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IDA -MARTHANDAM BRANCH OFFICE BEARERS-2013 President:Dr.G.Sathish Kumar Imm.Past President: Dr.S.Karthiga Kannan President-Elect:Dr. J.D. Dias Vice Presidents:Dr.Selva Libin ,Dr.Indra Kumar Hon. Branch Secretary:Dr.Subramonian.S Hon. Jt. Secretary: Dr.Sherin Leon Hon. Asst. Secretary:Dr.Sudha Rani Hon. Treasurer: Dr.LeonDurai Rep to C.D.E:Dr.Farakath Khan Rep to C.D.H:Dr.Beyanso.C.P.Daniel Rep to State: Dr.J.D.Dias ,Dr.Subramonian ,Dr. V. Manoj Executive Committee: Dr.SankarPandian ,Dr.JeslinBeyanso Dr. Harry NihilNayagam Journal Editor: Dr.R.Sambhu Journal Co-Editor:Dr. Krishna Prasad Website & Event:Dr. Merlin Raja Singh ,Dr.Jithin.G.Nelson Greeting Committee :Dr. Shine Manoj.D.J Student Membership:Dr.Anuroopa Membership Committee:Dr.Priya.M.S ,Dr.Manoj.J.R ,Dr.Dhano Legal Cell:Adv.Rtn. Mohanan Nair ,Dr. B. Krishna Prasad Advisory Committee: Dr.J.D.Dias ,Dr.M.IrwinAnand ,Dr.AnithaJeslin Dr.Jain.R.S Care and Concern:Dr.Selva Kumar

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It is interesting to note that JOMIDA provides a forum for the exchange of information about new and significant research in dentistry besides peer-reviewed research articles, clinical developments and key clinical opinions. I also found that some sections act as a bridge between the practice and research sections and ensures that the information from the research is easily available to both practitioners and researchers. It is clear that the Editor, President, Secretary and other office bearers have put in a lot of effort in this venture and the same reflects in the broad diversity of the articles published. I was impressed by the particular emphasis on knowledge that holds the potential to improve patient care in our clinics. This indeed is a reflection of sincere and commendable efforts to inculcate an environment conducive of research. I wish that the Journal will continue to embody scientific literature of highest quality, integrity and ethical standards. I extend my best wishes for the success of the Journal and hope that this enthusiasm will hence forth be a regular feature in the years to come.

Dr Thomas Manjooran Dean Faculty of Dental science Kerala University of Health Sciences

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Authorship criteria All persons designated as authors should qualify for authorship, and all those who qualify should be listed. Each author should have participated sufficiently in the work to take public responsibility for appropriate portions of the content. One or more authors should take responsibility for the integrity of the work as a whole, from inception to published article. Authorship credit should be based only on 1.Substantial contributions to conception and design, or acquisition of data, or analysis and interpretation of data; 2.Drafting the article or revising it critically for important intellectual content; and 3.Final approval of the version to be published. Conditions 1, 2, and 3 must all be met. Acquisition of funding, the collection of data, or general supervision of the research group, by themselves, do not justify authorship. The order of authorship on the byline should be a joint decision of the co-authors. Authors should be prepared to explain the order in which authors are listed. Once submitted the order cannot be changed without written consent of all the authors. For a study carried out in a single institute, the number of authors should not exceed six. For a case-report and for a review article, the number of authors should not exceed four. For short communication, the number of authors should not be more than three. A justification should be included, if the number of authors exceeds these limits. Only those who have done substantial work in a particular field can write a review article. A short summary of the work done by the authors (s) in the field of review should accompany the manuscript. The journal expects the authors to give post-publication updates on the subject of review. The update should be brief, covering the advances in the field after the publication of article and should be sent as letter to editor, as and when major development occur in the field. Sending the Manuscript to the Journal Articles can be submitted to: editoridamarthandam@yahoo.com,editor@idamarthandam. com 1.First Page File: Prepare the title page, covering letter, acknowledgement, etc., using a word processor program. All information which can reveal your identity should be here. Do not zip the files.

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Dear friends, I feel Wonderful as I pen down this editorial for the 4th issue of scientific journal of Marthandam IDA (JOMIDA).This journey with JOMIDA started in May 2012 and as we step forward to 2014, we the editorial board feel proud that a young brand new branch was successful in bringing out 4 successive issues of a scientific journal with quality in articles and printing which was appreciated and received whole heartedly by many great professionals in the field of dentistry. Few land marks in this short journey includes the recognition from ISSN and availability of journal online in the link www.jomida.idamarthandam.com We the editorial board would like to thank the support and motivation from head office, state office& reviewer board members. Unconditional support of the president, secretary, treasurer and all the members of IDA Marthandam family for the editorial board holds a great role in this successful journey and we request you all to support and motivate us in the future journey too. “Commitment doesn't guarantee success, but lack of commitment guarantee you will fall short of your potential� - Denis Waitely

The editorial board is committed to bring out the best for the readers and we would like to listen to your comments, remarks, suggestions, and critics about our journal. Kindly feel free to write to the editorial board. Feedbacks are always instrumental in improving and are always motivational force for us to move ahead. Looking forward for your feedbacks as email at editor@idamarthandam.com

Thanking you, With Warm Regards Yours Sincerely, Dr.R.Sambhu Editor in Chief

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Dear Friends, I am extremely happy to write to you through your journal again and probably for the last time as the President of IDA - Tamil Nadu. Clinical dental practices are so dependent on, forever changing and improving scientific research. Busy dental practitioners find it difficult, if not impossible to keep abreast with the latest developments in dentistry. To keep aside time to read scientific journals and literature and to incorporate it into their practices is not an easy task for a practitioner involved in the day to day routine. I congratulate you and your team of editorial board and whole of IDA Marthandam in the journey, as your journal JOMIDA has taken up the task of updating the general dental practitioners knowledge in your region and to keep them informed about the modern concepts in dentistry. Vazhga Bharatham, Valarga IDA.

Dear Friends, I have great privilege to communicate with you through your branch journal. We are growing with the world, knowledge with new inventions. Still we are lacking so much. Read More, Learn More. This year we have 2800 Members in our state IDA and 1560 Members in Care and Concern Family Security Scheme. Last year itself we discussed that all IDA TN members should join Care and Concern.This Year we Lost 6 Members. Through this Family Security Scheme we paid Fraternity amount to their families. But, this amount is very low which is only about 2, 50,000/-.I request each and every one of IDA Tamilnadu Member to join Care and Concern Scheme. I personally appreciate Dr.Sambhu for his effort put on this journal. It is like an International Journal. Congrats to the Office Bearers and Editorial Team of IDA Marthandam Branch. Jaihind

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BRANCH PRESIDENT’S MESSAGE Dear Friends, Warm wishes for a happy x-mas and a prosperous new year to all. Hope this year brings all prosperity to our profession. During my term as president of IDA Marthandam branch for past one year we were able to conduct regular CDE programs on various topics including medico legal aspects by eminent speakers. I feel really happy and strongly believe that these programs have been beneficial to all our members.IDA Marthandam branch has laid a platform for all the youngsters and seniors to interact and share knowledge through CDE and scientific journal. I congratulate the editor Dr.Sambhu and eminent academician Dr.S.Karthiga Kannan th for the efforts take to bring out the 4 successive issue of our scientific journal. I hope our journal will be PubMed indexed very soon with their hard work to publish each issue in a successful way. With wishes and warm regards, Dr.G.Sathish Kumar President IDA -Marthandam Branch

BRANCH SECRETARY’S MESSAGE Dear friends Warm Greetings. I am meeting you all in the last issue of JOMIDA during my tenure as secretary of MIDA. I feel deeply indebted to all members of MIDA for the great blessing and encouragement rendered towards me in last few years. My sincere thanks to hon. State secretary Dr.C. Sivakumar, Late. M.Sethuanandan, MIDA Presidents during my tenure Dr.Kartiga kannan, Dr. Sathish kumar for posting me with great ideas for the success of the office. Special thanks to the Editor for his perseverance in bringing up value added state of the art journal and website and for helping me remember about MIDA every moment. I am deeply thankful to the Head Office, State office, all members , editorial board, the designer-Dr. Sujan, the printers, the Guests, the speakers of all CDE, all sponsors, IMAMarthandam, Rotary club Marthandam, my students, my assistants, my family and so on… I congratulate and wish all success for the new team of office bearers headed by Dr.J.D.Dias sir. I wish the journal to get indexed at the earliest. Jai hind. With wishes and warm regards,

Dr. S. Subramonian MDS Hon.secretary IDA Marthandam

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Abstract The radiographic appearance of central giant cell granuloma is not pathognomic and may be confused with the other jaw lesions. The localization around the roots of the teeth, especially if these are root filled or if the vitality is negative or doubtful, can create diagnostic difficulty. The present report discusses a case of central giant cell granuloma in a 26 year old male, which appeared very similar to inflammatory periapical radiolucency. The report emphasizes the importance of routine and timely post-treatment

Keywords Central giant cell granuloma; Inflammatory; Mandible; Periradicular

Giant cell lesions of the maxillofacial skeleton and other bones are a controversial matter and uncertainty still exists 1 regarding their basic pathology and biologic behavior. Central giant cell granuloma (CGCG) is a benign lesion of the jaws of unknown etiology. Although initially believed to be the result of a reparative process caused by a variable 2 amount of bone formation, little evidence supports that concept. However, it is now considered as a non-neoplastic lesion exhibiting a spectrum of clinical behavior ranging from non-aggressive to aggressive variants.3 CGCGs occur over a wide age range, the lesion as being more common before age 30; more common in women by a factor of 2:1, and more common in the mandible by nearly a 3:1 margin. Lesions are reported also to be more common in 4 the anterior segments of the jaws and often cross the midline. Surgical curettage is the treatment of CGCG with a reported recurrence of about 15 - 20%.3 CGCG is generally classified amongst the multilocular well-circumscribed non-corticated radiolucencies. However, it may occasionally manifest as a unilocular well circumscribed and corticated radiolucency.5 Although not related to dental pathoses, CGCG may be localized near the roots of teeth or the tooth apex and therefore it may be diagnosed radiographically as a periapical granuloma or a radicular cyst, particularly if the dental pulp does not respond 3 to sensitivity tests. The literature reveals case reports of CGCGs associated with endodontically involved teeth. Because CGCG appears to be a non-inflammatory lesion with unknown etiology, root canal treatment would not be expected to resolve it. A potentially large and destructive lesion could result, caused by inadequate follow-up.3 Emphasizing the importance of post-treatment follow-up and routine submission of periapical surgical specimens for histopathological examination; the objective of this report is to present a case of periapical CGCG that was initially misdiagnosed and treated as an endodontic lesion.

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nt of a lesion located in the anterior tial clinical examination revealed a f the buccal cortex in the region of Case report ncisors covered byoldanmale intact normal A 26 year patient with a non-contributory medical history was referred by a general practitioner for evaluation and treatment of a lesion located in the anterior mandible region. An initial clinical examination revealed a hard painful swelling of the buccal cortex in the region of permanent mandibular incisors covered by an intact normal mucosa (Figure 1).

Fig .1 Intraoral photograph depicting hard swelling of the buccal cortex in the region of mandibular incisors covered by an intact normal mucosa.

Light microscopic examination of sections stained with H-E revealed numerous multinucleated giant cells of variable size and shape, diffusely distributed in a background of ovoid-to-spindle-shaped mononuclear cells showing foci of extravasated RBCs. Foci of new trabeculae of osteoid were seen at the periphery of the lesion (Figure 4). The appearance was consistent with central giant cell granuloma. Follow-up of the patient during a preliminary period of 16 months following surgical curettage of the lesion showed healing of the area with no signs of recurrence.

Fig .2 Intraoral photograph depicting extension of the swelling to the lingual cortex covered by intact mucosa (7 months after initial endodontic treatment)

History of the complaint revealed gradual increase in the size of the swelling during past year. Caries free permanent laint revealed gradual in the mandibular left centralincrease incisor was tested non-vital to electric pulp testing. Periapical radiograph revealed ing pastunilocular year. Caries free permanentwell-demarcated radiolucency in relation to mandibular incisors. ncisor wasThe tested non-vital to electric patient was referred to an Endodontist, where Fig endodontic treatment in relation to permanent mandibular adiograph revealed well-demarcated left central incisor was approached with a clinical view that in relation to mandibular incisors. the periapical radiolucency was most likely a periapical granuloma or a radicular cyst. Recurrence eferredcortex to expansion, an Endodontist, where of the buccal extension of the swelling to the lingual n relation to(Figure permanent cortex 2) and lackmandibular of periapical healing (Figure 3) with considerable enlargement of the radiolucency 7 months approached with a clinical view that after the initial treatment eventually lead to the proposal of ency was most likely alesion. periapical surgical intervention of the

Fig .4

.4

Photomicrograph of histopathologic section reveals numerous large multinucleated giant cells, diffusely distributed in a background of ovoid-to-spindle-shaped mononuclear cells (H-E, original magnification, x100).

lar cyst. Recurrence of the buccal nsion of the swelling to the lingual ack of periapical healing (Figure 3) gement of the radiolucency 7Figmonths .3 Intraoral periapical view revealed nonnt eventually lead to the proposal of corticated radiolucency that failed to respond to endodontic treatment of the lesion. permanent mandibular left central incisor.

Surgical curettage was carried out and the tissue specimen was subjected to the histopathological examination. In view of the acceptable quality of root canal filling in relation to left mandibular central incisor, no further endodontic treatment was undertaken. Gross examination of the tissue specimen revealed many small soft, reddish brown friable tissues of variable size that Fig .3 crumbled on manipulation.

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Since we are all expose to unnatural environmental influences, in one degree or another, the best precaution is to ensure the regular intake of antioxidant nutrients. Major recognized antioxidants include, beta-carotene, Vitamin E, Vitamin C, and a special group of antioxidants bioflavonoids, notably proacanthocyanidins found in the seeds and skins of blue violet and red pigmented fruits which they all work together synergistically for mutual benefit.1

Abstract At the molecular levels, antioxidants serve to deactivate certain particles called free radicals. Antioxidants play the house keeper role, “mopping up” free radicals before they get a chance to do harm in your body. It is postulated that antioxidants prevent the possible carcinogenic effects of oxidation. Together as antioxidants, these substances are thought to be effective in helping to prevent cancer, heart, diseases, and stroke. The antioxidants benefits help to prevent free radicals from tipping the scales to the wrong side of things.

Keywords

History: As part of their adaptation from marine life, terrestrial plants began producing non-marine antioxidants such as ascorbic acid (Vitamin C), polyphenols and tocopherols. The evolution of angiosperm plants between 50 and 200 million years ago resulted in the development of many antioxidant pigments as chemical defenses against reactive oxygen species that are byproducts of photosynthesis. 2, 3 Originally, the term antioxidant specifically referred to a chemical that prevented the consumption of oxygen. In the late 19th and early 20th centuries, extensive study concentrated on the use of antioxidants in important industrial processes, such as the prevention of metal corrosion, the vulcanization of rubber, and the polymerization of fuels in the fouling of internal combustion engines. 1

Antioxidants, Free radicals, Body protectors.

Introduction: The body's natural protector's antioxidants help our body combat excessive free radicals by fighting off their negative effect. Antioxidants are nutrients which donate extra hydrogen electrons to free radicals, thus neutralizing them and producing stable molecules. Antioxidants can be called “the body protectors”, a kind of life insurance for your cells. Since free radicals can multiply by the billions within only a few seconds, it is imperative that the body is constantly supply with these vital nutrients.

Antioxidants, Nature and Chemistry Definition: An antioxidants is a substance that when present in low concentrations relative to oxidation substrate significantly delays or reduces oxidation of substrate. Antioxidants get their name because they combat oxidation. They are the substances that protect other chemicals of the body from the damaging oxidation reactions by reacting with free radicals and other reactive oxygen species within the body, hence hindering the process of oxidation. During this reaction the antioxidants sacrifices itself by oxidation. However antioxidant supply is not unlimited as one antioxidant molecule can only react with a single free radical. Therefore there is a constant need to replenish antioxidants resources, whether endogenously or through supplementation.

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CLASSIFICATION OF MAJOR ANTIOXIDANTS (TABLE 1) ANTIOXIDANT

ROLE

REMARKS

Dismutases O2 to H2O2

Contains manganese

Dismutases H2O2 to H2O

Tetrameric hemoprotien present in peroxisomes

Superoxide Dismutase (SOD)

ENZYMES

Catalase

Removes H2O2 And lipid peroxidases

Glutathione peroxidase

VITAMINS

Selenoprotiens

Alphatocopherol

Breaks lipid peroxidation (Scavenger)

Fat soluble vitamin

Beta carotene

Scavenges free radicals Prevents oxidation of Vit A

Fat soluble vitamin

Ascorbic acid

Scavenger contributes to regeneration of Vit E

Water soluble vitamin

Mode of reaction of antioxidants 1.Chain breaking reactions 2.Reducing the concentration of reactive oxygen species 3.Scavenging initiating radicals 4.Chelating the transition metal catalysts

And the reason to get sick is because the amount of free radicals is greater than the antioxidants fighting them, causing an “imbalance” in the body. This imbalance, if nothing is done about it, can go from you feeling a little under the weather to potentially causing cancer

Oxidative Stress in Disease

Need of Antioxidants

Oxidative stress is thought to contribute to the development of a wide range of diseases including Alzheimer's disease, 4,5 Parkinson's disease6the pathologies caused by diabetes 7 , 8 rheumatoid arthritis, 7 and neurodegeneration in motor neuron diseases.8 In many of these cases, it is unclear if oxidants trigger the disease, or if they are produced as a secondary consequence of the disease and from general tissue damage; One case in which this link is particularly well-understood is the role of oxidative stress in cardiovascular disease. Here, low density lipoprotein (LDL) oxidation appears to trigger the process of atherogenesis, which results in atherosclerosis, and finally cardiovascular 9, 10 disease.

The antioxidants benefits include strengthening your immune system, slowing down the aging process and most importantly fighting off free radicals. This is big because free radicals are damaging to the body causing an increase in inflammation & can lead to many degenerative diseases (e.g. cancer, arthritis, Alzheimer's, heart disease, 5, 8, 9 etc

Antioxidants and the Immune System There are two prevailing theories on why we get sick: The Holistic Theory and the Disease Theory. The older of the two, the Disease Theory, states that a particular bacteria or virus will get “inside” your body and can cause you to be sick. The Holistic Theory states that your body is already full of foreign bodies and free radicals but is able to function normally because antioxidants will “disarm” the harmful stuff... thus keeping your body “in balance.”

Adequate amounts of antioxidants are needed to fight off damaging free radicals and to keep your immune system strong. Fortunately your bodies have its own antioxidant defenses against free radicals,mostly using oxygen. Harmful Effects of Antioxidants Nonpolar antioxidants such as eugenol , a major component of oil of cloves, have toxicity limits that can be exceeded with the misuse of undiluted essential oils. 11 ,Toxicity associated with high doses of water-soluble antioxidants such as ascorbic acid are less of a concern, as 12 these compounds can be excreted rapidly in urine. ,

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More seriously, very high doses of some antioxidants may have harmful long-term effects. The betaCarotene and Retinol Efficacy Trial (CARET) study of lung cancer patients found that smokers given supplements containing beta-carotene and vitamin A had increased rates of lung cancer.13; Subsequent studies confirmed these adverse effects.14. While antioxidant supplementation is widely used in attempts to prevent the development of cancer, it has been proposed that antioxidants may, paradoxically, interfere with cancer treatments. This was thought to occur since the environment of cancer cells causes high levels of oxidative stress, making these cells more susceptible to the further oxidative stress induced by treatments. As a result, by reducing the redox stress in cancer cells, antioxidant supplements could decrease the effectiveness of radiotherapy and chemotherapy.15,16, On the other hand, other reviews have suggested that antioxidants could reduce side effects or increase survival times.17,18 Potential Hazards of Antioxidants If antioxidants were harmless, it wouldn't much matter if you took them "just in case." A few studies, though, have raised the possibility that taking antioxidant supplements, either single agents or combinations, could interfere with health. The trial was stopped early when researchers saw a significant increase in lung cancer among those taking the supplement compared to those taking the placebo. 19, In another trial among heavy smokers and people exposed to asbestos, beta-carotene was combined with vitamin A. Again an increase in lung cancer was seen 20 in the supplement group.

Conclusion: "The Antioxidant Miracle makes it possible to prevent and perhaps even eradicate many of the diseases that were once considered an inevitable part of aging." Disease cannot live in an oxygen-rich environment. However, our world has an oxygen shortage. As a result our bodies are working overtime in order to keep free radicals in check. And this is causing extra stress & strain on the body. The antioxidants benefits help to prevent free radicals from tipping the scales to the wrong side of things. Antioxidants neutralize free radicals so they go from very harmful to practically harmless.

References: 1)Mattill, H A (1947). "Antioxidants". Annual Review of Biochemistry 16: 17792 2).Benzie, I (2003). "Evolution of dietary antioxidants". Comparative Biochemistry and Physiology 136 (1): 11326. 3)Venturi, Sebastiano; Donati, Francesco M.; Venturi, Alessandro; Venturi, Mattia (2000). "Environmental Iodine Deficiency: A Challenge to the Evolution of Terrestrial Life?". Thyroid 10 (8): 7279. 4) Christen Y (2000). "Oxidative stress and Alzheimer disease". Am J Clin Nutr 71 (2): 621S629S. 5)Nunomura A, Castellani R, Zhu X, Moreira P, Perry G, Smith M (2006). "Involvement of oxidative stress in Alzheimer disease". J Neuropathol Exp Neurol 65 (7): 63141. 6) Wood-Kaczmar A, Gandhi S, Wood N (2006). "Understanding the molecular causes of Parkinson's disease". Trends Mol Med 12 (11): 5218. 7) DavĂŹ G, Falco A, Patrono C (2005). "Lipid peroxidation in diabetes mellitus". Antioxid Redox Signal (12): 25668. 8)Giugliano D, Ceriello A, Paolisso G (1996). "Oxidative stress and diabetic vascular complications". Diabetes Care 19 (3): 25767. 9) Hitchon C, El-Gabalawy H (2004). "Oxidation in rheumatoid arthritis". Arthritis Res Ther 6 (6): 26578. 10)Cookson M, Shaw P (1999). "Oxidative stress and motor neurone disease". Brain Pathol 9 (1): 16586. 11)Prashar A, Locke I, Evans C (2006). "Cytotoxicity of clove (Syzygium aromaticum) oil and its major components to human skin cells". Cell Prolif 39 (4): 2418. 12)Hornig D, Vuilleumier J, Hartmann D (1980). "Absorption of large, single, oral intakes of ascorbic acid". Int J Vitam Nutr Res 50 (3): 30914. 13) Omenn G, Goodman G, Thornquist M, Balmes J, Cullen M, Glass A, Keogh J, Meyskens F, Valanis B, Williams J, Barnhart S, Cherniack M, Brodkin C, Hammar S (1996). "Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial". J Natl Cancer Inst 88 (21): 15509. 14) Albanes D (1999). "Beta-carotene and lung cancer: a case study". Am J Clin Nutr 69 (6): 1345S50S.. 15)Seifried H, McDonald S, Anderson D, Greenwald P, Milner J (2003). "The antioxidant conundrum in cancer". Cancer Res 63 (15): 42958. 16)Lawenda BD, Kelly KM, Ladas EJ, Sagar SM, Vickers A, Blumberg JB (2008). "Should supplemental antioxidant administration be avoided during chemotherapy and radiation therapy?". J. Natl. Cancer Inst. 100 (11): 77383. 17) Block KI, Koch AC, Mead MN, Tothy PK, Newman RA, Gyllenhaal C (2008). "Impact of antioxidant supplementation on chemotherapeutic toxicity: a systematic review of the evidence from randomized controlled trials". Int. J. Cancer 123 (6): 122739. 18)Block KI, Koch AC, Mead MN, Tothy PK, Newman RA, Gyllenhaal C (2007). "Impact of antioxidant supplementation on chemotherapeutic efficacy: a systematic review of the evidence from randomized controlled trials". Cancer Treat. Rev. 33 (5): 40718. 19)Albanes D, Heinonen OP, Taylor PR, et al. Alpha-tocopherol and beta-carotene supplements and lung cancer incidence in the alphatocopherol, beta-carotene cancer prevention study: effects of base-line characteristics and study compliance. J Natl Cancer Inst. 1996; 88:1560-70. 20) Omenn GS, Goodman GE, Thornquist MD, et al. Effects of a combination of beta-carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med. 1996; 334:1150-55.

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Abstract Bird Face is a common finding in patients with bilateral ankylosis. The retruded chin is generally not addressed during the primary surgery i.e. during the lysis of the ankylotic mass. In our technical note we are presenting a technique of augmenting the retruded chin using the osteotomised bony ankylotic mass. The advantage of this technique is no donor site is required, thereby reducing the donor site morbidity. The resected bone which would otherwise be thrown away is put to good use. Native bone is used for augmentation thereby maximizing the take-up chance. The total advancement of chin achieved with this technique was 22 mm.

Keywords Ankylosis, Retruded Chin, Bony Augmentation

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Case Report A 25 year old male reported to us with the chief complaint of inability to open mouth and retruded chin (Fig 1.). The patient gave a history of fall on the chin (1, 2) 17 years back that progressively lead to trismus. There was also difficulty in articulation due to the ankylosis. On examination the patient had bird face with a rudimentary chin almost flush with the hyoid bone. The mouth opening was nil with prominent bilateral antigonial notch. No movement was elicited at the preauricular region. The dentition showed Class II malocclusion with protrusive incisors. CT scans and OPG revealed bony ankylosis. Fibrooptic guided Nasotracheal intubation was done. Bilateral pop-wich incision was used for access, which was extended upto the lobule of the ear for better exposure & access. The fused condyle was identified and the mandible was exposed from the posterior border of the ramus to anterior border of the ramus.

Mandibular anterior vestibular incision was placed to expose the chin and reciprocating saw was used to make a horizontal cut extending under the mental foramen bilaterally. The cut was made 4 mm below the canine root apices. The osteotomised segment was slided ahead to augment the chin. The forward sliding of the genium increased the intra-oral mouth opening to 42 mm. 2 osteotomised ankylosed segments were contoured, augmented one over the other and fixed using 10mm titanium screws(Fig 2).

Fig .2 Augmentation using autogenous bone graft Fig .1 Pre-operative retruded chin

Osteotomy was carried out using reciprocating saw. The superior limit was 1.5 cms below the fused malformed joint and the inferior cut was 1.5 cms below the superior cut. The osteotomy was carried out in such a fashion the thick ramus was uniformly resected first and the outer table of the resected ramus was delivered as a rectangular block. Similarly, the inner table of the ramus was resected. The final osteotomy was carried using osteotome and mallet and the fused bone was delivered in 2 blocks of bone on each side. Thus 4 rectangular blocks were harvested. 35 mm mouth opening was achieved; further opening was restricted by the hyoid interfering with the posterior displacement of the chin. Interpositional arthroplasty was done using (3, 4, 5) the temporalis muscle graft . Drain was placed and the wound was closed in layers.

The other 2 osteotomised ankylosed segments were used for lateral augmentation(Fig 3). The discrepancy over the superior border of the augmented bony segment was filled with bone cement, which was further contoured to mimic the natural curvature of the mandible. Suturing was done in layers and pressure dressing was applied. Post-operative aggressive physiotherapy using mouth gag was given. Post-operative mouth opening:-Passive- 38mm Active- 41mm. The advantage of this technique is no donor site is required, thereby reducing the donor site morbidity. The resected bone which would otherwise be thrown away is put to good use. Native bone is used for augmentation thereby maximizing the take-up chance. The total advancement of chin achieved with this technique was 22 mm(Fig 4.).

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Fig .3 Post operative 3-D CT showing augmented chin

Fig .4 Post operative augmented chin

Reference 1.Topazian RG: Etiology of ankylosis of Tempromandibular joint analysis of 44 cases. J oral Surg Anesth Hospital Dent Serv 22:227,1964 2.Kaban LB, Troulis MJ: Peadiatric Oral & Maxillofacial Surgery. Philadelphia, PA, WB Saunders, 2004, p469 3.Guralnick WC , Kaban LB : Surgical Treatment of mandibular Hypomobility. J Oral Surg34:343, 1976 4.Norman JB : Ankylosis of the Tempromandibular Joint . Aust Dent J 23:56, 1978 5.Tideman H, Doddridge M: Tempromandibular joint ankylosis. Aust Dent J 32:171, 1987 6.Pogrel MA, Kaban LB: The role of of a temporalis fascia and muscle flap in tempromandibular joint surgery. J Oral & Maxillofacial Surgery 48;14, 1990 7.Umeda H, Kaban LB, Pogrel MA, etal : Long term viability of the temporalis muscle/fasia flap used for tempromandibular reconstruction. J Oral Maxillofacial Surg 51:530,4,1993 8.Su-Gwan K. treatment of tempromandibular joint ankylosis with temporalis muscle and fascia flap. Int J Oral Maxillofacial Surg 2001:30: 189-193 9.Topazian RG. Comparision of Gap & Interpositional arthroplasty in treatment of TMJ Ankylosis. J Oral Surgery 1966;24: 405-9 10.Gunaseelan R: Condylar resection in extensive ankylosis of tempromandibular ankylosis in adult using resected segment as autograft. A new technique. IJOMS 1997;26:405-407

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Abstract Complex maxillofacial injuries are often a challenging task for the maxillo facial surgeons in terms of diagnosis and reconstruction. Patient presenting with facial trauma may be distracted by other injuries. A missing teeth may be presumed to have been avulsed during the accident therefore, they might be overlooked if their presence is not suspected. We present a case report of maxillofacial trauma and avulsed maxillary anterior teeth dislocated into the nasal cavity which was diagnosed properly and surgically removed.

Keywords

Posterior dentoalveolar fractures are rare unless the impact is high. Previous studies showed that nearly 50% of all children experience some form of dentoalveolar fracture between the ages of 6 and 183 ,another study indicated that 30% of children suffer from a trauma to their primary dentition4 and 22% suffer from a trauma to their permanent 5 dentition .The occurrence rate of dentoalveolar fracture in 6 the maxillofacial trauma was changing from 1.9% to 76.3% according to recent studies.Thorali7 stressed the importance 8 of correct clinical and radiological examination , Andreasen stated that a sufficient radiographic evaluation increases the accuracy of making a correct diagnosis with over 10% from 80% to 91%.When traumatized teeth are left untreated it can lead to more complication because of its displacement into 1 the danger triangle of the mid face .

Nasal cavity, Teeth,Dentoalveolar fracture

Introduction Complex maxillofacial injuries are often a challenging task for the maxillo facial surgeons in terms of diagnosis and reconstruction. Trauma to the dentoalveolar structure are often masked or ignored because of the underlying fractures. Teeth in the nasal cavity is a rare incident and many theories have been proposed including developmental disturbances ,trauma, cysts, crowding of the dentition, persistent deciduous teeth and genetic factors1.The major causes are dentoalveolar trauma and less commonly to other factors2.The frequency of dentoalveolar trauma in maxillofacial injuries varies from different studies. Injury is more common to the maxillary anterior 6 teeth than the mandibular anterior teeth .

Case History A 30 year old man was admitted in our hospital followed by road traffic accident. On examination patient condition was stable and he got multiple facial lacerations with his upper anterior teeth were missing. He could not able to recollect whether his upper teeth was avulsed or not. There was no sign of tooth intrusion and on palpation also could not find the teeth, so it has given the impression of missing teeth. After the examination patient was send for radiological examination. skullantero posterior radiograph was taken and it demonstrated the teeth in the nasal cavity. other facial bones showed no abnormality. The patient was taken for the surgery under general anesthesia ,the wound was explored throughly. We found the teeth displaced posteriorly and lying on the nasal floor .Lateral incisor tooth was lying further posteriorly, its root has pierced the palate and turned upside down. All the tooth were removed .All the bony pieces were removed. Wound closed with 4.0 vicryl .

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Fig.1 Pre op lateral skull radiograph showing teeth in the nasal floor

Fig. 4 Exposed tooth in the palate

Fig.2 Pre op anteroposterior skull radiograph showing teeth

Fig. 5

in the nasal cavity

Removed teeth

Fig. 6 fig. 3

Post op radiograph showing clear nasal cavity

Exposed tooth in the nasal cavity

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Discussion Maxillofacial fractures are more dramatic,making the surgeons to save life as the prime effort diverting from the dental aspect. The major cause for tooth displacement into the nasal cavity is trauma followed by other possible etiologies such as infection, cysts, obstruction to the tooth 9 eruption and development disorders .Magnitude of force and impact determines the direction of the tooth displacement in 6 anterior,posterior,superior directions .The tooth most vulnerable to trauma is the maxillary central incisors which 6 sustains approximately 80% of all dental injuries .Unless the impact force is considerable, the posterior teeth are seldom involved because of their anatomic position and multiple roots6. In the primary dentition intrusions and extrusions comprise the majority of all injuries whereas in permanent dentition the number of the intrusive luxation injuries is considerably reduced which comprises 15 61 % 10. There have been reports of teeth in the nasal septum, mandibular condyle, coronoid process, palate, chin, and maxillary sinus 12. Martin11 has reported a traumatic intrusion of the maxillary permanent incisor into the nasal cavity in 13 patient with mixed dentition. Kamaraj and Paul reported a case of teeth in the frontal sinus of a completely dentulous patient. Case reports of teeth in the nasal cavity similar to our case are very rarely reported in the literature. In our case the patient did not feel the presence of any foreign body in the 14 nasal cavity similar to the case reported by Belostoky whose 15 patient was asymptomatic. In contrast, Jones et al reported a case with a persistent, foul smelling mucoid discharge and obstruction of his right nostril which gave him a sensation of a foreign body. A wide variety of other foreign bodies has been reported in the facial injuries including fillings, wood or bamboo splinters, pieces of cotton or gauze, bullets, knife blades and glass fragments16. Plain radiographs, computed tomograms (CT), magnetic resonance images (MRI) and ultrasound may guide the diagnosis and management. However in patients who have sustained significant trauma to the face, CT provides the reference standard for the diagnosis since it provides high spatial resolution images of the facial anatomy in both direct axial or coronal planes, thus eliminating the overlapping of osseous structures inherent in plain radiographic studies.We could able to manage the tooth position with the skull radiograph alone. Complete dislocation of a tooth can have lifethreatening ramifications, an airway complication, a respiratory tract obstruction, a complicated lung abscess, or sinusitis.

Fig. 7 - Post op

The other complications are nasal or cheek pain, speech problems, nasal obstruction, recurrent epistaxis, headache, 2 nasal discharge or nasal septal abscess . Aspergillosis, rhinitis withseptal perforation and naso-oral fistula has also been reported as complications. If a tooth is completely intruded into the nasal cavity, careful removal should be considered to avoid dislodging the tooth into the respiratory 9 tract .In our case the diagnosis was done at a right time and was prevented from complications. Conclusion patient presenting with a facial trauma may be distracted by other injuries, and a missing tooth may be presumed to have been avulsed during the accident therefore, they might be overlooked if their presence is not suspected. If an avulsed tooth is not present in the socket and is not recovered from the accident venue, it is prudent to rule out intrusion, aspiration, or ingestion of the missing tooth. maxillofacial trauma patients with gingival laceration suspicion of foreign bodies is essential to prevent the possibility of complications.

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References 1.Raichoor Anil Kumar.SivaKumar.Maxillary Permanent Tooth In The Nasal Cavity. Report Of Two Cases With Different Etiopathogenesis, Management And Review Of The Literature.The Internet Journal of Dental Science 2010;9(1). 2. Murthy P.S, Jaspal N etal.Foreign body in the ethmoid sinus. Int.J.oralmaxillofacsurg 1994; 23:74-75. 3.Andreasen JO, Andreasen FM (1990) Dental traumatology: quovadis. Endo Dent Traumatol 6:7880 4.Andreasen JO, Ravn JJ (1972) Epidemiology of traumatic dental injuries to primary and permanent teeth in a Danish population sample. Int J Oral Surg 1:235239 5.Ravn JJ, Rossen I (1969) Prevalence and distribution of traumatic injuries to the teeth of Copenhagen school children 196768. Tandlægebladet 73:19Ravn JJ, Rossen I (1969) Prevalence and distribution of traumatic injuries to the teeth of Copenhagen school children 196768. Tandlægebladet 73:19 6.Bruno Ramos Chrcanovic&SebastiãoCristianBueno et al.Traumatic displacement of maxillary permanent incisor into the nasal cavity.OralMaxillofacSurg 2009;10006-009-0191-3. 7.Thor AL (2002) Delayed removal of a fully intruded primary incisor through the nasal cavity: a case report. Dent Traumatol 18:227230 8.Andreasen FM, Andreasen JO (1985) Diagnosis of luxation injuries: the importance of standardised clinical, radiographic and photographic techniques in clinical investigations. EndodDentTraumatol 1:160169 9.Henrique Fernandes de Oliveira, Marcelo Braz Vieira etal.Tooth in Nasal Cavity of Non-traumatic Etiology: Uncommon Affection.Intl. Arch. Otorhinolaryngol 2009;13,(2):201-203. 10.Andreasen FM, Andreasen JO (1994) Luxations injuries. In: Andreasen JO, Andreasen FM (eds) Textbook and color atlas of traumatic injuries to the teeth, 3rd edn. Munksgaard, Copenhagen, pp 315378 11.Martin BS (2003) Traumatic intrusion of maxillary permanent incisors into the nasal cavity associated with a seizure disorder: report of a case. Dent Traumatol 19:286288 12.Altas E, Karasen MR, Yilmaz AB, et al. A case of a large dentigerous cyst containing a canine tooth in the maxillary antrum leading to epiphora. J LaryngolOtol 1997; 111(7) :641-3. 13.Kamaraj L, Paul G (2007) Unusual foreign body in frontal sinus. Int J Oral MaxillofacSurg 36:1098 14.Belostoky L, Schwartz Z, Soskolne WA (1986) Undiagnosed intrusion of a maxillary primary incisor tooth: 15-year follow-up. Pediat Dent 8:294295 15.Jones HB, Whitley SP, Morelli G, Tuffin JR (2006) Interesting case: spontaneous exfoliation of an upper central incisor through the nasal floor. Br J Oral MaxillofacSurg 44:500 16.Sedataydin, Arifsanli. Glass Particles in the Frontal Sinus. Turk J Med Sci 2009;39(2):313-315

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Abstract

Case Report

Maxillary anterior teeth are prone to traumatic injuries. In most cases, teeth can be saved by various treatment options involving restorative or endodontic therapy. But there are certain situations where extraction of the traumatized teeth may be required due to poor prognosis. This may cause esthetic, phonetic and psychological difficulties to the patient, necessitating an immediate replacement of the extracted tooth. The use of natural tooth pontic is a viable option in such cases. The present article reports utilization of the clinical crown of a fractured central incisor as a natural tooth pontic in a young patient. The abutment teeth were conserved with minimal or no preparation,by a simple chair side method avoiding laboratory costs.

A 22 year old healthy female patient reported to the Department of Conservative Dentistry and Endodontics, KLE Society's Institute of Dental Sciences, Bangalore, with a chief complaint of rotated and discoloured upper front tooth [Fig.1].

Keywords Cervical root fracture,Natural tooth pontic, In-office power bleaching. Fig.1- Pre operative view

Introduction Dentists occasionally are faced with the difficult esthetic situation of having to remove an anterior tooth because of trauma, advanced periodontal disease, root resorption or failed endodontic therapy1.Although a permanent replacement may be planned after the tissues have healed, the options available for a good esthetic temporary prosthesis are limited, which includes acrylic immediate removable partial dentures, prefabricated acrylic denture teeth used as a pontic or natural tooth pontic bonded to the adjacent teeth. Using the natural tooth as a pontic offers the benefits of being the right size, shape and color. The use of the extracted tooth, along with the help of modern dental adhesive systems provides an option to treat patients with less invasive tooth preparation, favourable esthetics and a natural feeling9. This article describes the immediate replacement of an extracted left central incisor with the natural tooth pontic, using a minimally invasive technique.

She gave a history of trauma due to a fall injury three years back. Patient noticed the colour change since the lastone year. Clinical examination revealed rotated and discoloured 21 with no mobility. Patient had anterioropen bite [Fig. 2].

Fig.2 -Patient's occlusion showing open bite

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Customization of the extracted tooth

Radiographic examination revealed horizontalcervical root fracture with resorption at the fracture line of the apical part of the toothwith a gap of 3-4 mm between the two parts [Fig.3].

By using a tapered fissurediamond point, the extracted coronal part was cut a few millimeters apical to the identification mark. As the pulp canal and chamber were completely calcified, the apical end was contoured to produce a modified ridge lap design [Fig.5].The amount of contouring was periodically evaluated by trying the pontic in patient's mouth. The pontic tip was smoothed and polished using polishing points to prevent plaque accumulation3.

Fig.3 -IOPAR showing root fracture with resorption

Both the pulp chamber and root canal showed calcification.Pulp sensibility tests showed a negative response. A decision was made to extract the tooth as both clinical and radiographic findings indicated poor prognosis for endodontic treatment. Since the patient demanded immediate esthetic rehabilitation, the option of Fig.5-Calcified pulp chamber & Modified ridge lap design of the pontic using the extracted clinical crown as a natural tooth pontic In-office power bleaching was considered. As the tooth was discoloured, whitening was carried 速 out using 40% hydrogen peroxide gel(Opalescence Boost, Extraction ULTRADENT PRODUCTS.INC) according to the manufacturer's instructions [Fig.6]. Care was taken while Before the tooth wasextracted, a small, round applying the whitening agent not to contaminate the proximal diamond point was used to place a shallow identifying surfaces, which were required for bonding. mark on the facial surface to indicate the level of the gingival crest. The coronal part was extracted atraumatically and was kept in saline to prevent dehydration. As the apical part of the root was ankylosed, the labial cortical plate was fractured during its removal. Two single interrupted sutures were placed to approximate the site [Fig.4]. Technique:

Fig.6-In-office power bleaching

Teeth preparation for bonding

Fig.4-Post extraction view

Isolation was done using cotton rolls. The proximal surfaces of the abutment teeth and the pontic were roughened with a coarse, diamond point and etched with 37%phosphoric acid (Scotchbond Etchant, 3M ESPE,St. Paul, MN, USA). The teeth surfaces were rinsed with water and airdried after etching.

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The bonding agent (AdperSingle Bond 2, 3M ESPE) was applied and light-cured according to the manufacturer's instructions. A small amount of composite resin TM (Filtek Z250, 3M ESPE) was applied on the proximal contact areas of pontic, and the pontic was inserted in the proper position in the mouth. After final verification of pontic position, composite was polymerized with light. Additional composite was applied on both the proximal areas, contoured, cured and polished. Adequate gingival embrasures were provided to facilitate oral hygiene [Fig.7]. The occlusion was evaluated for centric contacts and functional movements.

Fig.8- Post operative view (after suture removal)

Fig.9- Post operative intra oral view (at 4 weeks)

Fig.10-Patient's smile (at 6 weeks)

Fig.7-Teeth preparation & Bonding

Discussion: Follow up Suture removal was done seven days post operatively and the wound healing was satisfactory [Fig.8]. The patient was instructed to maintain proper oral hygiene. Recall appointments were made at threeweeks [Fig.9] and six weeks. The patient was satisfied with her appearance at six weeks [Fig.10].

Extraction of anterior teeth is a deeply traumatic experience for most patients warranting immediate replacement to temporarily restore the patient's esthetic and phonetic needs.The treatment options available for immediate replacement include removable tissue supported partial denture, temporary full coverage fixed partial denture, bonded partial denture using acrylic tooth or natural tooth pontic bonded to abutment teeth.Acrylic removable partial dentures placed immediately after the tooth is extracted are bulky, may be uncomfortable for the patient and may impede healing. Prefabricated acrylic denture teeth used as a pontic bonded to the adjacent teeth can present challenges in regard to matching color, size and shape, and often require substantial modifications to achieve an acceptable appearance1.

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Using the natural tooth pontic is superior to other options in being the right size and shape as that of the abutment teeth. Moreover, the positive psychological value to the patient in using his or her natural tooth is an added 1 benefit .Other advantages include improved aesthetics, unaltered phonetics and cost effectiveness. Being a chair side procedure, it can be completed in a single visit thereby avoiding laboratory procedures. Furthermore, this technique preserves the natural crown structure and allows the scope for other definitive treatment options, if needed at a later stage. Various pontic designs are available. The one chosen for this case was a modified ridge lap design.The modified ridge lap design with a well polished and smooth, convex surface results in pressure-free6 or mild contact with the alveolar ridge over a very small area for a better preservation of the soft tissue health7. This particular shape of pontic also helps to give the illusion of an emerging profile, like a natural tooth. The micro-resiliency of pontic allows stimulation of underlying tissue and avoids excessive post-extraction ridge resorption8.

Conclusion Natural tooth pontic can be placed as an interim restoration or a definitive prosthesis. In this case report, a simple,non-invasive chair side technique is used. The concept of natural tooth pontic promises an excellent transient esthetic solution for a lost tooth as well as enables good preparation of the extracted site for future prosthetic replacement. Patient's positive psychological response, cost effectiveness, and achievement of excellent soft tissue contours make this technique a viable option10. However, there are certain factors that should be kept in mind before formulating the treatment plan. The patient's occlusion should be evaluated for adequate clearance in centric and functional movements.Heavy occlusal load after splinting should be avoided. Also, the presence of any parafunctional habits that may interfere with the prognosis should be ruled out at the time of clinical examination. Both the abutment teeth and the pontic tooth should be in good condition to facilitate bonding.Proper case selection, precise technique and patient compatibility ensure a successful result.

Multiple case reports have been reported in the literature describing the use of natural tooth pontic in different clinical scenarios. Conventional methods of References splinting the natural tooth pontic to abutment teeth include 1.Kretzschmar JL. The natural tooth pontic: A temporary solution for a difficult use of wire or fibre with composite4,5.This often needs a esthetic situation. J Am Dent Assoc 2001; 132:1552-3 considerable amount of tooth preparation in the form of 2.Stumpel LJ 3 . The Natural Tooth Pontic; Simplified. J Calif Dent Assoc 2004; grooves or class III cavity preparation5 of the abutment teeth 32:257-60. 3.HaraldO.Heymann, Ch. 21: Bonded Splints and Bridges www.sturdevantsto accommodate these splinting materials and to aid in the operativedentistry.com/online retention. In this case, a novel method was used wherein the 4.SivakumarNuvvula, AbinashMohapatra, M Kiranmayi, and K Rekhalakshmi. tooth preparation can be considered as a non invasive or a Anterior fixed interim prosthesis with natural tooth crown as pontic subsequent to replantation failure. J Conserv Dent. 2011 Oct-Dec; 14(4): 432435. minimally invasive method. Only the proximal surfaces of 5.SachinGupta,VineetaNikhil,ShikhaGupta,MukulVerma. Conservative Bridge the pontic and abutment teeth were used for bonding. It is a with Natural Tooth Pontic: A Case Report. IJCDS.2011; 2(2):58-64. 6.Stein RS. Pontic-residual ridge relationship. A research report. J Prosthet Dent reversible process and preserves the healthy abutment teeth. 1996; 16: 25185. The presence of open bite favored this treatment plan. 7.Edelhoff D, Spiekermann H, Yildirim M. A review of esthetic pontic design rd

As the tooth was discoloured, in-office whitening of the pontic was done, following extraction and before placement into the oral cavity.Sachin Gupta et.al reported a case in which in office power bleaching of the natural tooth pontic was carried out at 12 months follow upintraorally5. Other options like veneering and intra coronal bleaching were also considered. But because of time constraints and pulp chamber calcification, both options were discarded.

options. Quintessence Int 2002. 8.Parolia, A., Shenoy, K. M., Thomas, M. S. and Mohan, M. Use of a natural tooth crown as a pontic following cervical root fracture:a case report. Aus End J. 2010; 36: 3538. 9.Bagis B, Satiroglu I, Korkmaz FM, Ates SM. Rehabilitation of an extracted anterior tooth space using fiber-reinforced composite and the natural tooth.Dent Traumatol. 2010 Apr; 26(2):191-4. 10.SudhirBhandari,RashiChaturvedi.Immediate natural tooth pontic: A viable yet temporary prosthetic solution: A patient reported outcome.Indian J Dent Res. 2012 Jan-Feb; 23(1):59-63.

Some authors have reported a long term follow up 9 5 upto 12 months and 24 months where it was used as a definitive prosthesis.Natural tooth pontic can also be used as an interim measure during the time period from immediate 2 implant placement till the definitive prosthesis is given .

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Abstract Necrotizing sialometaplasia is a benign, self limiting inflammatory disease of the mucous secreting glands and is mostly seen to affect the minor salivary glands. The presentation of this lesion often mimics a malignancy both in its clinical and histopathological appearance. We report a case in a 56 year old male, of necrotizing sialometaplasia on the hard palate simulating a malignant ulcer. An accurate diagnosis of this condition is of paramount importance in order to avoid unnecessary treatment.

About six days previously the patient experienced a peculiar feeling as if the mucosa overlying the swelling had “dropped off� and this was when he noticed that the swelling had ulcerated. Neither the swelling nor ulceration was associated with pain nor any associated symptoms. There was no history of any tingling or burning sensation in the region of the lesion and the patient gave no history of fever. There was also no history of direct trauma to the region or any recent dental or surgical procedures. The rest of the history was non contributory but the patient gave a personal history of having been a chronic smoker for the last 30years averaging about 10 15 cigarettes per day.

Keywords Necrotizing Sialometaplasia, Ulcer, Palate, Salivary gland Introduction: Necrotizing sialometaplasia was defined by Abrams et al. for the first time in 1973 as 'a reactive necrotizing inflammatory process involving the mucous salivary glands [1] of the hard palate' . 80% of this lesion is seen to affect the [2] minor salivary glands . The exact aetiology of necrotizing sialometaplasia is unknown but local vascular ischemia is popularly considered to be the main cause for this condition [3] . The clinical significance of this lesion lies in its ability to mimic malignancies both in appearance and histopathology and is currently classified by the WHO under 'tumour like lesions'. Case Report: A 56 years old male patient came to the department of Oral Medicine and Radiology with a chief complaint of an ulcer on the right side of the palate that had been present for 2 weeks. History revealed that it was initially noticed by the patient as a small peanut sized swelling which grew progressively over a span of one week to attain its present dimensions.

Fig.1 Frontal profile

Fig. 2 Intraoral view of the ulcerated lesion

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Fig. 3 Intraoral periapical radiograph of 16, 17

Fig. 5 Excised specimen

Fig. 4 Occlusal radiograph Fig.6 Histopathological section viewed under 40 x magnification.

On general examination the patient appeared to be of moderate build and nourishment. Thevital signs were all within normal limits. No gross facial asymmetry or abnormalities were noted on extraoral examination and the lymph nodes were non palpable. On intraoral examination a solitary ulcer was noticed on the posterolateral aspect of the hard palate located 2.5cm lateral to the midpalatine raphe and 1.5cm medial to the free gingival margin, in the region of the second molar. On inspection the ulcer was found to be approximately 1.5cm x 1cm, with irregular margins and surrounded by a zone of erythema. The floor of the ulcer appeared to be covered by a thick yellowish slough. The findings during inspection were confirmed on palpation and the ulcer was found to be non tender, the edges sloping and the base was firm in consistency. No bleeding was elicited during palpation. Hard tissue examination revealed that 17, 16 and 26 had been restored with silver amalgam and were found to be vital when subjected to pulp vitality test. Calculus and stains were present. After taking into consideration the history of smoking and the clinical presentation of the lesion we arrived at a provisional diagnosis of a malignant ulcer on the right side of the hard palate.A radiographic examination of the region revealed no periapical pathology or bony involvement.An incisional biopsy and local debridement of the lesion was done and the histopathological report showed squamous metaplasia of the ductal epithelium with a bland appearance of the nuclei and no evidence of any cellular atypia. Based on the histopathological features a final diagnosis of necrotizing sialometaplasia of the salivary glands of the hard palate was given. On reviewing the patient post operatively after one week, satisfactory healing was noted at the site of the biopsy.

Black arrow denotes the squamous metaplasia of the ductal epithelium

Figure 7 One week post-operative

Discussion: Necrotizing sialometaplasia (NSM) is a benign self limiting inflammatory lesion affecting the salivary glands. John Cornyn is credited as being the first to have recognized this lesion as a separate entity from [1] malignancies . NSM is a rare occurrence with a prevalence rate of only 0.03%[4]. It is seen to occur more frequently in males with a male to female ratio of 2:1 and it has also shown a white predilection. The age group affected ranges from 17 80 years with the mean age for males is 50 and for females 36 years[5], though a case has been reported in 2 year old girl following adenoidectomy[6]. The importance of this lesion is its potential to be misdiagnosed as a malignancy. According to Robert et al [5] 11.4% of these lesions received unnecessary therapy .

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The exact aetiology of NSM is still unknown but it is popularly believed to be the result of ischemia of the local vascular supply of the salivary glands and this assumption is supported by the presence of sites of infarction in the early [1][3][7] histopathological sections of the lesion . The possible aetiologies of this lesion include direct trauma, surgical and intubation procedures, smoking, alcohol use, chronic vomiting (bulimia), cocaine use, ill fitting dentures, upper [3][8] respiratory tract infections and radiation therapy . Also conditions like Raynaud's disease and Beurger's disease have [9] also been associated with the incidence of NSM . Of the aforementioned aetiologies the only possible cause found in our patient was the habit of smoking. The most commonly affected site is the salivary [3][6][10] glands of the hard palate . Other sites reported in literature include the maxillary sinus, retromolar pad region, lower lip, tongue and buccal mucosa. Three extraoral [11] variants, commonly termed as adenometaplasia , have also been reported in literature so far seen to affect the lung [12] [13] [14] tissue , breast and sweat glands . The clinical presentation of this ulcer can range from a rapidly growing submucosal swelling[15] to a shallow crateriform ulcer, as seen in our case. Lesions are usually asymptomatic, as seen in our patient. Though incidences of [13][10][16] pain, fever and occasionally parasthesia have been reported. Like in our case this lesion commonly occurs unilaterally but according to Brannon et al. 12% have a bilateral presentation5. Bony involvement is usually absent in cases of NSM and in the event that it is present it is seen only [5] as a mild saucerisation of bone . There was no bony involvement in the present case. The lesion usually resolves spontaneously within 3 12 weeks and recurrence has rarely been reported[17]. Abrams et al[1] outlined certain features that were characteristic of NSM and differentiated it from malignancies namely; 1. Lobular infarction or necrosis: 2. Bland-appearing nuclear morphology of the squamous cells: 3. Simultaneous metaplasia of ducts and mucous acini; 4.Prominent granulation tissue and inflammatory components, and 5.Maintenance of the general lobular morphology in spite of the fairly extensive inflammatory and metaplastic changes often involving more than one lobule. The features present in the histopathological examination of this case included the metaplasia of the ductal cells and the bland appearance of their nuclei. Based on the histopathological features Anneroth [18] and Hansen devised a classification that divided the progress of this lesion into 5 stages namely; the stage of infarction, sequestration, ulceration, repair and healing. During infarction, necrosis of the glandular acini predominates and culminates in the formation of the ulcer. At the beginning of the healing stage, proliferation of the overlying epithelium is observed, which is demonstrated microscopically by pseudoepitheliomatous hyperplasia. If infarction is limited, no sequestration occurs.

Healing becomes evident by the phagocytic activity of histiocytes and neutrophils and the presence of granulation tissue. In our case as the biopsy was obtained after ulceration and the only appreciable features were the squamous metaplasia of the ductal epithelium and the bland appearing morphology of the nuclei of these squamous cells. The differential diagnosis of this lesion includes mucoepidermoid carcinoma, subacute necrotizing sialadenitis, ulcers of deep fungal infection and tuberculous ulcer. The malignancies were ruled out on the lack of any evidence of cellular atypia, bland appearance of the nuclei of the metaplastic squamous cells and the healing at the site of biopsy post operatively. Though subacute necrotizing sialadenitis appears very similar to NSM it is usually seen as a submucosal swelling and was dismissed as a possible diagnosis due to the presence of an ulcer clinically and squamous metaplasia histopathologically. Ulcers of deep fungal infection show the presence of fungal hyphae and fungal granulomas and are often associated with immunocompromised patients or patients with severe debilitating diseases. Tuberculous ulcer was ruled out as the patient gave no history of tuberculosis, chronic cough or night sweats and the characteristic features of a tuberculous ulcer such as the undermined edges and bluish margins with tissue tags were absent. Also caseation necrosis and tuberculous granulomas were absent in the histopathological examination. Recent studies by Rizkalla and Toner have shown the use of immunohistochemical markers such as smooth muscle antibody, calponin, cytokeratins (CK 5, CK6, CK7, CAM 5.2), laminin ans p63 in order to differentiate between necrotizing sialomataplasia and malignancies such as mucoepidermoid carcinoma and squamous cell carcinoma[10]. As NSM is a self limiting condition there is no specific treatment criteria. The usual procedure involves an incisional biopsy to confirm the diagnosis of NSM, observation and reassurance of the patient and symptomatic treatment[19]. Conclusion Necrotizing sialometaplasia is a benign selflimiting disorder of the salivary glands that unfortunately mimics a malignancy both clinically and histopathologically. It is important to be aware of such an entity in order to prevent a misdiagnosis that can lead to unnecessary radiotherapy and surgical treatment that may alter the quality of life.

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References 1.Abrams AM, Melrose RJ, Howell FV. Necrotizing sialometaplasia: a disease simulating malignancy. Cancer. 1973 Jul;32(1):130-5.

17.Carlson DL. Necrotizing Sialometaplasia : A practical Approach to the diagnosis. Arch Pathol Lab Med 2009;133: 692 698.

2.Schmidt-Westhausen A, Philipsen HP, Reichart PA. Necrotizing

18.Anneroth G, Hansen LS. Necrotizing sialometaplasia: the relationship of

sialometaplasia of the palate. Literature report of 3 new cases. Dtsch Z

its pathogenesis to its clinical characteristics. Int J Oral Surg. 1982

Mund Kiefer Gesichtschir 1991;72:30-4

Oct;11(5):283-91.

3.Imbery TA, Edwards PA. Necrotizing sialometaplasia: literature

19.Lee T, Lee M, Chang H, Lee JY. Necrotizing sialometaplasia affecting

review and case reports. J Am Dent Assoc. 1996 Jul;127(7):1087-92.

the upper lip: A sheep in wolf's clothing. Dermatol Sinica 2004 March; 22:

4.Mesa ML, Gertler RS, Schneider LC. Necrotizing sialometaplasia:

88 - 92

frequency of histologic misdiagnosis. Oral Surg Oral Med Oral Pathol 1984;57:71-3. 5.Brannon RB, Fowler CB, Hartman KS. Necrotizing sialometaplasia: a clinicopathologic study of sixty-nine cases and review of the literature.Oral Surg Oral Med Oral Pathol. 1991 Sep;72(3):317-25. 6.Ylikontiola L, Siponen M, Salo T, SĂĄndor GK: Sialometaplasia of the soft palate in a 2-year-old girl. J Can Dent Assoc 2007, 73:333-336. 7.Randhawa T. Ipe Varghese, Shameena PM, Sudha S, Resmi G Nair. Necrotizing sialometaplasia of tongue. Journal of Oral and Maxillo Facial Pathology 2009, 13:1; 35 37. 8.Suckiel JM, Davis WH, Patakas BM, Kaminishi RM. Early and late manifestations of necrotizing sialometaplasia. J Oral Surg 1978;36:9025 9.Rye LA, Calhoun NR, Sedman RS. Necrotizing sialometaplasia in a patient with Buerger's Disease and Raynaud's phenomenon. Oral Surg 1980;49:233-6 10.Rizkalla H, Toner M. Necrotizing sialometaplasia versus invasive carcinoma of the head and neck: the use of myoepithelial markers and keratin subtypes as an adjunct to diagnosis. Histopathology. 2007 Aug; 51(2):184-9. 11.Romagosa V, Bella MR, Truchero C, Moya J. Necrotizing sialometaplasia (adenometaplasia) of the trachea. Histopathology 1992; 21 : 280-2. 12.Zschoch H. Mucus gland infarct with squamous epithelial metaplasia in the lung. A rare site of so-called necrotizing sialometaplasia. Pathologe 1992; 13 : 45-8. 13.Hurt MA, DĂ­az-Arias AA, Rosenholtz MJ, Havey AD, Stephenson HE Jr. Posttraumatic lobular squamous metaplasia of breast. An unusual pseudocarcinomatous metaplasia resembling squamous (necrotizing) sialometaplasia of the salivary gland. Mod Pathol 1988; 1:385-90. 14.King DT, Barr RJ. Syringometaplasia: mucinous and squamous variants. J Cutan Pathol 1979; 6:284-91. 15.Oliveira Alves et al.: Necrotizing sialometaplasia as a cause of a nonulcerated nodule in the hard palate: a case report. Journal of Medical Case Reports 2011 5:406. 16.Keogh PV, O'Regan E, Toner M, Flint S. Necrotizing sialometaplasia: an unusual bilateral presentation associated with antecedent anaesthesia and lack of response to intralesional steroids. Case report and review of the literature. Br Dent J. 2004 Jan 24;196(2):79-81.

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Abstract This article describes an unusual presentation of pleomorphic adenoma arising from accessory parotid tissue. Accessory parotid glands are an anatomic variation and are found in approximately only 21% of the population. Pathologies are very rare, with only 1% to 7.7% of all parotid gland tumors originating in them18 . Considering the minimal area of involvement, a facelift or direct cheek approach would run the risk of facial nerve injury and facial scar .In this report, we give an account of complete removal of the accessory parotid gland by a minimally invasive -oral approach.

Keywords Accessory parotid gland, pleomorphic adenoma, peroral approach

Background Accessory parotid glands, once believed to be simple extensions of the main parotid gland, are small, flat structures that function completely independently of the main parotid gland. It has secondary duct emptying into the Stensen's duct. The accessory parotid gland is located approximately 6 mm anterior to the main parotid gland, between the skin and the masseter muscle along an imaginary line that extends from the tragus to a point midway between the ala of the nose and the vermilion border of the lip. The diagnosis of an accessory parotid gland mass is usually reached after careful physical examination. The parotid gland drains its secretions through the Stenon duct into the oral cavity. According to cadaveric studies, accessory parotid glands are found in approximately 21% of the population. Pathologies are very rare, with only 1% to 7% of parotid tumors occur in the accessory parotid gland tissue1-8.

Because of local problems caused by the tumor, expansion, and the possibility of malignancy, tumors of the accessory glands need adequate diagnosis and treatment. Although resection is the first choice, preservation of the facial nerve and its function is one of the most important aims during surgery in this anatomic region. The literature favors the surgical approach, including a lateral parotidectomy or a standard face lift incision and tumor resection. We describe a per-oral resection for the treatment of these tumours. Anatomically, the main parotid gland and the accessory parotid gland drain into Stensen's duct through at least one minor tributary (at times two or three minor tributaries). In the main parotid gland, the trunk of the nerve courses deep to the superficial body of the gland. In the accessory parotid gland, the zygomatic and buccal rami run superficial to the gland. According to the literature, benign tumors of the accessory parotid gland account for approximately 50 to 74% of all accessory parotid neoplasms; the rate of malignancy ranges from 26 to 50%. In the main parotid gland, the rate of malignancy is far lower, approximately 18.5%. Compared with tumors developing in the parotid gland, tumors of the accessory glands show a more than 50% higher frequency of malignancy1-8. On histologic examination, the accessory parotid gland is made up of both serous and mucinous cells such as those seen in the submandibular gland. In contrast, the main parotid gland is predominantly serous. Despite this difference in histology, the most common benign tumor in both the accessory and main parotid gland remains the pleomorphic adenoma, a slow-growing, well-encapsulated neoplasm. The differential diagnosis of masses in the mid-anterior cheek area includes lesions arising from normal anatomic structures, as well as from variations of normal accessory parotid gland tissue, viz- lymphadenopathy, lipoma, neurofibroma, schwannoma, hemangioma, sebaceous cyst, fibroma, epidermal inclusion cyst and primary parotid duct tumors. .

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Case Presentation A middle aged woman complained of a painless mass in her right cheek, which slowly enlarged over the last 4 years. The mass was firm in consistency and was movable. The swelling had enlarged gradually but did not impair masticatory activity. The rest of the examination revealed no pathologic alterations in the head and neck area. There was no sign of infiltration into the surrounding tissue. Intraoral examination showed normal salivary flow from the parotid gland. Clenching the teeth made the mass more prominent. There was neither associated lymphadenopathy nor facial nerve dysfunction. Investigation Conventional plain radiographs were noncontributory to the diagnosis. Ultrasound examination showed an oval, nonhomogeneous hypoechoic mass that was solid with well-defined borders, located anterior of the masseter muscle suggesting sebaceous cyst (Fig.1) and sialography was normal (Fig.2). CT Scan shows right parotid mass (Fig.3)

Fig.1 Ultrasound

Differential Diagnosis Pleomorphic adenoma,Sebaceous Cyst, Neouroma of the facial nerve , Lipoma. Treatment Considering the possibility of avoiding a scar, the patient was not in favor of an external approach because of cosmetic concerns. She instead opted for a transoral approach. A lacrimal probe was inserted into the parotid duct during the procedure to enable easy location of the Stenson duct. A lazy “S” incision of the mucosa was made above and parallel to the duct over the tumour. Then blunt dissection was carried out around the tumor to isolate it.

Fig.2 Sialography

A branch of the facial nerve in close contact with the tumor mass was identified and preserved. The tumor was resected completely without macroscopic rupture of the capsule or damage of the duct. The intraoral wound was sutured with Vicryl 4-0 Ethicon (Johnson & Johnson Medical Products GmbH, Austria) without drainage. Final pathology revealed a completely excised 2.8 × 1.6 × 1.5-cm pleomorphic adenoma of the accessory parotid gland with an intact capsule (Fig.4).

Fig. 3 CT Scan

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Fig.4 Histopathology report

Outcome & Follow-Up Normal function of the facial nerve was tested postoperatively. There was weakness of the buccal branch of the facial nerve affecting full function of the upper lip. This was deemed to be due to tractional nerve injury. This was managed with 4 weeks of physiotherapy (balloon blowing, grimacing and rolling of lemon from one cheek to another) , which was started 2 weeks after surgery. Full function of the weak buccal nerve branch returned in about 6 weeks. Intra-oral examination 2 months postoperatively showed a well-healed oral mucosa (Fig.5), good facial nerve function and excellent cosmesis.

Fig.5 Post-op Healing

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Discussion 1-7 An accessory parotid gland is a rare entity (21%) . Clinical diagnosis of mid-cheek lesions is very difficult because of the presence of large number of accessory parotid gland in the population and there is a variety of lesions has to be considered in the differential diagnosis of an anterior cheek mass, including lymphadenopathy, lipoma neurofibroma, schwannoma, hemangioma, fibroma, epidermal inclusion cyst, primary parotid duct tumors, and accessory parotid gland lesions.1-6, 9, 10 Steiner et al concluded that clinical evaluation and digital palpation of a mass in the cheek are often indeterminate in defining the depth of tumors here. Diagnostic aids for evaluating accessory salivary gland lesions include plain radiographs, sialography, scintigraphy, ultrasound, CT, CT with sialography, MRI, MRI with sialography, and FNAC. Kronenberg et al12&Neneceket al1 recommended the use of CT and MRI for establishing anatomic relationships respectively. With combined axial and coronal views, the nature of the lesion 13 and its location can be easily determined. Smith et al concluded that parotid CT combined withsialography is an established method of determining intrinsic parotid gland tumor from extrinsic tumors. Some previous reports claim that sialography is of low diagnostic value with false negative results and a routine sialogram may not rule out the presence of an accessory parotid gland. During sialography, cannula should not be advanced past the junction between the accessory parotid duct and Stensen's duct because a lack of filling of the accessory gland will result.

The following criteria should be considered: 1) a single lesion without connection to the main parotid gland, 2) Clinical & Diagnostic tools favoring the diagnosis of a pleomorphic adenoma, and 3) size that should not exceed 3 cm in diameter. This approach is less invasive and provides a better cosmetic result. Risk of facial nerve injury can isminimal & can be further reduced with intraoperative nerve monitoring. In considering the rareness of this disease, it is difficult to compare the risk of the per-oral approach with that of lateral parotidectomy, but this approach should be kept in mind as a valuable alternative. References: 1. Nemecek JR, Marzek PA, Young VL. Diagnosis and treatment ofaccessory parotid gland masses. Ann PlastSurg 1994;33:75-9. 2. Kakulas EG, Smith AC, Sormann G. Pleomorphic adenoma of theaccessory parotid gland. J Oral MaxillofacSurg 1994;52:867-0. 3. Rodino W, Shaha AR. Surgical management of accessoryparotid tumors. J SurgOncol 1993;54:153-6. 4. Batsakis JG. Pathology consultation: accessory parotid gland.Ann OtolRhinolLaryngol 1988;977:434-5. 5. Polayes IM, Rankow RM. Cysts, masses and tumors of theaccessory parotid gland. PlastReconstSurg 1979;64:17-23. 6. Johnson FE, Spiro RH. Tumors arising in accessory parotidtissue. Am J Surg 1979;138:576-8. 7. Frommer J. The human accessory parotid gland: its incidence,nature, and significance. Oral Surg Oral Med Oral Pathol1977;43:671-6. 8. Horii A, Honjo Y, Nose M, et al. Accessory parotid gland tumor:a case report. AurisNasus Larynx 1997;24:105Y110 9. Kazumari S, Masahiro U, Hiromitsu K, Yumiko T, Suwako H,Takamichi Y.

Surgical approach is the only treatment objective . Because of the delicate anatomic region, framed by two branches of the facial nerve, in which these masses occur, surgical excision is difficult. The common surgical approach to soft tissue lesions in this area is the mid-cheek incision; however, this approach is not recommended because of anatomic considerations, such as the location of the buccal branch of the facial nerve, the proximity to the accessory duct, the vulnerability of Stensen's duct and the junction between the accessory and the main parotid ducts. The literature favors an approach through a standard lateral parotidectomy or a face lift incision. This procedure is favored because it provides excellent exposure of the 14, working field and minimizes the risk of facial nerve injury 15 . A few cases were treated through a direct cheek incision, with the result of an unpleasant scar and an approximately 40% risk of postoperative facial nerve deficit16. The intraoral approach to the accessory parotid gland is not favored because it provides inadequate exposure for the 17 control of bleeding and preservation of the facial nerve . In our experience, this procedure is a good alternative for wellselected tumors of the accessory parotid gland.

Primary squamous cell carcinoma of accessoryparotid gland duct epithelium. Oral Surg Oral Med Oral PatholOral RadiolEndod 1998;85:447-51. 10. Takenori I, Ryoichi Y, Takuya E Large retention cyst of theaccessory parotid gland associated with a mucoepidermoidtumor in the cyst wall. J Oral MaxillofacSurg 1991;49:884-6. 11. Steiner M, Gould AR, Miller RL, Johnson JA. Malignant tumorsof Stensen's duct. Oral Surg Oral Med Oral Pathol oral RadiolEndod 1999;87:73-7. 12. Kronemberg J, Horowitz A, Creter D. Pleomorphic adenomaarising in accessory salivary tissue with constriction of Stensen'sduct. J LaryngolOtol 1988;102:382-3. 13. Smith JRG, King WWK, Tang WY, Metreweli C. Differentiatingtumors of the deep and superficial lobes of the parotid gland bycomputed tomographic sialography. ClinRadiol 1987;38:345-9. 14. Johnson FE, Spiro RH. Tumors arising in accessory parotidtissue. Am J Surg 1979;138:576-578 15. Klotz DA, Coniglio JU. Prudent management of the mid-cheekmass: revisiting the accessory parotid gland tumor. Laryngoscope2000; 110:1627-1632 16. Lin DT, Coppit GL, Burkey BB, et al. Tumors of the accessorylobe of the parotid gland: a 10-year experience. Laryngoscope2004; 114:1652-1655 17. Polayes IM, Rankow RM. Cysts, masses, and tumors of theaccessory parotid gland.PlastReconstrSurg 1979;64:17-23

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Abstract True intrusion is one of the difficult and complex goal to achieve which requires clinical judgment, skills and experience. Intrusion requires less force level than other tooth movement but it requires delicacy since the entire stress is concentrated in the apex of the root. Although true intrusion alone is not challenging, eliminating the adverse effect while intruding requires tedious skills of the clinician.A17 yr old male patient with class I malocclusion with open bite has a prominent maxillary cortical bone.He had convex profile with unpleasant smile.Treatment objective was to reduce the bulkiness of cortical bone and to intrude the upper anteriors,so the decision was made to perform corticotomy

Keywords Intrusion, Corticotomy,

Introduction Alveolar corticotomy is a surgical procedure limited tothe cortical portion of the alveolar bone.Whereas in osteotomies both cortical and trabecular bone material is removed in considerable quantities,in alveolar corticotomy the incision must pierce the cortical layer, and at the same 8 time,penetrate into the bone marrow only minimally. This method claims to have several advantages.these include a reduced treatment time,enchanced expansion ,intrusion and open bite correction,manipulation of anchorage,increased traction of impacted teeth,accelerate canine retraction and also gives 1,3,13 post-treatment stability. Corticotomy facilitated tooth movement was first described by L.C. Bryan in 1893 and was introduced by Kole in 1959.Kole's used a combined inter-radicular corticotomy and supra apical osteotomy 4 technique. Because of the invasive nature of Kole's technique it was never widely accepted.1

In 1975 Duker used Kole's technique which preserves the health of the periodontium by avoiding the marginal crest bone during corticotomy cuts.8In 1978 Generson revised Kole's technique with a 1-stage corticotomy only technique without supra apical osteotomy.In 2000 Hajjii reported that corticotomy makes tooth movement faster because the bone blocks moves with the tooth,because the force applied to the tooth is transmitted into the osteotomy gap through the periodontal ligament.The most recent surgical orthodontic therapy was introduced by Wilcko 2001 which included combining corticotomy surgery with alveolar grafting technique referred as accelerated osteogenic orthodontics (AOO) and more recently as periodontally accelerated osteogenic orthodontics (PAOO) which is also termed as wilckodontics. 1,3

What are the possible limitations and contraindication of PAOO? (1)Patients with active periodontal disease1 (2)Individuals with inadequately treated endodontic problems (3)Patients intake of corticosteroids, (4)Persons who are taking any medications, such as bisphosphonates and NSAID'S 8 (5)Cases where bi-maxillary protrusion is accompanied with a gummy smile,which might benefit more from segmental osteotomy.14 Mechanism Underlying Corticotomy Healing event after corticotomy is regional accelerated phenomenon(RAP),which is responsible for the rapid tooth movement.RAP was first described by Frost in 1893.He noted that the original injury somehow accelerated the normal regional healing processes.This phenomenon is regional acceleratory phenomenon,ie increasing the activity of osteoclasts and osteoblasts which leads to bone remodeling and rapid tooth movement.RAP usually occurs after a fracture,arthrodesis,osteotomy, after placing implants procedure, and may involve recruitment and activation of precursor cells necessary for wound healing concentrated at the site of injury.6,7

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The increase of orthodontic tooth movement is influenced by bone turnover,bone density and hyalinization of the PDL.The RAP begins within a few days of injury,it peaks at 1-2months, lasts 4 months in bone and may take 6 to more than 24 months to subside.3,5 Case Report A 17yr old male patient had a chief complaint of proclination and spacing of upper and lower incisors.He had angle class2 malocclusion with anterior open bite and which he had an unpleasant smile,(fig-1) because of the presence of thick cortical bone in the anterior region, and to intrude the upper anteriors ,the decision was made to perform PAOO.

Surgical Procedures A modified corticotomy procedures was carried out by local anesthesia.A mucoperiosteal flap was elevated labially beyond the apices of the upper incisors.10The vertical cuts were performed from the distal of the right upper lateral incisor to the distal of the left upper lateral incisor and the cortical bone was removed by tungsten carbide bur with continuous saline irrigation.(fig-2)These incision preserves the interdental papilla on the buccal sides of the maxillary anteriors and noflap elevation or corticotomy was performed on the lingual or the palatal side in this case care was taken not to damage neurovascular bundles.9,10 Platelet rich fibrin(PRF) was placed on apical region of anteriors.(fig-3) The horizontal envelope mucoperiosteal flap was extended to the apical region of the anteriors. The mucoperiosteal flaps were replaced and sutured with 4-0 silk sutures. (Fig-4,5)The patient was given amoxicillin, 500 mg t.i.d. for 3days. The sutures were removed after a week and advised to use chlorhexidine mouthrinse 0.12% b.i.d for 2 weeks.

Fig-2 Cortical bone removed using tungsten carbide bur

Fig-3 Fig-1

PRF placed on the anteriorregion

Pre-operative photos

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Fig-4 Sutures Given

Fig-5 Coe Pack Given Fig-6 Continous burstone intrusive arch given

Orthodontic Procedures Full maxillary and mandibular braces (17x25ss) with conventional brackets were placed before periodontal s u r g e r y. S o o n a f t e r a w e e k o f p e r i o d o n t a l surgery,continuous burstone intrusive arch was given which was made in (17x 25TMA) wire.(fig-6)After 15 days of recall deep-bite got reduced from 6mm to 3mm.After 2 months of periodontal surgery continuous intrusive arch was removed.Eight months after surgery detailing of the occlusion was completed the following orthodontic results were achieved: 1)Ideal occlusion was obtained 2)Open bite correction were made 3)Anterior deep-bite was corrected from 6mm to 2mm 4)Straight profile 5)Pleasant smile

Discussion Optimal force for effective intrusion without root resorption 20 to 25g per tooth .If the PAOO procedure is performed,heavy intermediate force is the best protocol,because it will initiate RAP.Rapid tooth movement is explained by the bone remodeling which is coined as RAP. According to Hajii an average treatment time for the PAOO procedure was one-third to one-fourth of 11 traditional orthodontictreatment. Wilcko et al reported an average of 6.1months of treatment time for the PAOO 17 procedure. However,unlike the procedures described by Kรถle and Wilcko et al,corticotomy was performed only at the buccal aspects of maxilla in this case.3,4 This was in agreement with Germec et al, who reported rapid tooth movement when corticotomy was performed at the buccal 12 aspects of alveolar bone. The researchers noted that the elimination of palatal and lingual corticotomy reduced the length and the extent of the surgery and avoided the risk of violating vital lingual anatomy.

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References 1)GOYAL AMIT, KALRA JPS,BHATIYA PANKAJ,SINGLA SUCHINDER,BANSAL PARUL:periodontally accelerated osteogenic orthodontics (PAOO)- a review.j.clinexp 2012;4(5):e292-6 2)DAURO DOUGLAS OLIVEIRA,BRUNO FRANCO DE OLIVEIRA,HELIO HENRIQUE DE ARAUJO BRITO,MARGARETH MARIA GOMES DE SOUZA AND PAUTO JOSE MEDEIROS:selective alveolar corticotomy to intrude overeuptedmolars.AJODO 2008;133:902-8. 3)WILCKO WM, WILCKO MT,BOUQUOTJE:rapid orthodontics with alveolar reshaping:two case reports of decrowding.int j periodontics restorative dent.2001;21:9-19. 4)KOLE H. surgical operation on the alveolar ridge to correct occlusalabnormalities.oralsurg oral med oral pathol.1959;12:515-29 concl. 5)SCHILLING T,MULLER M,MINNE HW,ZIEGLER R.influence of inflammation mediated osteopenia on the regional acceleratory phenomenon and the systemic acceleratory phenomenon duringhealing of a bone defect in the rat.calcif tissue int.1998;63:160-6. 6)FROST HM the biology of fracture healing.an overview for clinicians part1.clin orthoprelat res.1989;248:283-93. 7)FROST HM.the regional acceleratory phenomenon:areview.henry ford hosp med j.1983;31:3-9. 8)DAURO DOUGLAS OLIVEIRA, BRUNO FRANCO DE OLIVEIRA, RODRIGO VILLAMARIM SOARES.Alveolar corticotomies in orthodontics: Indications and effects on tooth movement.dental press j orthod.2010 julyaugust;15(4):144-57. 9 ) D E R YA G E R M E C 存 B A H A D I R G I R AY; I L K E N KOCADERELI,AYHAN ENACAR Lower Incisor Retraction with a Modified Corticotomy .AO vlo.76,no5,2006. Post-operative photos

Conclusion Successful intrusion is a significant clinical challenge to orthodontists.2Alveolar corticotomy is an effective treatment to decrease the treatment time ,reduces the incidence of root resorption and it increases the quality of the 10 treatment. Conservative corticotomy technique, which eliminates the lingual approach which reduces the operation time and patient discomfort9. However this procedure should be carefully applied with respect to the teeth, bone, and surrounding tissues to avoid the risk of damage of neurovascular bundle, devitalization of the teeth and periodontal damage.9 The biological mechanisms generated by corticotomies is reflected in the structure of trabecular bone, which provides an opportunity to enhance certain orthodontic movements.8 Interest in the use of alveolar corticotomies as an adjunct to orthodontic treatment is growing thanks to a deeper understanding of its effects which brings about shortened 8 treatment time.

10)HESSAM NOWZARI, FRANK KAZUO YORITA AND HSUANCHEN CHANG Periodontally Accelerated Osteogenic Orthodontics Combined with Autogenous Bone Grafting CompendiumMay 2008Volume 29, Number4. 11) HAJJI SS. the influence of accelerated osteogenic responses on mandibular de-crowding [thesis]. St. Louis, MO; St Louis University:2000. 12) GERMEC D, GIRAY B, KOCADERELI I, ET AL. Lower incisor retraction with a modified corticotomy. Angle Orthod.2006;76(5):882890. 13)T. J. FISCHER.Orthodontic Treatment Acceleration with Corticotomy-assisted Exposure of Palatally Impacted Canines A Preliminary Study.AO VOL77,NO3,2007. 14)LEE JK,CHUNG KR,BAEK SH.treatment outcomes of orthodontic treatment,corticotomy assisted orthodontic treatment,and anterior s e g m e n t a l o s t e o t o m y f o r bimaxillarydentoalveolarprotrusion.plastreconstr surg.2007;120:102736.

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Abstract Surgical removal of tumours in mandible leaves us with a difficult scenario because of loss of lip support, inadequate sulcus depth, flabby tissue, loss of stability and insufficient bone support to withstand the occlusal force. However, a definite concentration in each of the steps used in the fabrication of removal prosthesis comes as a welcome hope for the patient in the midst of his catastrophe. This paper discusses a case report wherein the patient had a fibula graft after complete mandibulectomy who has rehabilitated with the removal prosthesis after 6 months based on the merits of neutral zone and polished surface to achieve stability and support to the maximum.

Case report The management of a grafted resorbed mandibular ridge with aneutral zone technique using an impression compoundmixed with a green stick in the ratio of 3:7 has beendescribed. A 57 year old male reported to Department of Prosthodontics, Tamilnadu Government Dental College,Chennai withcompletely edentulous and severely resorbed mandibularridge. On extra oral examination patient had obvious facial asymmetry(Fig.1) and a surgical scar below the chin which was skin grafted.

Keywords Mandibulectomy, Fibula graft,Neutral zone, Polished surface, Stability.

Introduction The human mandible contributes to facial contour, proper occlusion,mastication, airway support, deglutition and speech. Dentures fabricated over a grafted severely resorbed mandibular ridge by neutral zone impression technique will insure that the muscular forces aid in the retention and stabilization of the denture rather than dislodging the denture during function. These dentures will also have other advantages such as reduced food lodgement, good aesthetics due to facial support, proper positioning of the posterior teeth which allows sufficient tongue space. Clinicians must identify and record the neuromuscular dynamics of the oral tissues and this should be applied in the construction of the definitive prosthesis that will exist within the stabilizing boundaries of the neutral zone area.

Fig. 1: Extra oral view of the patient showing facial asymmetry

On intraoral examination there was a complete compliment of teeth in the maxillary arch,mandibular arch was irregular in shape and contour,severely resorbed (Atwood's class IV) shallow sulcus depth with thin flabby mucosa.From the above mentioned history, OPG X-ray and clinical examination we got to know that patient had a tumour on the right side of the mandible 3 years back, and right side of mandible was resected subsequently and reconstructed with fibula graft from left leg.After 2 years patient had a recurrence of reparative giant cell granuloma extending to left side(Fig.2). Six months before mandible was resected from angle to angle and reconstructed with osseocutaneous fibula graftfrom right leg(figure 3).

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Difficulties encountered in this case are,Compromised bone support, Unusual soft tissue configuration, Lack of attached mucosa and Obliteration of vestibule.

Fig. 2: OPG showing recurrence of Reparative Giant Cell Granuloma Fig. 4:Border moulding done and final impression made with addition silicone

Fig. 3: OPG showing mandible rehabilitated with Fibula graft

Treatment options considered were, ·Implant retained fixed prosthesis ·Implant retained over denture ·Removable denture with neutral zone and polished surfaces ·Removable denture with soft liner ·Removable denture with multiple suction cups We preferred to select the prosthesis of Removable denture with neutral zone and polished surfaces because of patient Unwilling for a second surgery.Implants are contraindicated because of uncontrolled diabetes and Economy. Treatment procedure: 1.Maxillary and mandibular alginate impression was made and cast was obtained with Type III dental stone. 2.Wax spacer adapted and custom tray was fabricated for mandibular arch 3. Border moulding done and final impression was made with addition silicone(aquasil) light body impression material(Fig.4) and master cast was poured with type III dental stone(Fig.5)

Fig. 4:Master cast poured with type III dental stone

4. Two record bases were fabricated, one for jaw relation one for neutral zone recording 5.Jaw relation done with wax occlusal rim and articulated 6. Neutral zone recording done with admix of impression compound and low fusing compound (3:7) with various movements like swallowing, sucking of the cheek and pursing movements of the lips,and levelled with lower occlusal rim in the articulator 7.Plaster indices were made as two labiobuccal matrices and one lingual matrix(figure 6) 8.Molten wax was poured in the hollow space created by the neutral zone record between the indices 9.Teeth arrangement done according to the neutral zone record(Fig.7) and wax trial done

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10.Labial and lingual wax was removed from the trial denture and polished surfaces was recorded with light body impression material(aquasil) in both buccal and lingual surfaces of the trial denture(Fig.8) 11. Processing of denture was done(Fig.9) and final denture inserted in the patient's mouth(Fig.10) and occlusal corrections were made with the articulating paper 12.Patient reviewed after one day, one week and one month and patient was comfortable (Fig. 11) and able to take soft and medium consistency food

Fig. 8: Polished surface recorded with light body

Fig. 9: Finished and polished denture Fig. 6: Neutral zone plaster indiced

Fig.7: Arragement of teeth confine to the neutral zone

Discussion Neutral zone Advocated initially by BERESIN & SCHIESSER1. According to GPT neutral zone “the potential space between the lips and cheeks on one side and the tongue on the other, that area or position where the forces between the tongue and cheeks or lips are equal'' dynamics of oral tissues.It is the zone where the natural dentition lie and this is the place where the artificial teeth should be positioned for Optimum retention ,stability and comfort Muscle forces are working more efficiently in harmony and gives advantage of stabilising potential of oral and perioral musculature. Health (1970) has demonstrated that there is a difference in the shape of the denture space and resultant arch from at rest or repose as compared to the denture space and arch form established by function.The Theory of the neutralization of forces that stabilize dentures and the rationale involved was one of the major contributions made by Dr.RUSSEL TENCH and his co-worker CAVALCANTI.

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For the muscular forces to be of a stabilizing nature, the dentures must be so constructed that they receive these forces at the proper angle. Dr FISH described the cross section of stable dentures in the molar region to be triangular in shape, with the tooth being the apex and the denture periphery the base of a triangle. A force exerted on the inclined plane may be broken down into two components. One component acts in a direction parallel to included plane. The other component called normal force, acts perpendicularly to the inclined plane. If the inclined planes of external surface are properly fashioned and forces are of equal magnitude the resultant normal force will be in a seating direction. By the same token, if the dentures are triangular but not properly located within the neutral zone, the lateral force will be unequal and not provide the equilibrium necessary for a stable denture. This will result either in the dislodgement of the denture or unequal pressure on the ridge. Many studies have demonstrated that neutral zone dentures are functionally more stable than conventional dentures. Neutral zone recording considers the actions of the tongue, lips, cheeks, and floor of the mouth during a specific oral function, to push the soft material into a position where buccolingual forces are neutralized. The technique employed for the present patient provides a more stable record base duringrecording of jaw relations, since the mandibular rim is functionally molded. Advantages of neutral zone in this case Enhanced stability,Control of saliva,Reestablished facial profile,improved mastication,Speech and Aesthetics.

Fig.11: Re-established facial symmetry after prosthesis

Conclusion The ultimate goal of any Prosthodontictreatment is to restore the form, function and aesthetics of the patient. Fish pointed that, out of the three surfaces of the denture like impression or denture bearing surface,occlusal surface and polished surface, the implication of the latter two surfaces assumes more importance as the degree of resorption increases .So we concentrate more on neutral zone and polished surface in this compromised clinical condition. These are involved in normal physiologic movements such as speech, mastication, swallowing, smiling, and laughing. Hence, the fabrication of the denture must be in harmony with these functions. Because physiologically unacceptable denture is responsible for poor prosthesis stability and retention insufficient facial tissue support, less tongue space and compromised phonetics. A successful attempt was made to provide the patient with a prosthesis simulating nature though replicating nature is impossible as nature proves to be supreme. References 1.Beresin VE, Schiesser FJ. The neutral zone in complete dentures. J Prosthet Dent 1976;36:356-67. 2. Fish EW: Using the muscles to stabilise the full lower denture,j Am DentAiSOC1933;2O:2I63-2169 3.Brill N, Tryde G, Cantor R. The dynamic nature of the lower denture space.J Prosthet Dent.1965;15:401418 4. Cagna DR, Massad JJ, Schiesser FJ. The neutral zone revisited:From historical concepts to modern application. J Prosthet Dent2009;101:405-12. 5. Jacobson TE, Krol AJ. A contemporary review of the factors involved in complete dentures. Part II: stability. J. Prosthet Dent. 1983;49:165-72. 6.Ohkubo C, Hanatani S, Hosoi T, Mizuno Y. Neutral zone approach fordenture fabrication for a partial glossectomy patient: A clinical report.J Prosthet Dent 2000;834:90-3. 7.Wright CR. Evaluation of the factors necessary to develop stability in mandibular dentures. J Prosthet Dent. 1966;16(3):414-30. 8. Russell AF. The reciprocal lower denture.J Prosthet Dent.1959;9:180190 9.E. M. The polished surfaces. Br Dent J. 1961;111(5):407-11.

Fig. 10: Prosthesis in occlusion

10.Wright SM. The polished surface contour: a new approach. Int J Prosthodont. 1991;4(2):159-63.

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Abstract Stem cells are defined as cells that have the ability to perpetuate themselves through selfrenewal and to generate mature cells of a particular tissue through differentiation.Stem cells are truly remarkable. They renew themselves, resisting the powerful pull towards differentiation that overcomes more prosaic cells. And depending on the source, they have the potential to form one, many or all cell types of an organism. Stem cells are not science fiction, but something that one day will become a part of each dentist's clinical practice. The immediate challenge is for dentists not only to be better able to address the questions that their patients have concerning stem cellbased therapy, but also to familiarize themselves with the spectrum of tools they may have in near future to restore form and function effectively.

Keywords Stem cells (SC), Dental pulp stem cells (DPSCs), Stem cells from human exfoliated deciduous teeth (SHED).

Stem cells have been isolated from various dental tissues till date. Flurry of research and studies have been done to isolate and characterize stem cells from various sources. Sources: (i)Dental pulp (ii)Periodontal ligament (iii)Human exfoliated deciduous teeth Dental pulp stem cells (DPSCs) Recently, a population of putative post-natal stem cells has been identified known as DPSCs.The most striking feature of DPSCs is their ability to regenerate a dentinpulp-like complex that is composed of mineralized matrix with tubules lined with osteoblasts,and fibrous tissue containing blood vessels in an arrangement similar to the dentin-pulp complex found in normal human teeth.These DPSCs were then compared with human bone marrow stromal cells (BMSCs), known precursors of osteoblasts. Although they share a similar immunophenotype in vitro, functional studies showed that DPSCs produced only sporadic, but densely calcified nodules, and did not form adipocytes, whereas BMSCs routinely calcified throughout the adherent cell layer with clusters of lipidladen adipocytes. When DPSCs were transplanted into immunocompromised mice, they generated a dentin-like structure lined with human odontoblast-like cells that surrounded a pulp-like interstitial tissue. The data presented here demonstrate that postnatal dental pulp contains cells that are clonogenic, highly proliferative, and capable of regenerating a tissue, properties that effectively define them as stem cells1. DPSCs were capable of forming ectopic dentin and associated pulp tissue in vivo.Stromal-like cells were reestablished in culture from primary DPSC transplants and retransplanted into immunocompromised mice to generate a dentin-pulp-like tissue, demonstrating their selfrenewal capability.DPSCs were also found to be capable of differentiating into adipocytes and neural-like cells.

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The odontogenic potential of 12 individual single-colony derived DPSC strains were determined. Two-thirds of the single-colony-derived DPSC strains generated abundant ectopic dentin in vivo, while only a limited amount of dentin was detected in the remaining one-third. These results indicate that single-colony-derived DPSC strains differ from each other with respect to their rate of odontogenesis. Taken together; these results demonstrate that DPSCs possess stem-cell-like qualities, including self-renewal capability and multi-lineage 2 differentiation .Mesenchymal stem cell populations in adult bone marrow and dental pulp reside in the microvasculature of their tissue of origin. Human bone marrow stromal stem cells (BMSSCs) and DPSCs were isolated by immunoselection using the antibody, STRO-1, which recognizes an antigen on perivascular cells in bone marrow and dental pulp tissue3. Freshly isolated STRO-1 positive BMSSCs and DPSCs were tested for expression of vascular antigens known to be e x p r e s s e d b y e n d o t h e l i a l c e l l s ( v o n Wi l l e b r a n d factor,CD146),smooth muscle cells, and pericytes(รก-smooth muscle actin,CD146,and a pericyte-associated antigen, by immunohistochemistry, fluorescence-activated cell sorting(FACS),and/or immunomagnetic bead selection. Both BMSSCs and DPSCs lacked expression of von Willebrand factor but were found to be positive for รก-smooth muscle actin 4 and CD146. DPSCs were isolated from erupted human molars, and the mitogenic potential of Dentonin in DPSCs was measured by BrdU immunoassay and cell-cycle gene SuperArray. Differentiation of DPSCs was characterized by western blot and by osteogenesis gene SuperArray. Dentonin enhanced DPSC proliferation by down-regulating P16,accompanied by up-regulation of ubiquitin protein ligase E3A and human ubiquitin-related protein SUMO-1.Enhanced cell proliferation required intact RGD and SGDG motifs in the peptide. This study shows that Dentonin can promote DPSC proliferation, with a potential role in pulp repair5. Based on the in vitro experiments, an in vivo evaluation of pulp progenitor/pulp stem cells in the dog was performed. The autogenous transplantation of the BMP2-treated pellet culture onto the amputated pulp stimulated reparative dentin formation. They concluded that BMP2 can direct pulp progenitor/stem cell differentiation into odontoblasts and result in dentin formation6. The cultured stem cells derived from human adult dental pulp of healthy subjects 30-45 years of age, and cells were selected using a FAC Sorter. Light microscope, histochemistry, immunofluorescence,and RT-PCR analyses were performed to study both stem and differentiating cells. A new c+ + kit /CD34 /CD45 cell population of stromal bone producing cells (SBP/DPSCs) has been selected by FAC Sorting, 7 expanded,and cultured .

These SBP/DPSCs were highly clonogenic and, in culture, differentiated into osteoblast precursors (CD44+/RUNX-2+), still capable of self-renewing, and in osteoblasts, producing, in vitro, a living autologous fibrous bone (LAB) tissue. This new-formed tissue was markedly positive for several antibodies for bone, including osteonectin, bone sialoprotein, osteocalcin, fibronectin,collagen III,and bone alkalinephosphatase(BALP).Cells producing LAB can ? be stored at -80 C for a long period of time and were an extraordinary source of osteoblasts and mineralized 8 fibrous bone tissue . Stem cells in the periodontal ligament The functional periodontal ligament attachment apparatus anchors the tooth and consists of periodontal fibers that run between alveolar bone and cementum lining the root surface. Further more, gingival connective tissues and epithelium overlay the alveolar bone and form a dentogingival junction at the interface with the tooth. The complex structure of the periodontium, which consists of the soft connective tissues of the gingival and periodontal ligament, as well as the mineralized tissues cementum and bone, makes periodontal wound healing a unique process. Following conventional periodontal therapy involving debridement of the root surface, the periodontal tissues heal by repair and the migration of the epithelium along the previously contaminated root surface (long junctional epithelium), which prevents connective tissue attachment to the root surface 9. Using a combination of immunohistochemistry and in situ hybridization on co-cultures of mesenchymal stem cells and periodontal ligament, they observed a significant increase in mesenchymal stem cells' expression of osteocalcin and osteopontin and a significant decrease in expression in expression of bone sialoprotein, characteristics of periodontal ligament in vivo. Increased osteopontin and osteocalcin and decreased bone sialoprotein expression was detected within 7 days and maintained through 21 days of coculture. They concluded that contact or factors from periodontal ligament induced mesenchymal stem cells to obtain periodontal ligament-like characteristics. Importantly, analysis of the data suggests the feasibility of utilizing mesenchymal stem cells in clinical applications for repairing and/or regenerating periodontal tissue10.

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In a Study periodontal ligament tissues from 25 surgically extracted human third molars and used them isolate PDL stem cells (PDLSCs) by single-colony selection and magnetic activated cell sorting. Immunohistochemical staining, RT-PCR, and northern and western blot analyses were used to identify putative stem-cell markers. Human PDLSCs were transplanted into immunocompromised mice (n=12) and rats (n=6) to assess capacity for tissue regeneration and periodontal repair. PDLSCs expressed the mesenchymal stem cell markers STRO-1 and CD146/MUC18.Under defined culture conditions, PDLSCs differentiated into cementoblast-like cells, adipocytes, and collagen-forming cells. When transplanted into immunocompromised rodents, PDLSCs showed the capacity to generate a cementum/PDL-like structure and contribute to periodontal tissue repair. Their findings suggest that PDL contains stem cells that have the capacity to generate cementum/PDL-like tissue in vivo. Transplantation of these cells, which can be obtained from an easily accessible tissue resource and expanded ex vivo, might hold promise as a therapeutic approach for reconstruction of tissues destroyed by periodontal diseases11. Stem cells from human exfoliated deciduous teeth (SHED) Exfoliated human deciduous tooth contains multipotent stem cells [stem cells from human exfoliated deciduous teeth (SHED)]. SHED were identified to be a population of highly proliferative, clonogenic cells capable of differentiating into a variety of cell types including neural cells, adipocytes, and odontoblats. After in vivo transplantation, SHED were found to be able to induce bone formation, generate dentin, and survive in mouse brain along with expression of neural markers. They have shown that a naturally exfoliated human organ contains a population of stem cells that are completely different from previously identified stem cells. SHED are not only derived from a very accessible tissue resource but are also capable of providing enough cells for potential clinical application. Thus, exfoliated teeth may be an unexpected unique resource for stem-cell therapies including autologous stem-cell transplantation and tissue engineering12. Applications Stem cells have numerous applications in dentistry namely (i) Basic dental research: To characterize the functional role of differentially expressed genes. (ii) Clinical dental research: §To repair damaged tooth structure endodontic therapy. §Induce bone regeneration. §To treat neural tissue injury or degenerative diseases.

(iii) Periodontal ligament regeneration. (iv) Dentin regeneration. (v) Tissue engineering. Some of the trials are: §Direct orthotopic transplantation into segmental defects §Alveolar ridge augmentation 13 §Vascularized bone graft . To summarize, the promise of stem cell therapies is an exciting one, but significant technical hurdles remain that will only be overcome through years of intensive research. Ethical and social considerations of stem cell research: Much recent interest has focused on whether stem cell therapy could alleviate or even cure common degenerative diseases. This has been accompanied by debate on the ethics of destructive research on early human embryos. Stem cells derived from various sources raise different ethical issues, but their contribution to medical research could be immense. Any use of stem cells should be subject to appropriate scientific and ethical review 14.

References 1.Gronthos S, Mankani M, Brahim J, Robey PG and Shi S.Postnatal human dental pulp stem cells (DPSCs) in vitro and in vivo. ProcNatlAcadSci USA, 2000; 97(25):13625-13630. 2.GronthosS,BrahimJ,LiW,FisherLW,ChermanN,Boyde A et al.Stem Cell Properties of Human Dental Pulp Stem Cells. J Dent Res, 2002; 81(8):531-535. 3.BatouliS,MiuraM,BrahimJ,TsutsuiTW,FisherLW,Gronthos S et al.Comparison of Stemcell-mediated Osteogenesis and Dentinogenesis. J Dent Res, 2003; 12:976-981. 4.Shi S and Gronthos S.Perivascular Niche of Postnatal Mesenchymal Stem Cells in Human Bone Marrow and Dental Pulp.Journal of Bone and Mineral Research, 2003; 18:696-704. 5.Lovell-Badge R.The future for stem cell research. Nature, 2001; 414:88-91. 6.McLaren A.Ethical and Social considerations of stem cell research.Nature, 2001; 414:129131. 7.Chang J, Zhang C, Tan-Ishii N, Shi S and Wang CY. NF-êB Activation in Human Dental Pulp Stem Cells by TNF and LPS.J Dent Res, 2005; 11:994-998. 8.Li A, Simmons PJ and Kaur P.Identification and isolation of candidate human keratinocyte stem cells based on cell surface phenotype.ProcNatlAcadSci USA, 1998; 95:3902-3907. 9.Ivanovski S, Gronthos S, Shi S and Bartold PM.Stem cells in the periodontal ligament.Oral diseases, 2006; 12:358-363. 10.Kramer PR, Nares S, Kramer SF, Grogan D and Kaiser M.Mesenchymal Stem Cells Acquire Characteristics of Cells in the Periodontal Ligament in vitro.J Dent Res, 2004; 83(1):27-34. 11.Sherley JL.Asymmetric cell Kinetics Genes; The key to expansion of adult stem cells in culture. Stem cells, 2002; 20:561-572. 12.Niemann C.Controlling the stem cell niche: right time, right place, and right strength. BioEssays, 2005; 28:1-5. 13.Rosenthal N.Prometheus's Vulture and the Stem-Cell Promise.N Engl J Med, 2003; 349:267-74. 14.Miura M,GronthosS,ZhaoM,LuB,FisherLW,Robey PG et al.SHED: Stem cells from human exfoliated deciduous teeth. ProcNatlAcadSci, 2003; 100(10):5807-5812.

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