcome on 12 months of follow-up visit is shown in [Figure 1f].</div>
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Case-2</h2>
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A female patient of 50 years reported with complaints of gum swelling and generalized sensitivity of teeth since 2 months. Patient was under treatment of essential hypertension for 5 months and was taking amlodipine 5 mg (OD) +telmisartan 40 mg (OD) since 5 months. Intraoral examination revealed very poor oral hygiene; generalized gingival enlargement covering one-third to half of the tooth surface. Gingival enlargement involved marginal, papillary gingiva as well as attached gingiva also. Gingiva was highly inflamed with multiple areas of spontaneous bleeding with generalized abrasion and staining of teeth [Figure 2a].</div>
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Figure 2</div>
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<span style="font-size: 15px; line-height: 21px;">Case 2 — (a) intraoral picture at first visit (b) ten weeks after phase-1 therapy (c) nine-month postoperative view</span>
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Investigation</h3>
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OPG revealed generalized horizontal bone loss. Report of hemogram and other blood test were within normal range.</div>
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Treatment</h3>
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Amlodipine was substituted to telmisartan 40 mg (OD) and verapamil 40 mg (BD). Phase-1 therapy was performed. After 10 weeks of follow-up inflammation was markedly reduced with some reduction in gingival enlargement [Figure 2b]. Remaining excess gingival was corrected by surgical periodontal treatment. Healing was uneventful.</div>
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Histopathology</h3>
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Microscopic picture revealed presence of hyperplastic-straitified squamous epithelium without dysplasia. The underlying connective tissue contained scanty inflammatory cells.</div>
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Followup visit</h3>
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Patient was recalled after every 3 months. The 9-month follow-up visit is shown in [Figure 2c].</div>
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Case-3</h2>
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A 60-year-old female patient presented with generalized gingival enlargement with localized pink fibrous, pedunculated, 2΄3 cm soft tissue mass in relation to maxillary left canine-premolar region. Poor oral hygiene with spacing in maxillary and mandibular anterior teeth was also observed [Figure 3a]. Patient was taking amlodipine 5 mg (OD) since last 10 years. ECG and blood investigation report was within normal limit.</div>
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Figure 3</div>
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<span style="font-size: 15px; line-height: 21px;">Case 3 — (a) intraoral picture at first visit (b) two months after phase-1 therapy</span>
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<span style="font-size: 15px; line-height: 21px;">Treatment</span></h3>
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Oral hygiene maintenance instructions were given to patient. Thorough scaling and root planning were performed and amlodipine was substituted with losartan 50 mg (OD).</div>
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After 2 months there was significant reduction in gingival enlargement. Patient is under regular follow-up [Figure 3b].</div>
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<span style="font-size: x-large;">DISCUSSION</span></h2>
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Gingival hyperplasia, with its potential cosmetic implication and tendency to provide niche for further growth of microorganism, possess a serious concern to patients and clinicians. Calcium channel blockers are considered as potential etiological agent for inducing gingival enlargement. Lafzi <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">et al</em>. (2006) had reported rapidly developing gingival hyperplasia in patient receiving 10 mg/day of amlodipine within 2 month of onset. The prevalence of amlodipine-induced gingival overgrowth was reported to be 3.3% (Jogersen, 1997). The underlying mechanism of gingival enlargement still remains to be fully understood. However, two main inflammatory and non-inflammatory pathways have already been suggested. The proposed non-in-flammatory mechanisms include defective collagenase activity due to decreased uptake of folic acid, blockage of aldosterone synthesis in adrenal cortex and consequent feedback increase in ACTH level and upregulation of keratinocyte growth factor. Alternatively, inflammation may develop as a result of direct toxic effects of concentrated drug in crevicular gingival fluid and/or bacterial plaques. This inflammation could lead to the upregulation of several cytokine factors such as TGF-β1. Marked reduction in inflammation and gingival overgrowth was observed in all three cases after phase-1 therapy and substitution of amlodipine to other drug. Meticulous oral hygiene maintenance by patient may also be responsible for reduction in gingival overgrowth. In the first two cases, surgery was performed after a follow-up period of nearly 3 months. In the third case, only a 2-month follow-up report is presented. Marvogiannis <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">et al</em>., 2006 suggested that there may be recurrence of gingival hyperplasia if medication is continued and also persistence of other risk factors. But no recurrence was noted in our case series.</div>
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<span style="font-size: x-large;">CONCLUSION</span></h2>
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Stringent maintenance of oral hygiene, switchover to alternative drugs and surgical therapy if required, remains the main stay of available treatment modalities. Better results were obtained where drug substitution along with oral prophylaxis were followed.</div>
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<span style="font-size: x-large;">REFERENCES</span></h2>
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com1tag:blogger.com,1999:blog-3393509504180156297.post-76448160661325659272012-07-10T23:06:00.000-07:002012-07-22T19:55:52.961-07:00Myoepithelial carcinoma of the nasopharynx: Case report of a rare entity<div dir="ltr" style="text-align: left;" trbidi="on">
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Myoepithelial carcinomas are rare tumors of salivary glands. Most occur in the parotid gland buta few other sites of origin have also been described. Myoepithelial carcinoma of the nasopharynx has only been reported very few times. Because the lesion is so rare in the nasopharynx, there are no specific guidelines for its treatment. We present a rare case of myoepithelial carcinoma in the nasopharynx and discuss its diagnostic and therapeutic aspects.</div>
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<span style="line-height: 18px;">Myoepitheliomas are relatively rare tumors of the salivary glands comprising only 1% of all. Most of these are benign but malignant variants, called myoepithelial carcinomas (MCs), are even rarer comprising about 10% of myoepitheliomas. </span><span style="line-height: 18px;">Most of these occur in the parotid gland; a few other sites of origin have been described such as lungs, trachea, oral cavity, larynx and breast.</span><span style="line-height: 18px;">To our knowledge there are very few countable reports of MCs of the nasopharynx in the literature which makes the nasopharynx an unusual location for MCs and considered difficult to access for the head and neck surgeon. So, there are no specific indications and guidelines for its management. We present a case of myoepithelial carcinoma in the nasopharynx and discuss its diagnostic and therapeutic aspects. </span><br />
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Case Report</span></h2>
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<span style="line-height: 18px;">A 60-year-old female reported to the department with a non-painful left laterocervical swelling measuring 3 cm in diameter. The patient complained of nasal blockage, hyponasal speech, conductive hearing loss and ear fullness since two months though the cranial nerve examination results were within normal limits. Posterior rhinoscopy examination revealed a fungating tumor on the roof and left lateral aspect of the nasopharynx. Endoscopic nasopharyngeal biopsy was taken which reported the lesion as a mucus-secreting minor salivary gland tumor. Fine needle biopsy of the nasopharygeal swelling was performed, and the lesion was diagnosed as myoepithelial cell carcinoma.</span><br />
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<span style="line-height: 18px;">Computed tomography (CT) scan depicted an irregular hypodense lesion measuring 4.5/3.8 cm in the left half of the nasopharynx, obliterating the </span><span class="spl" style="background-color: black; border: 3px dotted rgb(255, 255, 255); font-style: italic; line-height: 18px; margin-left: 2px; margin-right: 2px;"> Eustachian tube </span><span style="line-height: 18px;">opening and Rosenmuller fossa. On the left side the lesion was extending to the pterygopalatine fossa and involving the parapharyngeal space. On the ipsilateral side, the submandibular group of lymph nodes was enlarged. There was no intracranial extension noted (Figure 1)</span><span style="line-height: 18px;">. Chest X-ray and Ultrasound (USG) abdomen were performed as a part of the metastatic workup.</span>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 1: Axial CT scan showing the extent of the tumor in the nasopharynx</b>
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<span style="line-height: 18px;">The patient underwent excision of the tumor with paramedian mandibulotomy in conjunction with transpalatal approach (Figure 2)</span><span style="line-height: 18px;">. Supraomohyoid neck dissection was performed on the ipsilateral side with classical transcervical incision. Histopathology reports revealed myoepithelial carcinoma of the nasopharynx with infiltrating margins and the presence of numerous sheets and cords of both spindle-shaped and epithelioid neoplastic cells (Figure 3)</span><span style="line-height: 18px;">. Tumor was immunoreactive for actin, smooth muscle actin (SMA), S-100 and cytokeratin (CK) markers. The postoperative period was uneventful and the patient received external beam radiotherapy to the primary site {70 gy/ 35 fractions} as well as to the neck {56 gy/ 28 fractions} which was started within three weeks of surgery. The patient is on regular follow-up since 28 months with no evidence of recurrence at the loco-regional level till date.</span>
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<b><span style="background-color: black; font-size: 12px; line-height: 18px;">Figure 2: Intraoperative photograph showing the surgical site after excision of the tumor</span>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 3: Histopathological picture of myoepithelial carcinoma showing spindle-shaped cells in the background</b>
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Discussion</span></h2>
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<span style="line-height: 18px;">MCs are tumors of epithelial origin that may occur with preexisting benign lesions like pleomorphic adenomas or benign myoepitheliomas, but they also may arise </span><i style="line-height: 18px;">de novo</i><span style="line-height: 18px;">.</span><span style="line-height: 18px;"> Nilles and associates </span><span style="line-height: 18px;">and Tuncel and colleagues</span><span style="line-height: 18px;"> reported only two cases of malignant myoepithelioma in the rhinopharynx that were confirmed histologically and immunohistochemically. In 1983, Nofal</span><span style="line-height: 18px;"> described a poorly differentiated spindle-cell carcinoma that could have been the third case of rhinopharyngeal myoepithelial carcinoma.</span><br />
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<span style="line-height: 18px;">MC is usually insidious in onset, a painless mass that originates in the parotid gland. However, other sites such as the palate, larynx, gums, retromolar area, and breast have also been reported.</span><span style="line-height: 18px;"> In the parotid gland, MCs usually affect patients over 50 years of age with no sex predilection. Because they are relatively painless tumors, their diagnosis can be delayed by months or even years.</span><br />
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<span style="line-height: 18px;">When MCs occur in the nasopharynx, the symptoms are the same as those of other tumors that affect this region, such as nasal obstruction, ear fullness, serous otitis media, and conductive hearing loss. To ensure a correct early diagnosis of nasopharyngeal tumors, the lesion should first be evaluated via fiberoptic nasopharyngoscopy to identify the mass, which is usually covered with unaltered mucosa. Diagnostic imaging (CT and magnetic resonance imaging (MRI)) allows the site and the extension of the tumor to be established, thus permitting a correct surgical approach. The diagnosis can be further ascertained by taking a biopsy specimen for histological confirmation of the presence of a tumor and its type. Histologically, MCs appear to have pleomorphic spindle-shaped or more rounded cells, occasionally with eosinophilic cytoplasm (otherwise known as plasmacytoid cells).</span><span style="line-height: 18px;"> Immunohistochemistry can help to identify myoepithelial differentiation of the neoplastic cells. Chow </span><i style="line-height: 18px;">et al.,</i><span style="line-height: 18px;"> and Torlakovic and associates</span><span style="line-height: 18px;"> demonstrated that tumoral cells are immunoreactive to cytokeratin, smooth muscle actin, and S-100 protein. Our patient was no exception, and this profile allowed the final histological diagnosis of myoepithelial carcinoma. The criteria that indicate the malignancy of myoepithelial neoplasms include their destructive infiltrating growth, cellular pleomorphism, necrosis, and an increase in mitotic activity. </span><span style="line-height: 18px;">Locally, this type of tumor is particularly destructive, but its clinical and biological features are not yet fully understood. Some authors believe that metastases are uncommon,</span><span style="line-height: 18px;"> while others have reported metastases in 30% of the cases.</span><span style="line-height: 18px;"> It has been reported that MCs in the parotid may spread to the submandibular and supraclavicular lymph nodes, hence requiring neck dissection procedures. </span><br />
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<span style="line-height: 18px;">The treatment of choice for MCs is surgical excision, but there are no specific guidelines for the treatment of nasopharyngeal MCs. However, it seems reasonable to apply the criteria used for MCs involving the most common site, the parotid. So any type of selective neck dissection will prove to be a diagnostic as well as a therapeutic procedure. Unlike certain nasopharyngeal tumors for which chemotherapy and radiotherapy are the preferred treatments in some cases, the application of these treatments to MCs has not been encouraging. The mainstay of success is primary surgical management.</span><span style="line-height: 18px;"> Several surgical approaches have been proposed, depending on the size and site of the tumor.</span><span style="line-height: 18px;">We adopted excision of the tumor with paramedian mandibulotomy in conjunction with a transpalatal approach. To our knowledge, this patient is the only case of nasopharyngeal MC treated with this technique. It enabled complete resection of the lesion with negative margins, and there have been no signs of recurrence and metastasis during the 28-month follow-up period with stable dental occlusion, no velo-pharyngeal incompetence and no signs of trismus. </span><br />
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References</span></h2>
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<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">1.</span></td><td><span style="color: #cc0000; font-size: small;">Sciubba JJ, Brannon RB. Myoepithelioma of salivary glands: Report of 23 cases. Cancer 1982;49:562-72<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">2.</span></td><td><span style="color: #cc0000; font-size: small;">Barnes L, Appel BN, Perez H, El-Attar AM. Myoepitheliomas of the head and neck: Case report and review. J Surg Oncol 1985;28:21-8<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">3.</span></td><td><span style="color: #cc0000; font-size: small;">Dean A, Sierra R, Alamillos FJ, Lopez-Beltran A, Morillo A, Arévalo R, <i>et al</i>. Malignant myoepithelioma of the salivary glands: Clinicopathological and immunohistochemical features. Br J Oral Maxillofac Surg 1999;37:64-6.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">4.</span></td><td><span style="color: #cc0000; font-size: small;">Klumpp TR, Mohr RM, Silverman CL, Tang CK, Elfenbein IB, Dardick I. Malignant myoepithelioma of the parotid gland: case report and review of the literature. J Laryngol Otol 1995;109:995-8<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">5.</span></td><td><span style="color: #cc0000; font-size: small;">Young J, Barker M, Robertson T, Nasioulas S, Tannenberg A, Buttenshaw RL, <i>et al</i>. A case of myoepithelial carcinoma displaying biallelic inactivation of the tumour suppressor gene APC in a patient with familial adenomatous polyposis. J Clin Pathol 2002;55:230-2.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">6.</span></td><td><span style="color: #cc0000; font-size: small;">Nilles R, Lenartz T, Kaiserling E. Myoepithelial carcinoma of the nasopharynx: Case report and review of the literature. HNO 1993;41:396-400 <br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">7.</span></td><td><span style="color: #cc0000; font-size: small;">Tuncel U, Ergul G, Ozlugedik S, Unal A, Myoepithelial carcinoma in the nasopharynx: An unusual localization. Yonsei Med J 2004;45:161-5 <br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">8.</span></td><td><span style="color: #cc0000; font-size: small;">Nofal F. Spindle cell carcinoma of the nasopharynx. J Laryngol Otol 1983;97:1057-63.</span><br />
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<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">9.</span></td><td><span style="color: #cc0000; font-size: small;">Chow LT, Chow WH. Lee JC. Monomorphic epithelioid variant of malignant myoepithelioma of the parotid gland: Cytologic features in fine needle aspiration (FNA). Cytopathology 1996;7:279-87 <br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">10.</span></td><td><span style="color: #cc0000; font-size: small;">Torlakovic E, Ames ED, Manivel JC, Stanley MW. Benign and malignant neoplasm of myoepithelial cells: Cytologic findings. Diagn Cytopathol 1993;9:655-60.<br /> </span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">11.</span></td><td><span style="color: #cc0000; font-size: small;">Savera AT, Sloman A, Huvos AG, Klimstra DS. Myoepithelial carcinoma of the salivary glands: A clinocopathologic study of 25 patients. Am J Surg Pathol 2000;24:761-74</span></td></tr>
<tr><td valign="top" width="5%"><span style="color: #cc0000; font-size: small;">12.</span></td><td><span style="color: #cc0000; font-size: small;">Fisch U. The infratemporal approach for nasopharyngeal tumors. Laryngoscope 1983;93:36-44. </span></td></tr>
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com0tag:blogger.com,1999:blog-3393509504180156297.post-3934749760268092602012-07-10T14:27:00.001-07:002012-07-22T20:03:22.201-07:00Fanconi anemia manifesting as a squamous cell carcinoma of the hard palate: a case report<div dir="ltr" style="text-align: left;" trbidi="on">
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Fanconi Anemia is a rare autosomal recessive disorder characterized by various congenital malformations, progressive bone marrow failure at a very young age and of solid tumors development. The authors present a rare case of a squamous cell carcinoma of the hard palate in a Fanconi Anaemia patient. The atypical clinical manifestation rendered the diagnosis more difficult. This case, for age of appearance, sex and localization, is unique in international literature. We recommend a quarterly follow up of the oral-rhino-pharynx complex in FA patients and to consider as carcinomas, all oral lesions that last more than two weeks.</div>
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<span style="color: purple; font-size: x-large;">Background</span></h2>
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Fanconi Anemia (FA) is a rare autosomal recessive syndrome (birth incidence of 1 per 350000), first described in 1927 as a progressive lethal anaemia associated with brown pigmentation of skin. Subsequently, this term was extended to a syndrome that includes pancytopenia with hypoplastic bone marrow, skeletal, renal and ophtalmological malformations and chromosomal aberrations. The disease involves many organs including skin and genitourinary, musculoskeletal, cardiovascular and neurological systems. The clinical findings in FA patients are hyperpigmentation, small reproductive organs in males, kidney problems, thumbs and arm abnormalities, skeletal anomalies of hip, spine or ribs, low birth weight, short stature, growth retardation, defects of the tissue separating the heart chambers and mental retardation or learning disabilitym. Most cases of FA manifest anaemia symptoms during childhood. However, the symptoms may not become apparent until adulthood. FA patients are at risk for secondary malignancies, for example leukaemia, squamous cell carcinoma and hepatocellular carcinoma. The risk of squamous cell carcinoma development is expecially high in the anogenital region as well as the head and neck region. Increased susceptibility of the oral cavity and anogenital region to local predisposing factors, including environmental toxins and viruses . The authors report a new case of hard palate squamous cell carcinoma in a FA patient. The clinical history and localization of the tumour make this case unique.</div>
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The patient, a 27-year-old white male, was referred by a private oral surgeon to our hospital for evaluation of a hard palate lesion that had appeared six months before (Figure ). The lesion had been diagnosed initialing as gingivitis by the private oral surgeon and treated with local topical medicines without any remission.</div>
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<span style="background-color: black; line-height: 13.333333969116211px; text-align: left;">Preoperative hard and soft palate lesion</span></div>
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At the age of seven the patient was recovered for an orthopaedic trauma. He had been diagnosed with FA at the age of seven after that pancytopenia was noticed during routine blood examinations for orthodontic trauma. He had been treated with androgenic therapy and had not received a bone marrow transplant. The haematological test revealed an early stage of pancytopenia (3,4 × 109/l, Hb 12,3 g/dl, and platelets 13 × 10<sup style="margin: 0px; padding: 0px;">9</sup>/l).</div>
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Oral examination revealed a relatively well-defined, nearly circular, concave ulcer measuring 3 × 4 cm, which extended from the hard palatal mucosa in the upper molar region to the adjacent soft palatal mucosa. The surface was erythematous and smooth, with some telangiectasias. Clinical examination showed no regional lymphadenopathy. CT and MR imaging showed a hard and soft tissue mass extending from molar region mucosa to the soft palate mucosa. The nasopharynx appeared normal (Figure 2). No significant cervical lymphadenopathy was seen on the images. An incisional biopsy performed under local anaesthesia revealed a well-differentiated squamous cell carcinoma (Figure 3).</div>
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<span style="background-color: black;"> <span style="font-size: 11px; line-height: 14px;">Preoperative CT image.</span></span></div>
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<span style="background-color: #f7f7f7; font-size: 11px; line-height: 14px;"> </span><span style="background-color: black;"><span style="font-size: 11px; line-height: 14px;"> </span><span style="font-size: 11px; line-height: 14px;">Biopsy finding: Well-differentiated squamous cell carcinoma.</span></span></div>
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<span style="line-height: 17px;">The tumor was surgically removed with a right partial maxillectomy extendiney to homolateral soft mucosa and clear magins. Reconstruction was accomplished with a temporalis muscle flap. The patient has been followed up for 6 months without any evidence of recurrence or metastasis.</span>
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<span style="color: purple; font-size: x-large;">Discussion</span></h2>
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Fanconi Anemia is a rare autosomal recessive disorder characterized by various congenital malformations, progressive bone marrow failure at a very young age and of solid tumors development. FA is defined by its cellular hypersensitivity to DNA cross-linking agent such as diepoxybutane (DEB) and mitomycin (MML). Presence of mutations of in one of the different FA genes, FA can be divided into eight complementary groups (A, B, C, D1, D2, E, F, G), with each group having in common the cellular hypersensitivity to cross-linking agent. In the International Fanconi Anemia Registry (IFAR) complementation group A (65%), C (15%) and G (10%) are the most common .</div>
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The severity is determined by specific complementation group and over all by the type of genetic mutation. Because of these phenotypic differences among complementation groups, FA is a heterogeneous disease. If impaired genetic factors cause an early appearance of the FA syndrome, the same factors may cause an early appearance of malignancies. Thus, there are two distinct groups of patients: (1) severe genetic disturbance with early FA symptoms and early malignancies; (2) mild disturbances with delayed FA symptoms and late malignancies . Kaplan suggested that there are two defects determining the development of cancer in FA patients: defective chromosomal stability and immunodeficiency.</div>
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Patients that have endured bone marrow transplantation have a greater incidence of malignancies development. In these patients, there are four additional factors including pretransplant total body irradiation, cyclophosphamide treatment, chronic graft versus host disease, and prolonged immunosuppressive treatment after transplantation.</div>
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The highest incidence of cancer development in FA patients is reported by Kuttler. In this study he compared the incidence of Hard Neck Squamous Cell Carcinoma (HNSCC) in common population (0.038%) and in FA patients (3%). The first to describe a HNSCC in a FA patient were Esparza and Thompson. Jansisyanont reported that the commonest localizations of squamous cell carcinoma in FA patients in descending order are: tongue, anogenital region, pharynx, larynx, oral mucosa, mandible and skin.</div>
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Lustig published a review of the international bibliography on the HNSCC in FA patients. He presented 17 cases. In 13 patients the cancer localization was intra-oral. In 9 cases of these 13, the tongue was involved. According with this, in FA patients the tongue cancer incidence is 69%, while in non FA patients the incidence varies by 10 to 16%.</div>
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Kuttler in 2003 referred that 19 of 754 patients in the International Fanconi Anaemia Registry (3%) had HNSCC. In the same year Bremer presented two cases of HNSCC, but in international literature no article has reported a hard palate localization of HNSCC.</div>
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The male:female ratio of HNSCC in normal population is 2:1 while Reed asserted the reversed ratio in FA patients. FA patients develop squamous cell carcinoma at significantly earlier age than the general population. Kenedy and Hart reported an average age of 27 years in FA patients and the average time between age of FA diagnosis and cancer development is 10.5 years.</div>
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The treatment of malignancies in FA patients with HNSCC is similar to the general population with similar pathologies. The aim is the tumour resection oncologic radicality. The main preoperative problem in patients with FA is the associated bone marrow failure, requiring preoperative haematologic consultations. The possibility of blood and platelet transfusion before surgery must be considered. We think that the first approach in FA patients is surgical resection of primary HNSCC with, if necessary, neck dissection and reconstruction. Generally, FA patients withstand surgical procedures very well. A further concern for the surgeon is the development of postoperative complications, including wound infections and haematoma. Although our patient did not develop postoperative complications, FA patients can have serious problems in adjuvant therapy due to increased susceptibility to mutagenic stimuli.</div>
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In FA patients, radiotherapy and chemotherapy follow different therapeutic principles. In FA patients the increased susceptibility to XRT and CTx can present problems to determine and to deliver a cancericidal dose without causing significant damage to normal tissue. Thus, in these patients standard doses for adjuvant therapy are generally reduced. Furthermore, the use of conventional protocols, which include cross-linking agents, can cause severe systemic complications, including irreversible aplastic anaemia and catastrophic organ damage.</div>
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Because SCC in FA is difficult to treat once advanced, it is necessary to diagnose malignancies at early stage. We agree with the protocol proposed by Kutler. He suggests a careful biannual screening of the oral cavity and oropharynx that should start between the ages of 15 and 20. However, in patients with FA with histrory of leucoplakia or recurrent oral lesions, head and neck examinations are recommended every six or eight weeks.</div>
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<span style="color: purple; font-size: x-large;">Conclusion</span></h2>
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We report a unique localization of hard and soft squamous cell carcinoma in a FA patient. The atypical clinical manifestation rendered the diagnosis more difficult. We recommend a quarterly follow up of the oral-rhino-pharynx complex in FA patients and to consider as carcinomas, all oral lesions that last more than two weeks.</div>
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<span style="color: purple; font-size: x-large;">References</span></h2>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Jahrbuch für Kinderheilkunde und physische Erziehung</em> 1927, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">117</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>257-280. <a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B1" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<span style="color: #cc0000;">Swift MR, Hirschhorn K: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Fanconi's anemia. inherited susceptibility to chromosome breakage in various tissue.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Ann Intern Med</em> 1966, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">65</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>496-503. </span></div>
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<span style="color: #cc0000;">Esparza A, Thompson WK: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Familial hypoplastic anemia with multiple congenital anomalies (Fanconi's syndrome) – report of three cases. Cases presented are of two sisters and a female cousin with complete clinical and post mortem findings.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">R I Med J</em> 1966, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">49</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>103-110. <a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B4" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<span style="color: #cc0000;">Joenje H, Matthew C, Gluckman E: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Fanconi anaemia research: current status and prospects.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Eur J Cancer</em> 1995, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">31</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>268-272. <a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B5" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<span style="color: #cc0000;">dos Santos CC, Gavish H, Buchwald M: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Fanconi anemia revisited: old ideas and new advances.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Stem Cells</em> 1994, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">12</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>142-153. <a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B6" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<span style="color: #cc0000;">Linares M, Pastor E, Gomez A, Grau E: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Hepatocellular carcinoma and squamous cell carcinoma in a patient with Fanconi's anemia.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Ann Hematol</em> 1991, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">63</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>54-55. <a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B7" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<span style="color: #cc0000;">LeBrun DP, Silver MM, Freedman MH, Phillips MJ: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Fibrolamellar carcinoma of the liver in a patient with Fanconi anemia.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Hum Pathol</em> 1991, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">22</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>396-398. <a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B8" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<li id="B9" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Moldvay J, Schaff Z, Lapis K: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Hepatocellular carcinoma in Fanconi's anemia treated with androgen and corticosteroid.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Zentralbl Pathol</em> 1991, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">137</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>167-17</span></div>
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<li id="B10" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Oksuzoglu B, Yalcin S: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Squamous cell carcinoma of the tongue in a patient with Fanconi's anemia: a case report and review of the literature.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Ann Hematol</em> 2002, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">81</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>294-298. <a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B10" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<li id="B11" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Kutler DI, Auerbach AD, Satagopan J, Giampietro PF, Batish SD, Huvos AG, Goberdhan A, Shah JP, Singh B: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">High incidence of head and neck squamous cell carcinoma in patients with Fanconi anemia.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Arch Otolaryngol Head Neck Surg</em> 2003, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">129</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>106-112<a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B11" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<li id="B12" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Kaplan MJ, Sabio H, Wanebo HJ, Cantrell RW: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Squamous cell carcinoma in the immunosuppressed patient: Fanconi's anemia.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Laryngoscope</em> 1985, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">95</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>771-775. <a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B12" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<li id="B13" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Jansisyanont P, Pazoki A, Ord RA: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Squamous cell carcinoma of the tongue after bone marrow transplantation in a patient with Fanconi's anemia.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">J Oral Maxillofac Surg</em> 2000, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">58</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>1454-1457<a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B13" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<li id="B14" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Socie G, Scieux C, Gluckman E, Soussi T, Clavel C, Saulnier P, Birembault P, Bosq J, Morinet F, Janin A: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Squamous cell carcinomas after allogeneic bone marrow transplantation for aplastic anemia: further evidence of a multistep process.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Transplantation</em> 1998, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">66</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>667-670. </span></div>
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<li id="B15" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Bremer M, Schindler D, Gross M, Dork T, Morlot S, Karstens JH: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Fanconi's anemia and clinical radiosensitivity report on two adult patients with locally advanced solid tumors treated by radiotherapy.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Strahlenther Onkol</em> 2003, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">179</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>748-753. <a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B15" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<li id="B16" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Reed K, Ravikumar TS, Gifford RR, Grage TB: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">The association of Fanconi's anemia and squamous cell carcinoma.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Cancer</em> 1983, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">52</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>926-928<a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B16" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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<li id="B17" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Kennedy AW, Hart WR: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Multiple squamous-cell carcinomas in Fanconi's anemia.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Cancer</em> 1982, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">50</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>811-814<a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B17" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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</li>
<li id="B18" style="border: 0px; font-family: inherit; font-style: inherit; margin: 1.4em 0px 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><div style="border: 0px; clear: both; font-family: inherit; font-style: inherit; line-height: 1.3em; outline: 0px; overflow: visible; padding: 0px; vertical-align: baseline;">
<span style="color: #cc0000;">Alter BP: <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Radiosensitivity in Fanconi's anemia patients.</strong></span></div>
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<span style="color: #cc0000;"><em style="border: 0px; font-family: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Radiother Oncol</em> 2002, <strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">62</strong><strong style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">:</strong>345-347.<a href="http://www.head-face-med.com/sfx_links?ui=1746-160X-2-1&bibl=B18" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><img align="absmiddle" alt="OpenURL" src="http://www.head-face-med.com/sfx_links?getImage" style="border: 0px; font-family: inherit; font-style: inherit; margin: 0px; outline: 0px; padding: 0px; vertical-align: middle;" /></a></span></div>
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</ol>
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<br /></div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com0tag:blogger.com,1999:blog-3393509504180156297.post-40398012522907335222012-07-10T13:46:00.001-07:002012-07-22T20:15:09.926-07:00Basaloid squamous cell carcinoma of retromolar trigone: A case report with review of literature<div dir="ltr" style="text-align: left;" trbidi="on">
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Basaloid squamous cell carcinoma (BSCC) is a rare distinct histologic variant of squamous - cell carcinoma of the head and neck region. BSCC is more aggressive and has a poorer prognosis, although histologically, it is associated with squamous cell carcinoma and squamous atypia. The usual site of occurrence for BSCC is the upper aerodigestive tract, floor of the mouth and base of the tongue. This is a case report of an unusual case of BSCC of retromolar trigone, which is quite rare.</div>
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<span style="line-height: 18px;">Basaloid squamous cell carcinoma (BSCC) is an uncommon variant of squamous cell carcinoma. It was first described by Wain </span><i style="line-height: 18px;">et al</i><span style="line-height: 18px;"> in 1986.</span><span style="line-height: 18px;"> BSCC is included as a distinct entity in the revised classification of tumors of head and neck by </span><i style="line-height: 18px;">WHO</i><span style="line-height: 18px;"> in 1991.</span><span style="line-height: 18px;"> Generally, it has a predilection for head and neck region, particularly the upper aerodigestive tract, i.e. larynx </span><sup style="line-height: 18px;">,</sup><span style="line-height: 18px;"> hypo pharynx.</span><span style="line-height: 18px;"> In the oral cavity, BSCC has a predilection for the tongue, though it has been described in other locations such as floor of the mouth, palate, retromolar trigone and gingival mucosa. </span><span style="line-height: 18px;"> </span><br />
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<span style="line-height: 18px;">The aggressive biological behavior of BSCC has been commonly associated with early recurrence, cervical lymph node involvement and distant metastasis with spread to the lungs and liver.</span><span style="line-height: 18px;"> Most BSCC's are diagnosed at advanced clinical stages and have an unfavorable prognosis because of poor overall patient survival rate.</span><br />
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<span style="line-height: 18px;">Clinically, patients with BSCC present features similar to those of the patients with squamous cell carcinoma and have the same etiological risk factors, e.g. tobacco and alcohol consumption.</span><span style="line-height: 18px;"> The recommended treatment for BSCC is surgery followed by radiotherapy and chemotherapy.</span><br />
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Case Report</span></h2>
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<span style="line-height: 18px;">A 65 year - old male patient came to Dr. R. Ahmed Dental College reporting with a chief complaint of pain in right lower back tooth region of 6 months duration. The patient gave a history of difficulty in mouth opening and swallowing. He had a history of beedi smoking for a period of 50 years, with a frequency of 12/day.</span><br />
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<span style="line-height: 18px;">Extra oral clinical examination revealed palpable, mobile submandibular and upper jugular lymph nodes on the right side, measuring approximately 1×1 cm and they were firm and non-tender to palpation. On intra-oral examination, an ulceroproliferative lesion involving the right side of the retromolar trigone region, measuring about 2×2 cm. was seen (Figure 1)</span><span style="line-height: 18px;">. The ulcer was tender on palpation, exhibiting irregular margins with ill-defined borders and white slough surrounded by erythematous area. Oral hygiene was poor with generalized stains and calculus. Generalized attrition was present with right posterior teeth tender on percussion. No limitation of mouth opening was seen. Tongue movements were not affected.</span>
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<span style="line-height: 18px;">A provisional clinical diagnosis of malignant ulcer was given. After obtaining written consent from the patient, an incisional biopsy was performed under local anesthesia and sent for histopathologic examination. An orthopantomogram (Figure 2)</span><span style="line-height: 18px;"> was taken which showed irregular radiolucency distal to 3 </span><sup style="line-height: 18px;">rd</sup><span style="line-height: 18px;"> molar with erosion of the ascending border of the ramus of the mandible, measuring 2 × 2 cm. An ultrasonogram of neck was done. The report showed metastatic changes in submandibular and level II group of lymph nodes. The histopathologic report (Figure 3)</span><span style="line-height: 18px;"> was poorly differentiated squamous cell carcinoma. The lesion was T </span><sub style="line-height: 18px;">4</sub><span style="line-height: 18px;"> N </span><sub style="line-height: 18px;">1</sub><span style="line-height: 18px;"> M </span><sub style="line-height: 18px;">x</sub><span style="line-height: 18px;">.</span>
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<span style="line-height: 18px;">The treatment planned was hemimandibulectomy with supraomohyoid neck dissection under general anesthesia, followed by radiotherapy. An apron incision extending from the midline of the chin along the second crease of the neck extending to the mastoid process was made. Anteriorly, the incision was continued around the chin to split the lower lip in the midline. Dissection was done in the subplatysmal layer and supraomohyoid neck dissection was done. The nodes in the level I and level II regions of the neck were surgically removed. The submandibular salivary gland was excised (Figure 4)</span><span style="line-height: 18px;">. Hemimandibulectomy was done. Hemostasis was achieved. Wound closure was done. Postoperative recovery of the patient was uneventful. The histopathologic picture of the excised specimen was reported as BSCC. The histopathologic report was given by three oral pathologists from different centers.</span>
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<span style="line-height: 18px;">The patient has undergone radiotherapy with 5000 cGy fractionated over 6 weeks. Barium meal test, chest X-ray and endoscopic evaluation of the upper aerodigestive tract were done, which showed no evidence of lesion or metastasis. The patient has been reviewed regularly for the last 3 months and is disease free.</span><br />
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<span style="line-height: 18px;">BSCC has been defined in the 2005 WHO blue book as an aggressive high grade variant of squamous cell carcinoma of both basaloid and squamous components. </span><span style="line-height: 18px;"> Wain </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> first introduced this histopathological entity and called it as BSCC in 1986. Till date approximately 45 cases of BSCC involving the oral cavity have been reported in literature, with a strong predilection for base of the tongue (61%) and floor of the mouth (30%). </span><br />
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<span style="line-height: 18px;">The histogenesis of this neoplasm is controversial. It is suggested that the tumor originates from the totipotential cells in the basal layer of squamous epithelium. When we review the etiology, it is seen that the possible relationship of BSCC and viruses is a matter of debate and has been reported in some locations like nasopharynx and penis.</span><span style="line-height: 18px;"> The obtained data are controversial, while Kleist </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> and El mofty </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> have very recently detected a high frequency of HPV and HSV in basaloid tumors than in conventional squamous cell carcinoma in the head and neck, others have found no difference.</span><br />
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<span style="line-height: 18px;">The various sites of origin of BSCC reported by authors were gingiva (Eiji Hirai </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> ), oral mucosa and maxillary tuberosity (C. Wedenberg </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> ), floor of the mouth (Kunal Sah </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;">), retromolar trigone (Marcia Sampaio Campose </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> ), nasal cavity (Joong Seob Lee </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> ), hypopharynx with extensive spindle cell component (Tokuhiro kimura </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> ), conjunctiva and paranasal sinus (Pooja Vasudev </span><span style="line-height: 18px;">), urinary bladder (Funda Vakar -Lopez </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> ) and uterine cervix (Yong Soon Kwon </span><span style="line-height: 18px;"> ) (Table 1)</span><span style="line-height: 18px;">.</span>
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<b style="font-family: Arial, Verdana, Helvetica, sans-serif; font-size: 12px; line-height: 18px; text-align: -webkit-center;"> Table 1: Review of the site, clinical and immunohistological features</b>
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<span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">Domenico Coppola </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> studied the clinicopathological and immunohistochemical features of eight BSCC of floor of the mouth which reveals high recurrence, worse prognosis, metastasis, mortality and shorter survival than squamous cell carcinoma. Grossly, most of the previously reported BSCCs are flat or slightly elevated tumors, often with a central ulceration similar to our case. Very few cases show a polypoid pattern. Interestingly these cases are always associated with a spindle cell component.</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> Jung Yeon Kin </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> reported that all BSCC showed positivity for high molecular weight cytokeratin (HMW CK) with heterogenous or diffuse staining pattern, but lacked activity for neuroendocrine markers and bcl-2 oncoprotein. Pinar Atasoy </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> reported a case of BSCC of lungs whose cells showed a high mitotic rate and peripheral palisading. The immunohistological examination for neuroendocrine markers was negative. Tie-Jun Li </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> studied BSCC of esophagus without adenoid cystic features. Grazia Salerno </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> reported that low levels of p27 </span><sup style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">Kip I</sup><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> expression significantly correlated with poor prognosis, biological aggressiveness and consequent shortened survival. The supposed higher clinical aggressiveness of BSCC compared with the conventional Squamous cell carcinoma remains a continuous matter of debate. Banks </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">, Luna </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">et al</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> and De sampaio </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> did not find significant differences in behaviour between these two neoplasms in different anatomical sites while others did. Cosmo E </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">et al.</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> discussed the clinicopathological and follow-up study of 40 cases and review of literature and concluded that solid nest with typical cell population, basaloid at the periphery (Figure 5)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> and squamous at the centre, are the most common growth patterns of BSCC, which was the histopathologic picture seen in our case.</span>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 5: Histological picture of basal cell palisading (H and E stain, 40×)</b>
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Discussion</span></h2>
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<span style="line-height: 18px;">BSCC is a rare and aggressive variant of squamous cell carcinoma which is reported to occur predominantly in men between 60 to 70 years of age. </span><span style="line-height: 18px;"> It is reported in individuals with history of tobacco and alcohol abuse. The most frequent site to be affected by BSCC is the upper aerodigestive tract with strong predilection for the base of the tongue, supraglottic larynx and hypopharynx, but it is also found in the anus, thymus and uterine cervix. Clinically, it is an aggressive tumor with high rates of nodal (64%) and distant metastases (44%). Results of a case control study by Soriano </span><i style="line-height: 18px;">et al</i><span style="line-height: 18px;"> found a 6 times higher risk of distant metastases compared to the usual type of squamous cell carcinoma. Some authors recommend a chest CT and FDG- PET in all cases to rule out early distant metastases. Treatment of choice is complete surgical excision of the lesion with neck dissection supplemented by radiotherapy or adjuvant chemotherapy.</span><br />
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<span style="line-height: 18px;">Our case report was a BSCC in the retromolar trigone which is an unusual site of occurrence. Marcia sampaio campos </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> has also reported an atypical presentation of oral BSCC in the retromolar trigone in a 39 year old man, in which he described the immunohistochemical characteristics of the lesion. Due to its biological and morphologic features, it may be confused with adenoid cystic carcinoma of the solid subtype, small cell neuroendocrine carcinoma undifferentiated carcinoma, basal cell adenocarcinoma and squamous or adenosquamous carcinoma. In the large majority of cases, the distinction between these tumors is readily made on the basis of standard H&E morphology. However, immunohistochemical markers have been reported to be useful in differentiating these tumors.</span><br />
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<span style="line-height: 18px;">Our case mimics squamous cell carcinoma clinically and was reported on incisional biopsy as poorly differentiated squamous cell carcinoma. On examining the deeper sections of the excisional biopsy, the histologic picture showed nests and cords of closely packed pleomorphic basaloid cells with nuclear palisading along the periphery of the neoplastic nests surrounded by a fibrous stroma with prominent areas of comedo necrosis. Hence the histopathologic report of BSCC was given.</span><br />
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<span style="line-height: 18px;">Wain </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> and recently Barnes </span><i style="line-height: 18px;">et al</i><span style="line-height: 18px;">. </span><span style="line-height: 18px;"> put down the following criteria to diagnose cases of BSCC.</span><br />
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<span style="line-height: 18px;">The features included:</span><br />
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<li>Predilection for head and neck region in men in their 60s or 70s.</li>
<li>An ulcerated or exophytic mass with submucosal soft tissue infiltration.</li>
<li>Solid basaloid appearing dysplastic island with biphasic pattern showing comedo type necrosis (Figure 6) and pseudo-glandular pattern.</li>
<li>Abrupt foci of squamous differentiation with or without keratin pearls, and surface mucosal epithelium showing dysplastic features.</li>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 6: Histopathological picture on high power magnification showing comedo necrosis (H and E stain, 10×)</b>
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<span style="line-height: 18px;">Quite recently, however Coletta </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> have demonstrated the importance of cytokeratins 1, 7 and 14 in the diagnosis of SCC and have shown significantly higher AgNOR and PCNA positivity in BSCC when compared with squamous cell carcinoma. Immuno staining for p53 also showed a higher percentage of positive cells in BSCC. The glandular carcinomas can be excluded as glandular lesion present immunoreactivity for CK7 unlike BSCC. Expression of MMP-1, MMP-2 and MMP-9 were reported higher in cells of BSCC than in cells of squamous cell carcinoma, suggesting of aggressive behaviour. Emanuel </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> have stressed the value of p63 in making the distinction between BSCC and adenoid cystic carcinoma of head and neck.</span><br />
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<span style="line-height: 18px;">Though in a comparative study of oral BSCC and squamous cell carcinoma done by Ferrada C Grizza </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> they concluded that their study supported the opinion that the prognosis of BSSC does not differ from that of conventional squamous cell carcinoma of the oral cavity when matched for clinical classification. </span><span style="line-height: 18px;"> </span><br />
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<span style="line-height: 18px;">Nodal metastasis is quite common in laryngeal, hypopharyngeal and tracheal BSCC. Regional nodal metastasis was seen in 75% and distant nodal metastasis was seen in 35-50% of the cases in Wizenburg </span><i style="line-height: 18px;">et al</i><span style="line-height: 18px;"> series, lung is reported to be the main target for distant metastasis in BSCC. In our case, the patient showed no clinical or radiographic evidence of lung metastasis. Finding a second primary tumor is a common clinical situation in the head and neck. Cosmo E </span><i style="line-height: 18px;">et al.</i><span style="line-height: 18px;"> have observed in 17.5% of their patients, a second primary tumor and therefore support Thompson's advice for keeping in mind the possibility of finding a second primary tumor in any sites either synchronic or metachronic, when diagnosing a BSCC in the head and neck.</span></div>
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</span><span style="color: #783f04; font-size: x-large;">Conclusion</span></h2>
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<span style="line-height: 18px;">BSCC, a distinct clinicopathological entity with aggressive clinical behavior, which usually is reported to occur in the upper aerodigestive tract, has been reported by us occurring in the retromolar trigone area which is an uncommon site for an uncommon lesion such as BSCC.</span></div>
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<span style="color: #cf9aff; font-size: 17px;"> </span><span style="color: #783f04; font-size: x-large;">References</span></h2>
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<tr><td valign="top" width="5%"><span style="color: red;">1.</span></td><td><span style="color: red;">Wain SL, Kier R, Volmer RT. Basaloid squamous cell carcinoma of the tongue, hypopharynx and larynx report of 10 cases. Hum Pathol 1986;17:1158-6. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">2.</span></td><td><span style="color: red;">World Health Organization. Histological typing of tumour of upper respiratory tract and ear Berlin, Germany: Springer Verlag; 1991. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">3.</span></td><td><span style="color: red;">Sundharam BS, Krishnan PA. Basaloid squamous cell carcinoma report of a case and review of literature. Indian J Dent Res 2003;14:184-6. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">4.</span></td><td><span style="color: red;">de Sampaio Góes FC, Oliveira DT, Dorta RG, Nishimoto IN, Landman G, Kowalski LP. Prognoses of oral basaloid squamous cell carcinoma and squamous cell carcinoma. Arch Otolaryngol head neck surg 2004;130:83-6. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">5.</span></td><td><span style="color: red;">Sampio -Goes FC, Oliveira DT, Dorta RG, Nonogaki S, Landman G, Nishimoto IN, <i>et al</i>. Expression of PCNA, p53, BAXA and Bcl-X in oral poorly differentiated and Basaloid squamous cell carcinoma relationship with prognosis. Head Neck 2005;27:982-9. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">6.</span></td><td><span style="color: red;">Winzenburg SN, Niehans GA, George E, Daly K, Adams GL. Basaloid squamous cell carcinoma: A clinical comparision of two histological types with poorly differentiated squamous cell carcinoma. Otolaryngeal Head Neck Surg 1998;119:471-5. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">7.</span></td><td><span style="color: red;">Lu SY, Eng HL, Huang CC, Chien CY, Lui CC, Lin JW. Basaloid squamous cell carcinoma of the sinonasal tract - report of two cases. Otolaryngol Head Neck Surg 2006;134:883-5. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">8.</span></td><td><span style="color: red;">Cardesa A, Zidar N, Erenoc. Basaloid squamous cell carcinoma. World health organization classification of tumors. Lyon, france: IARC Press; 2005.p.124-5. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">9.</span></td><td><span style="color: red;">Ide F, Shimoyama T, Horie N, Kusama K. Basaloid squamous cell carcinoma of oral mucosa: A new case and review of 45 cases in literature. Oral Oncol 2002;38:120-4. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">10.</span></td><td><span style="color: red;">Wan SK, Chan JK, Lau WH, Yip TT. Basaloid squamous carcinoma of the nasopharynx. An epstein-barr virus-associated neoplasm compared with morphologically identical tumors occurring in other sites. Cancer 1995;76:1689-93. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">11.</span></td><td><span style="color: red;">Cubilla AL, Reuter VE, Gregoire L, Ayala G, Ocampos S, Lancaster WD, <i>et al</i>. Basaloid squamous cellcarcinoma: A distinctive human papilloma virus related penile neoplasm: A report of 20 cases. Am J Surg Pathol 1998;22:755-61.</span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">12.</span></td><td><span style="color: red;">Kleist B, Bankau A, Lorenz G, Jager B, Poetschet M. Different risk factors in basaloid and common squamous head and neck cancer. Laryngoscope 2004;114:1063-8. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">13.</span></td><td><span style="color: red;">El-Mofty SK, Patil S. Human papillomavirus (HPV)-related oropharyngeal nonkeratinizing squamous cell carcinoma: Characterization of a distinct phenotype. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101:339-45. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">14.</span></td><td><span style="color: red;">Hirai E, Yamamoto K, Yamamoto N, Yamashita Y, Kounoe T, Kondo Y, <i>et al</i>. Basaloid squamous cell carcinoma of mandible: Report of two cases. Oral Surg Oral Med OralPathol Oral Radiol Endod 2009;108:e54-8. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">15.</span></td><td><span style="color: red;">Wedenberg C, Jesslén P, Lundqvist G, Lundgren J, Hellquist HB. Basaloid squamous cell carcinoma of the maxilla. Oral Oncology 1997;33:141-4. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">16.</span></td><td><span style="color: red;">Sah K, kale A, Hallikerimah S. Basaloid squamous cell carcinoma involving floor of the mouth. J Oral Maxillofac Surg2008;12:61-3. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">17.</span></td><td><span style="color: red;">Campos MS, Modolo F, de Oliveira JS, Pinto-Júnior DS, de Sousa SC. Atypical presentation of oral basaloid squamous cell carcinoma. J Contemp Dent Pract 2009;10:98-104. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">18.</span></td><td><span style="color: red;">Lee JS, Ko IJ, Jun SY, Kim JY. Basaloid squamous cell carcinoma in nasal cavity. Clin Exp Otorhinolaryngol 2009;2:207-10 </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">19.</span></td><td><span style="color: red;">Kimura T, Mukai M, Shiotani A, Moro K, Ikeda A, Okada Y. Basaloid squamous cell carcinoma of the hypopharynx with an extensive spindle cell component exhibiting a pedunculated polypoid mass. Arch patho lab med 2005;129:e94-6. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">20.</span></td><td><span style="color: red;">Vasudev P, Boutross-Tadross O, Radhi J. Basaloid squamous cell carcinoma: Two case reports. Cases J 2009;2:9351. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">21.</span></td><td><span style="color: red;">Vakar-López F, Abrams J. Basaloid squamous cell carcinoma occurring in the urinary bladder. Arch Pathol Lab Med 2000;124:455-9. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">22.</span></td><td><span style="color: red;">Yong SK, Yong MK, Choi GW, Kim YT, NamJH. Pure basaloid squamous cell carcinoma of the uterine cervix: A case report. J Korean Med Sci 2009;24:542-5. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">23.</span></td><td><span style="color: red;">Coppola D, Catalano E, Tang CK, Elfenbein IB, Harwick R, Mohr R. Basaloid squamous cell carcinoma of floor of mouth. Cancer 1993;72:2299-05. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">24.</span></td><td><span style="color: red;">Kim JY, Cho KJ, Lee SS, Khang SK, Shim YS. Clinicopathologic study of basaloid squamous cell carcinoma of the upper aerodigestive tract. J Korean Med 1998;13:269-74. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">25.</span></td><td><span style="color: red;">Atasoy P, Bozdogan N, Dizbay SS, Akay H. Basaloid carcinoma of the lung. Turk J Cancer 2000;30:36-9. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">26.</span></td><td><span style="color: red;">Li TJ, Zhang YX, Wen J, Cowan DF, Hart J, Xiao SY. Basaloid Squamous cell carcinoma of the esophagus with or without adenoid cystic features. Arch Pathol Lab Med 2004;128:1124-30. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">27.</span></td><td><span style="color: red;">Salerno G, Di Vizio D, Staibano S, Mottola G, Quaremba G, Mascolo M, <i>et al</i>. Prognostic value of p27Kip1 expression in basaloid squamous cell. BMC Cancer 2006;6:146. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">28.</span></td><td><span style="color: red;">Banks ER, Frierson HF, Covell JL. Fine needle aspiration cytologic findings in metastatic basaloid squamous cell carcinoma of the head and neck. Acta Cytol 1992;36:126-31. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">29.</span></td><td><span style="color: red;">Cosme E, Ayman G, Maddi G, Carmen E, Francisco J. Bilbao J, <i>et al</i>. Basaloid squamous cell carcinoma of the head and neck. Head Neck Pathol 2008;2:83-91. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">30.</span></td><td><span style="color: red;">Barnes L, Ferlito A, Altavilla G, MacMillan C, Rinaldo A, Doglioni C. Basaloid squamous cell carcinoma of head and neck: Clinicopathological features and differential diagnosis. Ann Otol Rhino Laryngol 1996;105:75-82. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">31.</span></td><td><span style="color: red;">Coletta RD, Cotrim P, Vargas PA, Villalba H, Pires FR, de Moraes M, <i>et al.</i> Basaloid squamous cell carcinoma of oral cavity report of 2 cases and study of AGNOR, PCNA, p53 and MMP expression. Oral Surg Oral Med Oralpathol Oral Radiol Endod 2001;91:563-9. </span><br />
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<tr><td valign="top" width="5%"><span style="color: red;">32.</span></td><td><span style="color: red;">Emanuel P, Wang B, Wu M, Burstein DE. p63 immunohistochemistry in the distinction of adenoid cystic carcinoma from basaloid squamous cell carcinoma. Mod Pathol 2005;18:645-50. </span><br />
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<br /></div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com1tag:blogger.com,1999:blog-3393509504180156297.post-20883260340864284042012-07-10T02:27:00.002-07:002012-07-22T20:26:58.687-07:00Management of intrusive luxation with immediate surgical repositioning<div dir="ltr" style="text-align: left;" trbidi="on">
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Intrusive luxation is one of the most severe forms of traumatic injuries in which the affected tooth is forced to displace deeper into the alveolus. As a consequence of this type of injury, maximum damage occurs to the pulp and all the supporting structures. This report presents a case of severe intrusive luxation of mature maxillary central and lateral incisor in a 40-year-old male. The intruded tooth was immediately repositioned (surgical extrusion) and splinted within hours following injury. Antibiotic therapy was initiated at the time of repositioning and maintained for 5 days. Pulp removal and calcium hydroxide treatment of the root canal was carried out after repositioning. Splint was removed 2 months later. Definitive root canal treatment with Gutta percha was accomplished at a later appointment. Clinical and radiographic examination 6, 12 and 24 months after the surgical extrusion revealed satisfactory progressive apical and periodontal healing.</div>
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<span style="line-height: 18px;">Luxation lesions account for 15.0% to 61.0% of traumas in permanent teeth.</span><sup style="line-height: 18px;"> </sup><span style="line-height: 18px;">Intrusion injury has a rarer occurrence in permanent dentition when compared with other types of luxation injuries. It comprises 3% of all traumatic injuries in the permanent dentition</span><span style="line-height: 18px;"> and 5%-12% of dental luxations.</span><span style="line-height: 18px;"> Pulp necrosis, inflammatory root resorption, ankylosis, loss of marginal bone support, pulp canal obliteration, paralysis or disturbance of radicular development and gingival retraction may occur as a consequence of an intrusive luxation.</span><span style="line-height: 18px;">This case report discusses the management of traumatic injury in which three permanent teeth, including two central incisors and one lateral incisor, were severely intruded.</span></div>
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<span style="line-height: 18px;"><span style="color: #750810; font-family: Verdana, Arial, sans-serif; font-size: x-large;">CASE REPORT</span></span></h2>
<span style="line-height: 18px;"><br style="font-size: 12px; line-height: 18px;" /><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">The patient was a healthy, 42-year-old male (Figure 1)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> who had suffered a roadside accident 2 h before and after initial examination and soft tissue management, he was referred to the conservative Dentistry PG Clinics of Dr. R. Ahmed Dental College and Hospital by Oral Surgery Department of the same college Clinical examination revealed that the injury had resulted in 5-6 mm intrusion</span></span><span style="background-color: black;"><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">(Figure 2)</span><span style="line-height: 18px;"><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">and unco</span></span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">mplicated crown fracture of maxillary permanent central incisors and left lateral incisor</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">(Figure 3)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">. </span></span><br />
<span style="line-height: 18px;"><br style="line-height: 18px;" /><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">Subluxation of both maxillary canines was also noted. There was additional injury to alveolar bone, teeth and surrounding soft tissues with minor lacerations on both upper and lower lips. Lower central incisors were also mobile due to trauma.</span><br style="line-height: 18px;" /><br style="line-height: 18px;" /><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">Because of the severity of intrusion and completed root development, immediate surgical repositioning of intruded incisors was planned. Prior to surgical operation, the patient was given doxycycline (100 mg, oral). After the administration of local anesthesia, the intruded tooth was initially luxated. An artery forcep was used for this purpose</span></span><span style="background-color: black;"><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">(Figure 4)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">.The tooth was brought into a position by applying careful and very gentle force incisally. The teeth were repositioned to a level such that the cementoenamel junction (CEJ) was in plane with the free gingival margin. Following repositioning of the teeth, space was found to be present between the upper and lower teeth. Patient's history of pre-existing open-bite justified the relative positions </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">(Figure 5)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">. After bringing the upper lateral incisor and central incisors into their respective positions, these teeth were splinted using Erich's arch bar technique</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">(Figure 6)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">. The lower incisors with slight mobility were splinted using 22 gauge wire and light-cured composite resin. Arch bar was used in the upper teeth because of the </span><i style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">associated alveolar fractures and extreme mobility</i><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> of the teeth involved in intrusion and mobility of both the canines as well. Another reason for avoiding composite splint in upper teeth was the continued bleeding from the traumatized supporting structures in upper teeth.</span></span><br />
<span style="line-height: 18px;"><br style="line-height: 18px;" /><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">Upper left lateral incisor (tooth no. 22) was symptomatic 3 weeks later with patient complaining of pain and sensitivity in the same. Intra oral periapical radiograph (IOPA) showed external root resorption with loss of marginal bone support. Therefore, access was done in tooth no. 22, and the necrosed pulp was removed. Calcium hydroxide was placed as an intracanal medicament.</span><br style="line-height: 18px;" /><br style="line-height: 18px;" /><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">Splints were removed after 6 weeks. Both upper and lower central incisors were stable, while the upper left lateral incisor was found to be slightly mobile. Soft tissue injuries had healed. Therefore, continued need for support of tooth no. 22 was addressed to and a resin composite-wire splint was placed for 2 more weeks.</span><br style="line-height: 18px;" /><br style="line-height: 18px;" /><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">Follow-up IOPA radiograph showed narrowing of root canal lumen of upper central incisors and no response to pulp vitality tests. Hence a diagnosis of non-vital pulp was made and root canal therapy was completed. </span><br style="line-height: 18px;" /><br style="line-height: 18px;" /><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">Fractured incisal edges of both central incisors were built up with resin composite. Teeth were stable and patient was completely asymptomatic 6 months post-operatively. Further follow up at 1 year and 2 year post-operatively showed no changes in asymptomatic status of the patient clinically. Radiograph of the teeth involved was taken, and the peri-apical area shows normal healing </span></span><span style="background-color: black;"><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">(Figure 7)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> and</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">(Figure 8)</span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;"> </span><span style="font-family: Arial, Verdana, Helvetica, sans-serif; line-height: 18px;">. </span></span><br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiWyV829HXmZhdf23DmIBIp9q4Y7kteORtplOTEOP_dMek7BLzsTw41gpfbuV7RG_9JEhSZl8ZcrBLZ4HIZ-lmEbQAhKpo8X6oPgmRkU5tFM4jSF7HVlt3DICFrwRPzB5EJOid5DiM0bZpM/s1600/JConservDent_2009_12_2_69_55621_f2.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="231" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiWyV829HXmZhdf23DmIBIp9q4Y7kteORtplOTEOP_dMek7BLzsTw41gpfbuV7RG_9JEhSZl8ZcrBLZ4HIZ-lmEbQAhKpo8X6oPgmRkU5tFM4jSF7HVlt3DICFrwRPzB5EJOid5DiM0bZpM/s320/JConservDent_2009_12_2_69_55621_f2.jpg" width="320" /></a></div>
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<b>Figure 2: Intra-oral view showing intruded upper central incisors and left lateral incisors, with loss of upper right lateral incisor</b></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEisQDoQ0VKy96JGrfiLRLshoco5-VptlBvMOZpoIBdjoJkSEXQT13ZGYfcFNLJpOhyAFXj4b5Gn2Kbf53XSsovUK7YB3Xs9cWADCYblydJC4qPBSgai1o1qtZrbXj4qsIzg-DkjCLvyUX4n/s1600/JConservDent_2009_12_2_69_55621_f3.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="231" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEisQDoQ0VKy96JGrfiLRLshoco5-VptlBvMOZpoIBdjoJkSEXQT13ZGYfcFNLJpOhyAFXj4b5Gn2Kbf53XSsovUK7YB3Xs9cWADCYblydJC4qPBSgai1o1qtZrbXj4qsIzg-DkjCLvyUX4n/s320/JConservDent_2009_12_2_69_55621_f3.jpg" width="320" /></a></div>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 3: Orthopantomograph of the patient showing the intruded upper incisors with their abnormal relative position with other teeth</b>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhGPheOzFOph9eSOcESN_8k4JyUeOp0IB-eIMMFBk9VPj0YiqlUp7qWlcbYeKGJj6-sN4DvPovvhToZON1PZQxLzyvPMStyG5HU0s_UglQQxBt_A_JJ-bJTGb6TxUvmzrLniIwoeoXuxk6I/s1600/JConservDent_2009_12_2_69_55621_f4.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="231" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhGPheOzFOph9eSOcESN_8k4JyUeOp0IB-eIMMFBk9VPj0YiqlUp7qWlcbYeKGJj6-sN4DvPovvhToZON1PZQxLzyvPMStyG5HU0s_UglQQxBt_A_JJ-bJTGb6TxUvmzrLniIwoeoXuxk6I/s320/JConservDent_2009_12_2_69_55621_f4.jpg" width="320" /></a></div>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 4: An artery forcep used to apply a very gentle downward force to position the teeth properly</b>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhnTmNyC79hzw4gJB7Dff8jOCjUmlbV-7F3h39tk0dRcTh7gxc09K6KBO2aQS5kOQqJcApHXpKUlr1HH9YKA1iOcN_U5qBuKJY8ppXsZJtIuYP-PsFPshPKGiJiXyLouVQezU3EmyEsP-YS/s1600/JConservDent_2009_12_2_69_55621_f5.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="231" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhnTmNyC79hzw4gJB7Dff8jOCjUmlbV-7F3h39tk0dRcTh7gxc09K6KBO2aQS5kOQqJcApHXpKUlr1HH9YKA1iOcN_U5qBuKJY8ppXsZJtIuYP-PsFPshPKGiJiXyLouVQezU3EmyEsP-YS/s320/JConservDent_2009_12_2_69_55621_f5.jpg" width="320" /></a></div>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 5: Space was present between the upper and lower teeth. Patient gave history of an pre-existing open-bite</b>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiPKArIPwHHFHqcHi7ElD7kfGn_Bc1T-2ycKITr6PDgp65JAcjrqhd-SZZ27JsHAD10PeGce0bAohRfLYc3UJXUcZ-Ry4PTlufd0BzKdSQMJnmHmpGjmzMKIWHtLWUSXgxhIiJvcY4zaA93/s1600/JConservDent_2009_12_2_69_55621_f6.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="231" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiPKArIPwHHFHqcHi7ElD7kfGn_Bc1T-2ycKITr6PDgp65JAcjrqhd-SZZ27JsHAD10PeGce0bAohRfLYc3UJXUcZ-Ry4PTlufd0BzKdSQMJnmHmpGjmzMKIWHtLWUSXgxhIiJvcY4zaA93/s320/JConservDent_2009_12_2_69_55621_f6.jpg" width="320" /></a></div>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 6: Splinting done using Erich’s arch bar technique</b>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjQ5YvyiXDQ09OlbOD7AMTUmF53Xd0S9J7Sj6ccImcrV1sLbxhqNox8NLoI7cD1xPtBCa2NOsvI1t5WPIe7sdHu6gzjMOHMhnR2ZRAPq5MTeQx7mKm7AtfrdwxxDBfycwFnhPSr5C4qBbN7/s1600/JConservDent_2009_12_2_69_55621_f7.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="231" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjQ5YvyiXDQ09OlbOD7AMTUmF53Xd0S9J7Sj6ccImcrV1sLbxhqNox8NLoI7cD1xPtBCa2NOsvI1t5WPIe7sdHu6gzjMOHMhnR2ZRAPq5MTeQx7mKm7AtfrdwxxDBfycwFnhPSr5C4qBbN7/s320/JConservDent_2009_12_2_69_55621_f7.jpg" width="320" /></a></div>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 7: IOPA radiograph at 1-year follow up</b>
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<b style="font-size: 12px; line-height: 18px; text-align: -webkit-center;">Figure 8: IOPA radiograph at 2-year follow up</b>
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<span style="line-height: 18px;">Intrusion injuries have the poorest prognosis and complex treatment among all tooth injuries. No consensus has been reached on the optimal treatment of this type of injuries. The recommended treatment options for intruded teeth include the following (3): Allowing spontaneous re-eruption of the teeth. Immediate surgical repositioning and fixation. Orthodontic repositioning (extrusion).</span></div>
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<span style="line-height: 18px;">The aim of the treatment was to restore the tooth to its original position by decompressing the injured tissues and re-establishing the normal relationship between bone and tooth.</span></div>
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<span style="line-height: 18px;">Andreasen and Andreasen</span><span style="line-height: 18px;"> postulated that fully mature intruded teeth must be extruded by orthodontic means over a 2-3 week period. According to them, total repositioning by surgical means in such cases may increase the risk of resorption. However, their study is based on a pooled sample of different injury types, including subluxation, extrusion and intrusion. The unique nature of the intrusion injury distinguishes it from other luxations. </span></div>
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<span style="line-height: 18px;">In addition, many previous studies, including that of 29 intruded permanent teeth by Kinirons, Sutcliff and Ebeleseder </span><i style="line-height: 18px;">et al.,</i><span style="line-height: 18px;"> failed to show that surgical repositioning increased the prevalence of resorption. </span></div>
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<span style="line-height: 18px;">In the presented case, immediate surgical repositioning was used for treating intruded incisors with favorable results at 2-year follow up. Still further follow up is continued to obtain a better interpretation of the result. </span></div>
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<span style="line-height: 18px;">There are many advantages of this surgical technique for managing intruded teeth. First, it can be easily repositioned and provides the original anatomic situation for healing of the adjacent tissues and also provides adequate room for endodontic access. However, inadvertent ex-articulation during the repositioning procedure and possible additional damage to the periodontal ligament, leading to a higher risk of ankylosis, are disadvantages of the surgical procedure, which perhaps can be minimized depending on the caution and the skill of the operator. </span></div>
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<span style="line-height: 18px;">The elapsed time for repositioning of the tooth was approximately 2 h in the presented case, which is an unfavourable factor, according to Andearsen delay in mechanical repositioning, more than 90 min facilitated replacement root resorption in the intruded position. In this case, more complications occurred in the lateral incisor, which may be correlated with severe injury encountered by this particular tooth. </span></div>
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<span style="line-height: 18px;">Pulp tissue and periodontal structures require constant attention in intrusive injuries. The treatment has to be adaptable according to complications. Further surgical repositioning in the presented case with 2-year follow up proved to be a viable treatment method for intruded teeth without any additional risk of resorption. The occurrence of such complications seems to be related to the degree of severity of the original injury</span><i style="line-height: 18px;"> .</i><span style="line-height: 18px;"> Further interpretation of results requires continued long-term follow up of the case.</span></div>
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<span style="color: #783f04; font-size: x-large;">REFERENCES</span></h2>
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">1.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Andreasen FM, Andreasen JO. Luxation injuries. In: Andreasen JO, Andreasen FM, editors. Textbook and Color Atlas of Traumatic Injuries to the Teeth, 3<sup> rd</sup> ed. Copenhagen: Munksgaard; 1994. p. 315-82.</span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">2.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Andreasen JO. Etiology and pathogenesis of traumatic dental injuries: A clinical study of 1298 cases. Scand J Dent Res 1970;78:329-42.</span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">3.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Zerman N, Cavallieri G. Traumatic injuries to permanent incisors. Endod Dent Traumatol 1993;9:61-4.</span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">4.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Altay N, Gungor HC. A retrospective study of dentoalveolar injuries of children in Ankara, Turkey. Dent Traumatol 2001;17:201-4.</span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">5.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Andreasen JO. Luxation of permanent teeth due to trauma: a clinical and radiographic follow-up study of 189 injured teeth. Scand J Dent Res 1970;78:273-86. </span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">6.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Andreasen FM, Vestergaard-Pedersen B. Prognosis of luxated permanent teeth - the development of pulp necrosis. Endod Dent Traumatol 1985;1:207-20. </span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">7.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Andreasen JO, Andreasen FM. Essentials of traumatic injuries to the teeth: a step-by-step treatment guide. Copenhagen: Munksgaard; 2000. </span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">8.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Cunha RF, Pavarini A, Percinoto C, Lima JE. Influence of surgical repositioning of mature permanent dog teeth following experimental intrusion: a histologic assessment. Dent Traumatol 2002;18:304-8. </span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">9.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Al-Badri S, Kinirons M, Cole BO, Welbury RR. Factors affecting resorption in traumatically intruded permanent incisors in children.<b></b>Dent Traumatol 2002;18:73-6.</span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">10.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Gungor HC, Cengiz SB, Altay N. Immediate surgical repositioning following intrusive luxation: a case report and review of the literature. Dent Traumatol 2006;22:340-4. </span><br />
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<tr><td valign="top" width="5%"><span style="background-color: black; color: #cc0000; font-size: small;">11.</span></td><td><span style="background-color: black; color: #cc0000; font-size: small;">Ebeleseder KA, Santler G, Glockner K, Hulla H, Pertl C, Quehenberge RF. An analysis of 58 traumatically intruded and surgically extruded permanent teeth. Endod Dent Traumatol 2000;16:34-9.</span></td></tr>
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com2tag:blogger.com,1999:blog-3393509504180156297.post-25444676330244009422012-07-09T23:12:00.001-07:002012-07-22T20:31:59.698-07:00Non surgical perforation repair by mineral trioxide aggregate under dental operating microscope<div dir="ltr" style="text-align: left;" trbidi="on">
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Root perforation repair has historically been an unpredictable treatment modality, with an unacceptably high rate of clinical failure. Recent developments in the techniques and materials utilized in root perforation repair have dramatically enhanced the prognosis of both surgical and nonsurgical procedures. Mineral Trioxide Aggregate is a relatively new material that is being successfully used to repair perforations. Technological advancements such as the use of a Dental Operating Microscope for correction of these inevitable procedural errors are a major breakthrough in dentistry today. This article presents one clinical case of nonsurgical root perforation repair by Mineral Trioxide Aggregate, using the Dental Operating Microscope.</div>
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INTRODUCTION</b></span></h2>
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Root perforations are undesired complications of endodontic treatment. Once a perforation has been diagnosed, treatment must be rendered to seal the perforation site effectively to minimize injury and prevent contamination of the surrounding periodontal attachment apparatus. Although successful treatment and prognosis depend on many factors, the location of the perforation and the time lapse between exposure and repair are the two most important factors for determining the treatment and prognosis of the tooth. Perforations have been treated mainly through surgical means earlier. However, now, with the introduction and widespread use of the operating microscope, together with the power of ultrasonics, the nonsurgical repair of perforation is more predictable, safe, and easy.</div>
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This present case illustrates concepts and techniques of using the operating microscope to visualize and repair the perforation nonsurgically.</div>
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CASE REPORT</b></span></h2>
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A 35-year-old female patient reported to the Department of Conservative Dentistry and Endodontics, Dr. R. Ahmed Dental College and Hospital, Kolkata, with pain in tooth No 11. She gave a history of root canal treatment (RCT) having been attempted elsewhere on that tooth, about one month prior.</div>
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Clinical examination revealed that access preparation had been attempted in the grossly carious maxillary right central incisor. Under rubber dam isolation, the access opening was carefully examined under a Dental Operating Microscope (FS – 1-11; MOELLER – WEDDEL INTERNATIONAL, Germany) (16X Magnification). Distolateral midroot perforation with ledge formation was clearly visualized under the microscope [Figure 1].</div>
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Figure 1</h4>
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Perforation site in disto-lateral mid-root area of tooth 11 under Microscope in 16X magnification</span></div>
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span style="font-size: 15px;">An intraoral periapical radiograph was taken with a #60 size gutta percha (GP) point placed in the perforation, which aided in further localizing the site of the perforation, and it was confirmed that the defect was subcrestal [</span>Figure 2<span style="font-size: 15px;">]. A slight periodontal ligament (PDL) widening was seen.</span>
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Figure 2<br />
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">IOPA radiograph of tooth 11 with GP point placed through the perforation</span></span></div>
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">The decision to nonsurgically manage the perforation using Mineral Trioxide Aggregate, under a Dental Operating Microscope, was taken with the patient's consent.</span></div>
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">The lateral walls of the perforation were refined and cleaned with light brushing strokes using an Endo 4 ultrasonic tip (Dentsply Tulsa Dental, Tulsa, Oklahoma). Hemostasis was achieved. A #60 size gutta percha point was used to establish the length from the incisal reference point up to the perforation site inside the root canal. Healiguide (ENCOLL, Fremont, CA, USA), an absorbable collagen material was chosen to provide complete hemostasis and a controlled barrier, to pack the restorative material against it. Working length was established and a #40 size GP point was placed in the canal [Figure 3]. Pieces of healiguide were appropriately cut and carried out into the access cavity [Figure 4]. These were progressively placed into the chamber with an appropriate plugger and firmly pressed through the perforation defect. A solid barrier was established [Figure 5]. The access cavity and perforation defect were flushed thoroughly with normal saline and dried. Mineral trioxide aggregate (MTA – ANGELUS; Peterborough, UK) was mixed and carried to the perforation site with the help of a carrier and packed with an appropriately fitted plugger. Repair of the perforation was carried out by progressive placement and packing of small increments of the Mineral Trioxide Aggregate. The gutta percha point was removed and moist cotton pellets were placed over the Mineral Trioxide Aggregate, and closed with noneugenol temporary restoration (Cavit, 3MESPE). The Mineral Trioxide Aggregate was allowed to set for approximately four hours and the patient was recalled after four hours. The canal was opened and it was found that the well-adapted, hard Mineral Trioxide Aggregate had sealed the perforation site and ledge area [Figure 6]. Biomechanical preparation was carried out using the step back method. Apical preparation was performed up to size #60 and obturation was done by lateral condensation of the gutta percha [Figure 7].</span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEihNjS1vjD6s2lVie0Tu3oc60gkK5n11yi8P8mCDFGdbVFyL4o-qhuh7ADDWstTIrqXdOuhk6-Lc_ZfuDUbc6yJJ6OK79-tIcQgf74cZr7rRaVlZg2mXqJIurNqujoS0fSF6lBtsAmS1uA1/s1600/JCD-14-83-g004.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="237" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEihNjS1vjD6s2lVie0Tu3oc60gkK5n11yi8P8mCDFGdbVFyL4o-qhuh7ADDWstTIrqXdOuhk6-Lc_ZfuDUbc6yJJ6OK79-tIcQgf74cZr7rRaVlZg2mXqJIurNqujoS0fSF6lBtsAmS1uA1/s320/JCD-14-83-g004.jpg" width="320" /></a></div>
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Figure 4<br />
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Piece of Healiguide resorbable collagen matrix carried out into the access cavity</span></span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhtUSw397BSWF9ewZM9OXq38tQuELg_YbtF49xrVeAy55kCMARvRT_F9E6w6l6w1HR9400v-95YzHSKC4sB0pxekVZIl0rOTTwOvZx_PpSmJi2KnRsiWsSEfoqqxHHQkqHEj8Cfp_upq8Co/s1600/JCD-14-83-g005.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="237" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhtUSw397BSWF9ewZM9OXq38tQuELg_YbtF49xrVeAy55kCMARvRT_F9E6w6l6w1HR9400v-95YzHSKC4sB0pxekVZIl0rOTTwOvZx_PpSmJi2KnRsiWsSEfoqqxHHQkqHEj8Cfp_upq8Co/s320/JCD-14-83-g005.jpg" width="320" /></a><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"></span><br />
Figure 5<br />
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Collagen matrix placed corresponding to the cavosurface of the root</span></span><br />
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">After 48 hours well adapted hard MTA visible under 24X magnification - completely filled the perforation defect</span></span></div>
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span style="font-size: 15px;">After one month the patient was recalled and was found to be asymptomatic. The glass fiber post was cemented by dual cure resin cement (Calibra - DENTSPLY). The crown was restored by a light cure composite resin [</span>Figure 8<span style="font-size: 15px;">]. A one-year recall examination, clinically demonstrated an asymptomatic tooth, with normal attachment and architecture of the soft tissues. A radiographic analysis at this recall evaluation revealed no development of a periapical lesion and no further widening of the PDL [</span>Figure 9<span style="font-size: 15px;">]. The patient was advised to put in a crown, but she did not report back, as she had migrated.</span>
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">A perforation is defined as the pathological or iatrogenic communication between the root canal space and the periodontal tissue. In the present case, the perforation was present in the distolateral midroot area of the upper right central incisor, which might have been caused during access preparation. To avoid such an occurrence, preparation of the access cavity should be carried out with regard to the anatomy of the tooth, and help of the microscope should be taken, to locate the canal orifice. In the present case the Dental Operating Microscope was used to repair the perforation defect. A midrange magnification (16×) was used because it was the recommended magnification for any surgical purpose.</span></div>
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">The increased magnification and dual light source of the microscope is invaluable to diagnose and locate accurately the exact perforation site. Incremental placement of restorative material like the Mineral Trioxide Aggregate over the perforation site can be carried out successfully and precisely under a microscope.</span></div>
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">As the perforation was in the middle third of the root and sufficient access was available through the pulp chamber, the perforation was repaired <span style="line-height: 20px;">non-surgically</span>. The perforation site was cleaned and refined by Endo 4 ultrasonic tip (Dentsply Tulsa Dental, Tulsa, Oklahoma) to ensure an environment free of microbial contamination and necrotic tissue.</span></div>
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<span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">The internal matrix concept, in conjunction with the microscope, is an efficient and effective technique for treating accessible perforations non-surgically. In the present case we placed a sterile, resorbable, and biocompatible collagen material Healiguide into the perforation site, to control hemostasis and prevent overfills, and it acted as an internal matrix.</span></div>
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The Mineral Trioxide Aggregate forms a colloidal gel upon hydration, which solidifies in approximately four hours. Therefore, when used as a root repair material, moisture must be provided from the internal aspect of the root (using a moist cotton pellet). The Mineral Trioxide Aggregate was initially introduced as a root end filling material, however, because of its biocompatibility it is now also considered as a material of choice to seal perforations. Although Mineral Trioxide Aggregate is an expensive material, it has become indispensible in procedures such as perforation repair.</div>
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The location of the perforation is an important factor for its successful repair. More apical the perforation, the better the prognosis. In the present case the perforation was in the midroot, but yet prognosis was favorable even after one year.</div>
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<span style="color: #660000; font-size: x-large;"><b>
CONCLUSION</b></span></h2>
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Training, practice, and technology allow clinicians to expand their abilities greatly in endodontic treatment. Correction of procedural errors can now be performed with a higher degree of clinical confidence by using a Dental Operating Microscope. The use of the microscope and its inherent precision is closing the gap between theoretical possibility and clinical reality.</div>
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<span style="color: #660000; font-size: x-large;"><b>
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<span style="color: #cc0000;"><span class="ref-label" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">7.</span> <span class="ref-cit" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="element-citation" id="__element-citationid1767206" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Aziz S, Ali AK, Moeen F. Two successful cases of root perforation repair using mineral trioxide aggregate. <span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="ref-journal" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Pak Oral Dent J. </span>2008;<span class="ref-vol" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">28</span>:103–6.</span></span></span></span></div>
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<span style="color: #cc0000;"><span class="ref-label" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">9.</span> <span class="ref-cit" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="element-citation" id="__element-citationid1781297" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Schwartz RS, Mauger M, Clement DJ, Walker WA 3rd. Mineral trioxide aggregate: A new material for endodontics. <span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="ref-journal" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">J Am Dent Assoc. </span>1999;<span class="ref-vol" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">130</span>:967–75.</span> </span></span></span></div>
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<span style="color: #cc0000;"><span class="ref-label" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">10.</span> <span class="ref-cit" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="element-citation" id="__element-citationid1463911" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Castellucci A. Magnification in endodontics: The use of the operating microscope. <span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="ref-journal" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Pract Proced Aesthet Dent. </span>2003;<span class="ref-vol" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">15</span>:377–84.</span> </span></span></span></div>
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<span style="color: #cc0000;"><span class="ref-label" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">14.</span> <span class="ref-cit" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="element-citation" id="__element-citationid1471373" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Moghaddame-Jafari S, Mantellini MG, Botero TM, McDonald NJ, Nör JE. <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">In vitro</em> Effect of ProRoot MTA on pulp cell apoptosis and proliferation. <span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="ref-journal" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">J Endod. </span>2005;<span class="ref-vol" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">31</span>:389–91.</span></span></span></span></div>
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<span style="color: #cc0000;"><span class="ref-label" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">15.</span> <span class="ref-cit" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="element-citation" id="__element-citationid1858879" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Qatharni HA. <em style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">In vitro</em> Effect of root perforation repair materials on morphology and attachment behavior of human PDL fibroblasts. <span style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><span class="ref-journal" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">Saudt Dent J. </span>2004;<span class="ref-vol" style="border: 0px; font: inherit; margin: 0px; padding: 0px; vertical-align: baseline;">16</span>:113–7.</span></span></span></span></div>
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</div>Anonymoushttp://www.blogger.com/profile/00836440572469934136noreply@blogger.com4