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Journal of MaxilloFacial Science & Research - 2014, Volume-1, Issue-1

Journal of Maxillo Facial Science and Researchis the official publication of PMS College of dentalscience & research ,Golden hills ,Vattappara ,Trivandrum 695028.Kerala.India. The Journalis intended to be researchperiodical, the purposeof which is to publish original clinical and basicinvestigations and review articles concernedwith every aspect of dentistry and relatedsciences. Brief communications are alsoaccepted and a special effort is made to ensurerapid publication.Only articles written in Englishare accepted and only if they have not been andwill not be published elsewhere. Manuscriptsand editorial correspondents should be send tothe editors at the addresses given. Journalofdental science and research has no objectionsto the reproductions of short passages andillustrations from this Journal without furtherformality than the acknowledgement of thesource. All rights are reserved. The editor andor its publisher cannot be held responsible forerrors or for any consequences arising from theuse of the information contained in this journal.The appearance of advertising or productinformation in the various sections in the journaldoesn’t constitute an endorsement or approvalby the journal and or its publisher of the qualityor value of the said product or of claims madefor it by its manufacturer. The journal is publishedand distributed by PMS College of dentalscience & research . The copies are send tosubscribers directly from the publishers address.It is illegal to acquire copies from any othersource. If a copy is received for personal useas a member of the Association / Society, onecan not resale or give – away the copy forcommercial or library use.

Editorial Office :Dr. (Capt) Vivek .VEditor, Journal of dental science & researchPMS College of dental science & researchGolden hills ,Vattppara,Trivandrum.695028e-mail : [email protected] : [email protected]

Published by :Dr PS ThahaThe ChairmanPMS College of dental science & researchGolden hills ,Vattppara,Trivandrum.695028

JANUARY TO JUNE 2014; VOLUME1,ISSUE 1

PatronDr.PS Thaha

Chairman.PMS College of dentalscience & research

Editor in Chief :Dr. (Capt.) Vivek .V

Associate EditorDr Suvy Manuel

Assistant editorsDr. Sherin A Kalam

Dr. Vinod Moni

Advisory BoardPadmashree Dr. Mahesh Varma

Dr. Manjith Singh, Dr. Iype Varghese, Dr. N.O. Varghese, Dr. K. Nandakumar

Expert PanelDr.Rajesh Pillai, Dr Bindu J nair

Dr.Seba Abraham, Dr. Alex Mathews MuruppelDr Surej Kumar LK, Dr Roopesh, Dr Sajeena George, Dr Jayalekshmi

Oral medicine & RadiologyDr Tatoo JoyDr Sreela LSDr Twinkle S. PrasadDr Tinky BoseDr Sunila Thomas

Oral pathology &microbiologyDr Beena VTDr HeeraDr Hari SDr SivaKumarTT

ProsthodonticsDr Harsha KumarDr Murugan PADr Shyam MohanDr Sudeep SDr Dinesh N

Conservative dentistry& endodonticsDr Rajesh GopalDr GibiPaulDr GaneshDr Unu S

PeriodonticsDr Prasanthila JanamDr Bindu R NairDr Elizabeth KoshyDr MiniJoseDr Betsy JosephDr Ambili R

PedodonticsDr Sheela SreedharanDr Rita ZarinaDr Suchitra MSDr Anand Raj

OrthodonticsDr Anil KumarDr Sreejith Kumar GDr KoshyDr Vinod KrishnanDr Madhav ManojDr DeepuLeander

Oral & MaxilloFacial SurgeryDr Geeta C.R.Dr Shobana C.R.Dr Sooraj S.Dr Ravindran NairDr Ajith Kumar

CommunityDentistryDr Vivek .S

REVIEW BOARD

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Instructions to the Authors.....GUIDELINESManuscripts: Articles should be type written on one side of A4 size (21x28cm) White paper in double spacing with a sufficientmargin. One Original and two high quality photostat copies should be submitted. The author’s name is to be written only on theoriginal copy and not on the two photostat copies. In addition to the printed version, a CD containing the article file alsoshould be submitted compulsorily. Use a clear and concise reporting style. Journal of Maxillofacial Science and Researchreserves the right to edit manuscript, to accommodate space and style requirements. Authors are advised to retain a copy for thereference.

Title Page: Title page should include the title of the article and the name, degrees, positions, professional affiliations of eachauthor. The corresponding authors, telephone, e-mail address, fax and complete mailing address must be given.

Abstract: An abstract of the article not exceeding 200 words should be included with abbreviated title for the page head use.Abstract should state the objectives, methodology, results and conclusions.

Tables: Tables should be self explanatory, numbered in roman numbers, according to the order in the text and type on separatesheets of paper. Number and legend should be typed on top of the table.

Illustrations: Illustrations should be clearly numbered and legends should be typed on a separate sheet of paper, while eachFigure should be referred to the text. Good black and white glossy photographs or drawings drawn in black Indian ink on drawingpaper should be provided. Colour photographs will be published as per availability of funds. It will incur printingcost. Otherwise the cost of printing will be at the expense of authors. Photographs of Raadiographs should be sent andnot the original Radiograph. Prints should be clear and glossy. On the back of each print in the upper right corner, write lightly theFigure number and author’s name; indicate top of the photograph with an arrow of word Top’ Slides and Raadiograph photographsshould be identified similarly.

Reference: Reference should be selective and keyed in numerical order to the text in Vancouver Style. Type them doublespaced on a separate sheet of paper. Journal references must include author’s names, article tide, journal name, volume number,page number and year. Book reference must include author’s or editor’s names, chapter title, book title, edition number, publisher,year and page numbers.

Copy right: Submission of manuscripts implies that the work described has and not been published before (except in the formof on abstract or as part of published lectures, review or thesis) and it is not under consideration for publication else where, andif accepted, it will not be published else where in the same form, in either the same or another language without the comment ofcopyright holders. The copyright covers the exclusive rights of reproduction and distribution, photographic reprints, videocassettes and such other similar things. The views/opinions expressed by the authors are their own. The journal bears noresponsibility what so ever.

The editors and publishers can accept no legal responsibility for any errors, omissions or opinions expressed by authors. Thepublisher makes no warranty, for expression implied with respect to the material contained therein. The journal is edited andpublished under the directions of the editorial board who reserve the right to reject any material without giving explanations. Allcommunications should be addressed to the Editor. No responsibility7 will be taken for undelivered issues due to circumstancesbeyond the control of the publishers.

Books for review: Books and monographs will be reviewed based on their relevance to Journal of Maxillofacial Science andResearch readers. Books should be sent to the Editor and will become property of Journal of Maxillofacial Science andResearch .

Return of articles: Unaccepted articles will be returned to the authors only if sufficient postage is enclosed with the manuscripts.

All correspondence may please be send to the following address:

Dr. Capt. Vivek .VEditor, Journal of Maxillofacial Science and Research ,Prof. and Head, Dept. of Oral Medicine & Radiology,

PMS College of Dental Science & Research, Golden Hills, Vattappara, Trivandrum - 695028Mobile : 09447341035 e-mail: [email protected]


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CONTENTS

MESSAGESMessage by Chairman 6Dr P.S. Thaha

Message by Principal 7Dr N.O. Varghese

EDITORIALJournal of Maxillofacial Science and Research (JMFSR) 8Vivek V

CASE REPORTSAn inverted impacted maxillary 3rd molar, what to do? 9A case report with reviewJacob BM, Paulose DE, Cherian NM, Thomas N, Vinod V.S

Clinical and surgical treatment dilemma of ankyloglossia: 12A case report with review of literatureMenon V, Kumar LKS, Zacariah RK, Khalam SA

Pyogenic granuloma in a one and half year old child 15A case reportBharathamVV, Mehta RS, Reshma VJ, Anwar AS

The myth and reality of “ The Free Fibula” 19Varghese MP , Kumar LKS, Suvy Manuel, Kurien NM, Khalam SA

Emotional woes : A strain to the periodontium 24Anju Samuel, Nithin Mathew Cherian

Zygomatic implants - A case report with review of literature 28Khalam SA, Kumar SLK, Kurien NM, Gopal KV

Intraoral nevi - A review 32Raman RK, Raj NS , Joseph AP, Mony V, Nair BJ

Inclusion bodies : A significant clue in pathologic diagnosis 37Denny SE, Nair A, Sivakumar TT, Varun B.R, Nair BJ

ABOUT THE JOURNAL 46


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Dental education is a continuous process and it is mandatory to

stay up to date with the recent advancements in dentistry. It is the need

of the hour to have a good platform to take the advancements in the

field to the masses and the best medium for this is to bring out scientific

publications of the nature of “JOURNAL OF MAXILLOFACIAL

SCIENCE AND RESEARCH”.

I understand that that this journal is enriched with original articles,

case studies and reports, and research articles from all over India.

I congratulate all who have contributed to bring out such a publication

and wish all success.

Dr P S ThahaChairman

Messages

Message by ChairmanPMS College of Dental Science & ResearchGolden Hills, Venkode P.O.,Vattappara, Trivandrum - 695028

Thaha P S

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I am very much pleased to notice that the PMS College of Dental Science is

coming out with a Journal which is a debut venture of its kind. This will definitely

provide a platform to the faculty as well as students of our College to publishing

the Scientific articles. More over this will encourage scientific aptitude. I appreciate

the editor and the management for all their support. All the very best for the

venture.

Principal

Dr. N.O. VARGHESE

Messages

Message by PrincipalPMS College of Dental Science & ResearchGolden Hills, Venkode P.O., Vattappara, Trivandrum - 695028

Varghese N O

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Editorial

Journal of Maxillofacial Science and Research (JMFSR)Dentistry which revolved only around the teeth, has over a short period of timeevolved from its humble beginnings to become a very important branch of medicinethat involves the health of oral and maxillofacial structures. Imbibing new informationand experiences in this fast and ever changing oral and maxillofacial world, is oftenvery challenging. Considering the present day evidence based practice, communicatingthe information gained for the benefit of our patients, profession and society, is evenmore challenging. In spite of all developments in communication, documentation andinformation sharing, scientific journals are still considered the gold standard in providingevidence based information.

Our visionary chairman Dr PS Thaha, a widely travelled educationist, entrepreneur ,quite interested in keeping abreast with the latest in dentistry , is the man behind the ideaof a scientific journal for our college by our college “JOURNAL OFMAXILLOFACIAL SCIENCE & RESEARCH”. By leading us [the editorial board]to create a critical and reactive journal, Dr. Thaha intends to create a space where thestudents and faculty, can “test the academic waters” and think deeply on their invaluableexperiences.

JOURNAL OF MAXILLOFACIAL SCIENCE & RESEARCH [JMFSR], the officialpublication of PMS College of Dental Science & Research is intended to be a researchperiodical that aims to inform its readers of ideas, opinions, developments and keyissues in dentistry - clinical, practical and scientific - stimulating interest, debate anddiscussion in all disciplines of dentistry. Rigorous peer review by our excellent reviewboard is the hall mark of JMFSR. The Journal is designed with a view to enable fastand easy access to information for its readers. I take this opportunity to request, all thestaff and students of PMS college of dental science and research, to supportJOURNAL OF MAXILLOFACIAL SCIENCE & RESEARCH by contributingarticles, letters, opinions, and last but not the least, identifying and procuring finance formaking the journal self sustainable.

Dr. (Capt) V. Vivek,Editor in Chief

JOURNAL OF MAXILLOFACIAL SCIENCE & RESEARCHProf. and Head, Dept. of Oral Medicine & Radiology,

PMS College of Dental Science & Research, Golden Hills, Vattappara, Trivandrum - 695028Mobile : 09447341035 e-mail: [email protected]

Vivek .V

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An inverted impacted maxillary 3rd molar, what to do?A case report with reviewBasil. M. Jacob1, Dheeraj Eldho Paulose2, Nithin Mathew Cherian3, Ninan Thomas4, Sankar Vinod V5.

CASE REPORT

IntroductionArcher defined an impacted tooth as one

which is completely or partially unerupted and ispositioned against another tooth or bone or softtissue so that its further eruption is unlikely1. Anincreased awareness among the general population,easyaccess to surgical treatment along withadvances in the surgical practice and equipment’shave resulted in increased number of surgeries forremoval of impacted teeth.

Surgical extraction of impacted third molarsis the most common procedure performed by theoral surgeon. Any tooth including the deciduousand the permanent can be impacted but the morecommon are the maxillary and mandibular thirdmolars and the maxillary cuspids followed by the

premolars and the supernumerary teeth[2]. Amongthe third molar impactions the most common isthe mandibular. Maxillary third molar impactionsbeing equally present but have been overlooked.Still rare are literature about inverted impactedmaxillary third molars. Here we present a case reportwith review of literature.

Case reportA 50 year female patient reported to the OPD

of Mar Baselios Dental college with complaintsof pain with respect to upper right back tooth. Ahistory of pain since 1 week and decay since 6months were elicited. On examination a grosslydecayed upper right maxillary first molar was

1. Junior Resident2. Junior Resident3. Senior Lecturer4. Senior Lecturer5. Prof & HOD

Division Of OMFS, Mar Baselios Dental College,Kothamangalam, Ernakulam District, India.

Adress for correspondence :Dr Basil. M. Jacob, Dept: of OMFS, Mar Baselios Dental College,Kothamangalam, Ernakulam District, India. Pincode:686691Email:- [email protected]

Jacob BM, Paulose DE, Cherian NM, Thomas N, Vinod V.S

Abstract

Surgical extraction of impacted third molars is the most common procedure performed by the oralsurgeon. Any tooth including the deciduous and the permanent can be impacted but the more commonare the maxillary and mandibular third molars and the maxillary cuspids followed by the premolars andthe supernumerary teeth2. Among the third molar impactions the most common is the mandibular.Maxillary third molar impactions being equally present but have been overlooked. Still rare are literatureabout inverted impacted maxillary third molars. Here we present a case report with review of literature.

Keywords : Inverted tooth, Maxillary impaction, impaction

Figure - 1

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noticed which was tender on percussion. The upperright maxillary second and third molars weremissing. A routine IOPA was taken whichconfirmed the clinical diagnosis of apicalperiodontitis of upper right maxillary first molar.In addition the IOPA revealed an invertedimpacted upper right maxillary third molar.

A panoramic radiograph was taken whichconfirmed the presence of the inverted impactedright maxillary third molar, with minimumradiolucency around the crown and close proximityto the maxillary sinus.

The patient was informed of the presenceof the impacted tooth and pros and cons of surgicalremoval versus the conservative management werediscussed. The patient opted for the surgicalremoval of the inverted impacted tooth and thesame was done along with the removal of thedecayed maxillary right first molar under localanaesthesia.

DiscussionInverted impacted maxillary molar is a rare entity.The first case was reported by Gold and Demby in19733, followed by this another 12 cases of invertedimpacted maxillary molars have been reported sofar4-12. An inverted impacted tooth is called acomplicated impaction5. Third molars in both themandible and maxilla may develop at a distancefrom their normal location because of unusualproliferation of odontogenic epithelium beforedevelopment of tooth germ thus leading these toget impacted4. Indications for surgical removal ofimpacted teeth include dental caries, recurrentpericoronitis, periodontal disease involving theadjacent tooth, obstruction to eruption of adjacenttooth, resorption of adjacent tooth, to facilitateorthognathic surgery, if related to any pathology,prosthetic considerations (prior to dentureconstruction or implant placement) and toeliminate any potential sources of infection priorto radiotherapy. Contraindications includeadvanced age, excessive risk of damage to adjacentstructures and asymptomatic deeply impacted thirdmolars.

Archer in 19751 classified impaction of maxillarythird molars as mesioangular, distoangular, vertical,horizontal, buccoangular, linguoangular andinverted. According to depth of impactioncompared to the second molar Archer classifiedmaxillary impactions into three categories:

Class A - Occlusal surface of impacted tooth is atapproximately the same level as the occlusal surfaceof second molar.

Class B - Occlusal surface of impacted tooth is atthe middle of the crown of the adjacent secondmolar.

Class C- Occlusal surface of impacted tooth isapical to the cervical line of the adjacent secondmolar or even deeper.


Figure - 2

Figure - 3

Figure - 4

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The factors that increases the difficulty of surgicalremoval of impacted maxillary third molars aresurgical removal performed with mouth openinggreater than 45mm, occlusal level is high, elevatortip is high, relation to maxillary sinus is positive(vs patients with no contact) and close relation toroot of second molar13 (vs patients in whom thereis no contact or contact only with crown of secondmolars).

The treatment options for inverted impacted toothinclude conservative management with routineradiographic follow up, autotransplantation andsurgical removal. In our case an option of surgicalremoval of impacted inverted third molar alongwith extraction of grossly decayed upper right firstmaxillary molar was given and the patient optedfor the same.Literature search shows no exacttreatment protocols for removing invertedimpacted maxillary molars so the most conservativemanagement is considered to be the best protocol.

Complications during removal of inverted impactedmaxillary third molars include a significantly largepost extraction socket, risk of tooth displacementinto infratemporal space or into the maxillary sinus,fracture of maxillary tuberosity and bleeding14.

Conclusion

As a conclusion inverted impacted third molars canbe surgically extracted but a conservative approachis more appropriate considering the complicationthat is foreseen.

References

1. Archer William H. Oral and MaxillofacialSurgery, Vol.1, edn.5, Philadelphia, WBSaunders Co.1975.

2. R Rajendran, B Sivapathasundrharam (2006)Shafer’s textbook of oral pathology, 5thedn.Elsevier, pp 83-86.

3. Gold J, Demby N (1973) Rare invertedmaxillary third molar impaction: report ofcase. J Am Dent Assoc 87: 186-188.

4. Held HW (1979) Inverted maxillary molar.Dent RadiogrPhotogr 52: 87. 10.


5. AlShamrani SM (2001) Inverted and impactedmaxillary third molar. Report of two cases.Odontostomatol Trop 24: 15-17.

6. Pai V, Kundabala M, Sequeira PS, Rao A(2008) Inverted and impacted maxillary andmandibular 3rd molars; a very rare case. OralHealth Comm Dent 2: 8-9.

7. Yuvaraj, Agarwal GD (2011) Invertedmaxillary third molar impaction – A casereport. People’s J Sci Res 4: 57-58.

8. Mohan S, Kankariya H, Fauzdar S (2012)Impacted inverted teeth with their possibletreatment protocols. J Maxillofac Oral Surg11: 455-457.

9. Togoo RA (2013) Rare occurrence of invertedmaxillary third molar impaction: a case report.J Int Oral Health 5: 85-87.

10. Rammal M, Alfonso C (2013) An unusualcase of an inverted and impacted maxillarythird molar. Oral Surg(in press).

11. Chhabra S, Chhabra N, Dhillon N (2012)Inverted and impacted maxillary third molar- Removal by lateral transposition method. IntJ Dent Exper Dent Sci 1: 26-29.

12. Chen CY, Wang WC, Lin LM, Chen YK (2014)Incidental detection of a rare inverted andimpacted maxillary third molar in a patientof mandibular unicysticameloblastoma.Dentistry 4: 213.

13. Carvalho, De AraujoFilho, Do EgitoVasconcelos (2013) Assessment of factorsassociated with surgical difficulty duringremoval of impacted maxillary third molars. JOral MaxillofacSurg 71: 839-845.

14. Togoo R A (2013) Rare occurrence ofinverted maxillary third molar impaction: Acase report. J Int Oral Health 5(3):85-87.

Source of Support : NilConflict of Interest : Nil

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Clinical and surgical treatment dilemma of ankyloglossia:A case report with review of literatureVarun Menon1, Surej Kumar LK2, Rakesh Koshy Zacariah3, Sherin.A.Khalam4.

CASE REPORT

IntroductionAnkyloglossia, or tongue tie, is an uncommoncongenital anomaly characterized by an abnormallyshort lingual frenum which may restrict tongue-tip mobility and may subsequently lead to a rangeof problems such as difficulties in breast feedingduring infancy, inability to chew age-appropriatesolid foods, speech impediments, poor oral hygieneand behavioural problems1. Ankyloglossia has beendefined as the condition in which the tonguecannot make contact with the hard palate or cannotprotrude more than 1–2 mm past the mandibularincisors2. According to Lalakea and Messnerincidence of ankyloglossia reported vary from 2 to4.8% and were observed to occur more commonlyin males with a male to female ratio of 3 to 1 withno racial predilection3.The reported prevalencevaries from 0.02 to 4.8%4.

Case Report:An 18year female patient reported with complaintsof difficulty in protruding the tongue and toapproximate the tip of the tongue to the palate.She also finds difficulty in speaking certain letterslike t; d etc.She had a history of previous surgicalprocedure done for correction of same difficultyduring childhood. Morphologically, lingual frenumwas abnormally short and thick and functionally;the tongue was unable to protrude past the gumline and could not contact the palatal vault (Figure1a). Even lateral movements of tongue were

1. Junior Resident2. Prof & HOD3. Reader4. Senior Lecturer

Division of OMFS, PMS College Of Dental Science &Research, Vattappara, Trivandrum.

Adress for correspondence :Division of OMFS, PMS College Of Dental Science & Research,Vattappara, Trivandrum.

Abstract:Ankyloglossia, or tongue-tie, refers to an abnormally short lingual frenulum. It is a well recognized

but poorly defined condition and has been reported to cause difficulties in feeding, dysarthria, dyspnea,and social or mechanical problems. Questions pertaining to the age, appropriate time of treatment andthe most optimal method to treat are still a dilemma to the clinicians. It has been reported to causefeeding difficulties, dysarthria, dyspnea, and social or mechanical problems, which may warrant surgicalcorrection in symptomatic cases. The literature regarding treatment remains inconclusive. In this articlewe report a case of 18 year old girl with tongue-tie who underwent the frenectomy procedure underlocal anaesthesia, along with review of literature.

Keywords : Ankyloglossia, tongue, surgical treatment.

Menon V, Kumar LKS, Zacariah RK, Khalam SA

Figures and Legends

Figure 1a: Ankyloglosia showing short and thicklingual frenum with restricted tongue movement

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Journal of MaxilloFacial Science & Research - 2014, Volume-1, Issue-1 Menon V, Kumar LKS, Zacariah RK, Khalam SA

mildly restricted (Figure 1b). The surgicalcorrection was performed sequentially, taking intoconsideration the vital anatomical structurespresent in the vicinity ,a vertical incision was placedalong the lingual frenum.Fibrotic bands excised,improved mobility of the organ was visibleimmediately after post intervention . Followingtotal release, closure was done with 3, 0 vicryl(Figure 1c). Haemostasis was achieved.

Discussion

Ankyloglossia, or tongue-tie, refers to anabnormally short lingual frenulum. Ankyloglossiais derived from the Greek words ‘ankylo’ meaningstiff and ‘glossa’ meaning tongue. The exactpathophysiology of tongue-tie is unknown and themost likely cause of abnormal frenulum length andattachment is the deviation from normaldevelopment. The clinical finding of ankyloglossiahas been associated several syndromes, includingEhlers-Danlos syndrome, Beckwith-Wiedemannsyndrome, Simosa syndrome, X linked cleft palate,orofaciodigital syndrome, and several others5, 6.In the early 1900s, tongue-tie was believed toimpact breastfeeding and was routinely divided. Asformula milk gained popularity, tongue-tie releasefell out of favor as infants could bottle feed as an

alternative7. History reveals treatment ofankyloglossia dates back to the New Testament:‘‘one...had an impediment in his speech...the stringof his tongue was loosed, and he spake plain.’’(Mark 7:32) and midwives ,in the 18th centurywould use their fingernails to divide thefrenulum.Since then a variety of treatment options,including simple division, frenulotomies, and four-ap Z-frenuloplasty have been described inliterature2.Kotlow LA8 ,from his clinical research gave acomprehensive classification to describe theseverity of ankyloglossia1. Clinically acceptable, normal range of free

tongue: greater than 16 mm2. Class I: Mild ankyloglossia: 12 to 16 mm3. Class II: Moderate ankyloglossia: 8 to 11mm4. Class III: Severe ankyloglossia: 3 to 7 mm5. Class IV: Complete ankyloglossia: less than 3

mmAccording to American Academy of Paediatrics9

different grading system for tongue tie: Grade 1: isthe attachment of the lingual frenulum to the tipof the tongue, in front of the alveolar ridge in thelower lip sulcus.Grade 2: is 2-4mm behind the tongue tip andattaches on or just behind the alveolar ridge. Grade 3: is the attachment of the lingual frenulumto the midtongue and the middle of the floor ofthe mouth and is usually tighter and less elastic.Grade 4: is essentially attached against the base ofthe tongue and is thick, shiny and inelastic.The Hazelbaker Assessment Tool for LingualFrenulum Function 10 (HATLFF) was developedto provide a quantitative assessment ofankyloglossia and has been proven to be highlyreliable. It includes five appearance items, such aslength, attachment site, and elasticity, as well asseven functional items, such as extension, spread,cupping, and peristalsis of the tongue4,10,11.Ankyloglossia can be diagnosed using the followingcriteria: impossibility of touching palate withtongue tip when the mouth is open; bifid tongueduring protrusion; curvature of the intermediatepart of the tongue, preventing it from movingforward out of the oral cavity;

Figure 1b: Lingual frenum with limited lateral movement

Figure 1c: Surgical correction and closure of Ankyloglosia

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Journal of MaxilloFacial Science & Research - 2014, Volume-1, Issue-1 Menon V, Kumar LKS, Zacariah RK, Khalam SA

and reduced sublingual space. The treatmentoptions for ankyloglossia involve observation,language articulation therapy and three possiblesurgical techniques: frenotomy, which consists ofsimply cutting the frenulum; frenectomy, completeexcision of the frenulum; and frenuloplasty, whichinvolves freeing the tongue and correcting itsanatomy12,13,14. Depending on the consequences ofthe abnormality, radical and urgent treatment maybe required.Berg15 reported that frenectomy is normallyperformed in 1–3-year old children, under generalanaesthesia, in most cases. It should be performedas soon as possible, because if performed later,the child might have incorrect swallowing anddisturbed speech muscle movement patterns. Thereare no conclusive parameters about the age forperforming the surgical technique in the literature16.ConclusionThough Clinical and surgical treatment dilemmaof Ankyloglossia still exist and it varies fromclinicians to clinicians but from our experience, wefeel timely and appropriate surgical intervention,followed by speech therapy when indicated ismandatory for optimal management of tongue tie;It is being more and more accepted across by allclinicians associated with infants, children andadults with tongue tie that , early intervention isthe optimal form of management when the frenumhas been identified and diagnosed as abnormal.Reference1. Lalakea M.L., Messner A.H. Ankyloglossia:

Does it matter? Pediatric Clin North Am2003;50:381-97.

2. Heller.J,Gabbay J, O’Hara .C, et al., Improvedankyloglossia correction with four-ap Zfrenuloplasty, Ann. Plast. Surg 2005;54: 623–628.

3. Messner A.H., Lalakea M.L.Ankyloglossia:Controversies in management. Int J PediatrOtorhinolaryngol 2000; 54:123-31.

4. Amir LH, James JP, Donath SM. Reliabilityof the Hazelbaker Assessment Tool for lingualfrenulum function. Int Breastfeed J 2006;1:3–8

5. Kummer,A: Ankyloglossia: to clip or not toclip? that’s the question. ASHA Leader, 2005;10(17):6,7-30.

6. De Felice C, Toti P, Di Maggio G etal.Absence of the inferior labial and lingualfrenula in Ehlers-Danlos syndrome. Lancet.2001;357(9267):1500–1502.

7. Wallace H, Clarke S. Tongue tie division ininfants with breast feeding difficulties. Int JPediatr Otorhinolaryngol. 2006;70(7):1257–1261

8. Kotlow L.A. Ankyloglossia (tongue-tie): Adiagnostic and treatment quandary.Quintessence Int 1999; 30:259-62

9. Shafer WG, Hine MK, Levi BM.Developmental disturbances of oral and paraoral structures. In: Oral Pathology. 4th ed.Philadelphia, Pa: Harcourt; 2000

10. Hazelbaker A. The Assessment Tool forLingual Frenulum Function (ATLFF): Use ina Lactation Consultant Private Practice.Pasadena, CA: Pacific Oaks College; 1993

11. Hogan M, Westcott C, Griffiths M.Randomized, controlled trial of division oftongue-tie in infants with feeding problems. JPaediatr Child Health.2005;41(5–6):246–250

12. Cunha RF, Silva JZ, Faria MD. Clinicalapproach of ankyloglossia in babies:report oftwo cases. J Clin Pediatr Dent 2008: 32: 277–281.

13. Kupietzky A, Botzer E. Ankyloglossia in theinfant and young child: clinical suggestions fordiagnosis and management. Pediatr Dent 2005:27: 40–46.

14. Suter VG, Bornstein MM. Ankyloglossia: factsand mytis in diagnosis and treatment. JPeriodontol 2009: 80:1204–1219.

15. Berg KL. Two cases of tongue-tie andbreastfeeding. J Hum Lact 1990: 6: 109–112.

16. Segal Lm. Stephenson R, Dawes M, FeldmanP. Prevalence, diagnosis, and treatment ofankyloglossia. Can Fam Physician 2007: 53:1027–1033.


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Pyogenic granuloma in a one and half year old child:A case reportVadi V. Bharatham1, Raj Gopal Singh Mehta 2, Reshma V J3, Shihab Anwar A4

CASE REPORT

Introduction

OPG is a kind of inflammatory hyperplasia.The term inflammatory hyperplasia is used todescribe a large range of nodular growths of theoral mucosa that histologically represents inflamedfibrous and granulation tissues. It includes fibrousinflammatory hyperplasia palatal papillaryhyperplasia, giant cell granuloma and pregnancyepulis.

The term Pyogenic granuloma was first introducedby Hartzell in 1904 although Hullihen was thefirst person to describe the lesion in 1844 for thefirst time in the English literature.

Although it is a common disease in the skin, it isextremely rare in the gastrointestinal tract exceptfor the oral cavity where it is often found onkeratized tissue. There are two kinds of PG namelythe lobular capillary hemangioma and non lobularcapillary hemangioma which differs in theirhistological appearances.

Because of the high incidence of oral PGespecially in pregnant women and the critical needfor its proper diagnosis management and treatment,it is important to recognize this problem and dealwith it suitably.

The etiology for oral pyogenic granuloma isunknown. Some investigators believe it to be a kindof benign neoplasm. It is also a reactive-tumorlike lesion which arises in response to variousstimuli such as a low grade local irritation,traumatic injury, hormonal factors or certain kindsof drugs.

1. Reader, MES Dental College, Perinthalmanna, Kerala.2. Professor, Jaipur Dental College, Jaipur.3. Senior lecturer, MES Dental College, Kerala.4. Senior lecturerEducare Institute of Dental Sciences, Kerala.

Adress for correspondence :Dr. Vadi V. Bharatham, MDSReaderMES Dental College, Perinthalmanna, Kerala, India.

BharathamVV, Mehta RS, Reshma VJ, Anwar AS

Abstract

Oral pyogenic granuloma (OPG) is defined as kind of inflammatory hyperplasias on any kind of softtissues of the oral cavity. It is very similar to pyogenic granuloma that occurs on the other part of thebody. The term pyogenic granuloma is a misnomer because the lesion is unrelated to infection and inreality arises in response to various stimuli such as low grade local irritation traumatic injury or hormonalfactors. This lesions is predominantly seen in younger individuals, specially in the females and aroundthe second decade of life. The reason could be possibly because of the high vascularity and due tochanges in the hormones in these individuals. Clinically, the oral pyogenic granuloma is a smooth orlobulated exophytic lesion manifesting as small red erythematous papules on a pedunculated or sometimessessile base which is usually hemorrhagic. The surface ranges from pink to red to purple depending onthe age of the lesion. Excisional surgery has the treatment of choice although some other treatmentprotocols such as the use of ND YAG laser, flash lamp, pulsed dye laser, cryosurgery, intralesionalinjection of ethanol or corticosteroid and sodium tetradecyl sulfate, sclerotherapy have been proposed.

Keywords : Pyogenic granuloma, child.

16

Journal of MaxilloFacial Science & Research - 2014, Volume-1, Issue-1 BharathamVV, Mehta RS, Reshma VJ, Anwar AS

Oral pyogenic granuloma is a smooth or lobulatedexophytic lesion manifesting as a small rederythematous papule or a pedunculated orsometimes sessile base which is usuallyhemorrhagic and compressible and may developas dumb bell shaped masses. The size varies indiameter from a few millimeters to severalcentimeters and usually reaches its full size withinweeks or months remaining inefinitely thereafter.Clinically the development of the lesion is slowasymptomatic and painless but it may also growrapidly. The surface is characteristically ulceratedand friable which may be covered by a yellowfibrinous membrane and its color ranges from pinkto red to purple depending on the age of the lesion.Young oral pyogenic granulomas are highly vascularin appearance because they are composed ofpredominantly of hyperplastic granulation tissuein which capillaries are prominent. Minor traumato the lesion may cause considerable bleeding dueto its pronounced vascularity where as older lesionstend to become more collagenized and pink.

Although, it has been reported even in children, itis a rare finding in the children. Here we reportsuch a case of oral pyogenic granuloma in a one-and-half year old child in the upper maxillarygingiva.

Case report

An 15-month-old male child patient reported tothe department of oral medicine and radiology atMES Dental college and Hospital with a chiefcomplaint of bleeding from swelling on the gumssince 15 days.

History of presenting illness revealed that thepatient was apparently normal about a month daysago when he had a fall. The upper front tooth wasbroken in the in the event with a laceration of theupper lip. The patients’ parents rushed the childpatient to a child health care provider where hewas subsequently treated for the broken tooth andlaceration of the upper lip with antibiotics andanalgesics. About 15 days ago the patients’ parentsnoticed a growth on the upper gums in the placeof the broken tooth. The swelling was bright redin color and would easily bleed during feeding. The

child patient was then subsequently referred to thishospital for further diagnosis and management.

Figure-1 Clinical photograph showing he gingival growth

Clinical examination revealed that the patient hadgingival overgrowth in relation to 61 Descriptionof the lesion: a solitary reddish peduculated growth,measuring roughly about 1.5 cm in diameter, roundto ovoid in shape was present on the upper labialgingival in relation to 61. the growth was smoothwith no surface ulceration, discharge, or bleeding.On palpation, all the inspectory findings wereconfirmed. The swelling was soft in consistency,attached to the maxiallary labial gingival with apedicle and immobile. The growth bled easily withmanipulation.

The remaining hard tissue such as the decidousteeth were intact with no significant pathologicalfindings. Similarly, other soft tissue such as tonguebuccal mucosa, vestibule, labial mucosa, tonguehad no noticeable change or abnormality.

Based on chief complaint, history and clinicalexamination a working diagnosis of oral pyogenicgranuloma was given.

DIFFERENTIAL DIAGNOSISDifferential Diagnosis of Peripheral giant cellgranuloma, Peripheral ossifying fibroma,Metastatic cancer, Hemangioma, Conventionalgranulation tissue, Kaposi’s sarcoma,Angiosarcoma and hon hodgkins lymphoma wasalso considered

As part of the routine investigative procedure anIntra Oral Periapical Radiograph was advised inrelation to 61 and an anterior maxillary occlusalview was taken.

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The radiographs revealed no change in the bonemorphology and indicating the lesion was arisingfrom the soft tissue.

Figure - 2 Radiograph showing the missing 61

The patient was then referred to the Departmentof Pedodontics for further management where anexcisional biopsy was done under local anesthesiaand the specimen subsequently sent to the Oralpathology department for histopathological studies.

Biopsy report

Electron microscopy of the fixed lesionrevealed parakeratized stratified squamousepithelium in focal areas and connective tissuestroma, loosely arranged collagen fibers numberousblood vessels filled with RBCs and inflammatorycells. Connective tissue stroma also exhibited

moderate infiltration of mixed inflammatory cellslike neutrophills lymphocytes plasma cells.

Figure - 5 photohistomicrograph of the oral pyogenic granuloma

Based on the histopathological findings a finaldiagnosis of Oral pyogenic granuloma was given.

The pyogenic granuloma also known as, granulomapyogenicum, is a response of tissues to nonspecificinfection of staphylllococci or streptococci.

Oral pyogenic granuloma is relatively common andaccounts for 3 to 7 % of all biopsy findings frommoral cavity lesions. In study the most common intraoral site was the gingival followed by the lips tonguepalate and buccal mucosa. Oral pyogenicgranuloma on gingiva is more common in themaxilla than in the mandible. Oral pyogenicgranuloma if on the gingival tissue is present ismore common in the anterior region than in thepostherior region

Oral pyogenic granuloma is a non neoplastic growthin the oral cavity proper most commonly seen inyoung individuals, especially the females. Althoughits occurrence in children and infants is rare, manycases have, however, been reported previously.Since it is seen pretty commonly in pregnant womenand young individuals, its diagnosis prevention,management, and treatment of the lesion are veryimportant. The exact etiology for this lesion isunknown although it is seen arising in response tovarious stimuli such as low grade local irritation,traumatic injury, sex hormones or certain kinds ofdrugs. Hence , our primary objective should beaimed at removal of causative irritants such asplaque calculus foreign materials and source oftrauma if such is the cause followed by treatmentby excisional surgery. New modalities of treatment


Figure - 3 Photograph of the excised specimen

Figure - 4 photohistomicrograph of the oral pyogenic granuloma

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include cryosurgery excision by ND YAG laser,flash lamp, pulsed dye laser, injection of ethanolor corticosteroid and sodium tetradecyl sulfate. Inspite of these treatments, recurrence is notinfrequent. So, in some case re-excision may benecessary. It should be emphasized that one ofthe most important point about pyogenic granulomais the effect of sex hormonal imbalances duringpregnancy and the body’s over zealous response toirritants. Although it is rarely seen in children, it issome times seen in these individuals also

References

1. Ramirez. K, Bruce G: carpenter. pyogenicgranuloma: case report in a 9-year old girl.General Dentistry 2002, 50(3):280-1.

2. Nevile BW, Damm DD, Allen CM, BouquotJE: oral and maxillofacial pathology. Secondedition. W.B. saunders co; 2004:444-449.

3. Svirsky J: Oral pyogenic Granuloma.[http://emedicine.medscape.com/article/1077040-overview] webcite 2007. (10 pages), web medAccessed Mar 10, 2007

4. karthikeya Patil, mahima VG, Lahari K:Exragingival pyogenic granuloma. Indianjournal of dental research 2006, 17(4):199-202.

5. Regezi JA, sciubba , James J, Jordan RichorsCK: Oral Pathology, clinical pathologiccorrelation. Fourth edition. Sanders Company;2003:115-76.

6. Akyol MU, Yalciner EG, Dolan AI: Pyogenicgranuloma (lobular capillary hemangioma) ofthe tongue. Int J Pediatr Otorhinolaryngol2001, 58(3):239-241.

7. Glorgi VD, sestini S, Nardini p, cali p: A 42-year – old man with a rapidly growing lesionof the soft palate. CMAJ 2005, 173(4):367.

8. Greenberg MS, Glick M: Burket’s oralmedicine Diagnosis & treatment. Tenthedition. B C Decker inc; 2003:141-142.

9. Cawson RA, Odell EW: Cawson’s essentialsof oral pathology and medicine. 7th edition.Churchill Livingston; 2002:277

10. Mueller BU, Mulliken JB. The infant with avascular tumor. Semin Perinatol. 1999;23:332-340.

11. Mills SE, Cooper PH, Fechner RE: Lobularcapillary hemangioma: the underlying lesionof pyogenic granuloma: a study of 73 casesfrom the oral and nasal mucous membranes.Am J Surg Pathol. 1980;4:470-479.

12. Isaacs H Jr. Tumors of the Fetus andNewborn. Vol 35. Philadelphia, Pa: WBSaunders Co; 1997.

13. Dilley DC, Siegel MA, Budnick S. Diagnosingand treating common oral pathologies. PediatrClin North Am.1991;38:1227-1264.

14. Sato M, Tanaka N, Sato T, Amagasa T. Oraland maxillofacial tumours in children: a review.Br J Oral Maxillofac Surg. 1997;35:92-95.

15. Kershisnik M, Batsakis JG, MacKay B.Pathology consultation: granular cell tumors.Ann Otol Rhinol Laryngol. 1994;103:416-419.



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The myth and reality of “ The Free Fibula”Mathew.P.Varghese1, Surej Kumar LK2, Suvy Manuel3, Nikhil Mathew Kurien3, Sherin.A.Khalam4.

CASE REPORT

Introduction

Over the past few decades, the use ofreconstructive plates alone for the reconstructionof large mandibular defects has almost completelybeen replaced by osseous microsurgical free flaps,such as the fibula flap, iliac crest, and scapula freeflap. Such reconstructive options have improvedthe functional and cosmetic outcomes afterreconstruction of extensive mandibular defects.In 1973, the fibula transfer was developedsimultaneously by O’Brien1 in Australia and Ueba2

in Japan and was first published by Taylor et al 3

from Melbourne in 1975 & Gilbert4 in 1979. Theosteocutaneous tissue transfer from the calf regionwas first described by Chen & Yan5 in 1983.Hidalgo6 popularised the technique and the flapcame into widespread use for mandible

microsurgical reconstruction. Since then, severalrefinements for flap harvesting and insetting hasbeen described for meeting better aesthetic andfunctional demands.

Free fibula graft allows for adequate prostheticrehabilitation of the patient through implants andthus has greatly enhanced masticatory and speechfunctions of patients with mandibular defects.This flap has thus emerged as the workhorse formicrosurgical mandibular reconstruction7,8.

Case report

We report a case of reconstruction of a segmentaldefect of the mandibular body using free fibula flap.The patient reported with a swelling on the rightmandibular body which was investigated anddiagnosed to be ameloblastoma. The patientunderwent segmental resection of the rightmandibular body and reconstruction with a plateat our centre. Due to certain technical constraintswe were not able to rehabilitate with a free flap atthe time. Three years later the patient reported withpain and swelling, which was investigated to reveala fractured reconstruction plate. We then decidedon rehabilitation with a free fibula flap. A free

1. Junior Resident2. Prof & HOD3. Reader4. Senior Lecturer

Division of OMFS, PMS College of Dental Science &Research, Vattappara, Trivandrum.

Adress for correspondence :Dr Suraj Kumar L.K.Prof. & HoD, Dept. of OMFS, PMS College of Dental Science &Research, Vattappara, Trivandrum

Varghese MP , Kumar LKS, Manuel S, Kurien NM, Khalam SA

Abstract

Segmental resection of the mandible may cause considerable functional, esthetic, and social problems.Immediate reconstruction of the mandible is, therefore, preferred, with the aim to achieve restorationof function and esthetics. Over the past decade, the use of reconstructive plates alone for thereconstruction of large mandible defects has essentially been replaced by the use of osseous microsurgicalfree flaps, of which the free fibula flap has emerged as the primary choice among surgeons. The freefibula flap has improved the functional and cosmetic outcomes after reconstruction of extensive mandibledefects. I present a case of free fibula microvascular flap transfer for reconstruction of the mandible.

Keywords : Free Fibula flap, mandibular defects.

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Figure - 8 OPG showing flap in place

Figure - 1 OPG revealing the initial lesion - ameloblastomaof right mandibular body

Figure - 2 Intraoperative view of the lesion

Figure - 3 Segmental resection of the mandibular body done

Figure - 4 Post operative OPG showing reconstruction plate in place

Figure - 5 OPG showing fractured reconstruction plate

Figure - 6 Harvested Free fibula free flap

Figure - 7 Free fibula fixed with plates


fibula transfer was planned and executed andadequate results were achieved using the procedure.

The prosthetic rehabilitation of the patient is beingplanned currently.

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Figure - 9 One month postoperative review

Figure - 10 One month postoperative review

Discussion

There are wide varieties of mandibulardefects and no single type of free flap is capableof meeting the demands of all the defects. Thechoice of flap depends on several factors includingthe type of bone and soft tissue (skin and/or oral)defect, vessel geometry of the donor and recipientsites, donor site morbidity, whether the patient isdentate or edentulous, need for dental implantrehabilitation, and often the type of training andindividual preference of the surgical team9.

The fibula free flap remains the first choice for theedentulous mandibles or for extensive mandibularresections 9. Blood supply to the fibula is bothintraosseous and segmental which allows multipleosteotomies to be made. This free flap can provideup to 30cm of bone length which is sufficient forreconstructing any length of the mandible. Theheight of bone often becomes inadequate relativeto a dentate mandible which may become aproblem when dental implants are planned for

prosthetic rehabilitation. This problem may beovercome by the use of a ‘double barrel’ flap10 ora vertical distraction of the fibular flap11. Donorsite morbidity often is relatively mild but pre-existing peripheral vascular disease may precludeuse of this flap.

Ghara et al12 have summarized, the potentialadvantages of the fibula flap, as follows:1. Straight shape and high mechanical resistance

to pressure and torsion2. Rapid incorporation and healing of the highly

vital flap due to the excellent perfusion,3. Composition - with a high content of cortical

bone,4. Great length, which allows the bridging of large

defects,5. Possibility of osteotomizing it at various points

allowing adaptation6. Relatively simple harvesting of the flap with

conveniently sized blood vessels foranastomoses

7. Low morbidity of the donor region

8. Can be elevated with skin and muscle asan osteomyocutaneous flap Ferri etal13 have listedseveral limitations in using the fibula flap. Whenbone modelling is required, and achieved by oneor more osteotomies, there is destruction of thecentromedullary fibular pedicle. Although manyauthors consider periosteal vascularisationadequate, Ferri etal found that a large number ofosteotomies of the fibular diaphysis led to reducedvitality of distal fragments, especially in cases ofsmall fragments. This risk is greater the smallerthe fragment. For this reason, we attempt to limitthe number of osteotomies of the fibula to amaximum of two. This problem is not seen withthe other bone flaps, which can be modelledwithout risk. Aesthetic sequele can sometimes beimportant, especially in women. A scar may runalong the entire length of the lateral part of theleg, which many may consider as unsightly.

The fibula flap procedure is not be used inpatients with ischemic disease involving the lowerlimbs. In patients with arteritis, the fibular artery isoften the lone remaining permeable vascularising


22


vessel in the lower limb. Arteriosclerotic diseaseinvolving the fibular artery does not allow for goodvascularisation and can lead to even failure of theflap. .

Another limitation of the fibula flap is thesmall length of its pedicle, which makes it difficultto perform anastomoses. When the entire fibula isremoved, no more than 5 cm is available, comparedwith 10 cm for iliac crest, lateral brachialis, andparascapular flaps. When a considerable quantityof soft tissue is to be reconstructed, the skin paddleof the fibula flap often becomes inadequatebecause of its limited thickness.

For our case, careful treatment planning andmethodical execution as per planned was adheredto, throughout the procedure. We did not wish tocompromise the vasculature by osteotomising thefibula for use of a double barrel, as adequate resultswere achieved by the procedure alone. At the timeof preparation of this article, prostheticrehabilitation of the patient is being planned,which will thus add to the benefit the patient,functionally.

Conclusion

The free fibula flap does have its advantagesand limitations, but the fact that, it is one of themost versatile and reliable option for microsurgicalreconstruction of large mandibular defects; iswithout question. It provides a large quantity ofbone, which can be shaped easily to adapt to theremaining mandible passively. The bone height isadequate for implant-based prostheticrehabilitation. Preoperative mapping of thecutaneous perforators help in improving theversatility of the flap design, thereby decreasingthe donor site morbidity.

While opting for free flaps, one should bearin mind that most patients with head and necktumours often have medical co morbidities. Aproper and critical preoperative assessment of therisk of postoperative complications is essentialbefore such patients are selected for extensiveoncological and reconstructive surgery. The freefibula is the ideal tool for a good surgeon wantingto put a smile back onto the faces of his patients.

References

1. O’Brien BMcC, Morrison WA. Reconstructivemicrosurgery. New York: ChurchillLivingstone, 1987

2. Ueba Y, Fujikawa S; Nine years follow up ofa free vascularised fibula graft inneurofibromatosis -a case report and literaturereview. J Orthop Trauma Surg 1983:26: 595-600.

3. Taylor GI, Miller DH, Ham FJ: The freevascularised bone graft: A clinical extensionof microvascular techniques. Plast ReconstrSurg 55:533, 1975

4. Gilbert A: Vascularised transfer of the fibularshaft. Int J Microsurg 1:100, 1979

5. Chen ZW, Yan W The study and clinicalapplication of the osteocutaneous flap offibula. Microsurgery 1983: 4: 11-6.

6. Hidalgo A: Fibula free flap: A new method ofmandible reconstruction. Plast Reconstr Surg84:71, 1989

7. P. Sieg, A. Hasse, C E. Zimmermann.Versatility of vascularised fibula and softtissue graft in the reconstruction of themandibulofacial region. Int. J. Oral Maxillofac.Surg. 1999; 28.” 356-361.

8. López-Arcas JM, Arias J, Del Castillo JL,Burgueño M, Navarro I, Morán MJ, ChamorroM, Martorell V. The FibulaOsteomyocutaneous Flap for MandibleReconstruction: A 15-Year Experience. J OralMaxillofac Surg 68:2377-2384, 2010

9. TinGoh B, Lee S,Tideman H, Stoelinga PJW:Mandibular reconstruction in adults: a review.Int. J. Oral Maxillofac. Surg. 2008; 37: 597–605

10. Horiuchi K, Hattori A, Inada I, KamibayashiT, Sugimura M, Yajima H, Tamai S.Mandibular reconstruction using the doublebarrel fibular graft. Microsurgery 1995: 16:450–45.


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11. Nocini PF, Wangerin K, Albanese M,Kretschmer W, Cortelazzi R. Verticaldistraction of a free vascularised fibula flapin a reconstructed hemi mandible: a casereport. J Craniomaxillofac Surg 2000: 28:20–24.

12. Ghara A, Darwich K, Li L, et al: Long-termresults of jaw reconstruction withmicrosurgical fibula grafts and dental implants.J Oral Maxillofac Surg 65:1005, 2007.



13. Advantages and Limitations of the Fibula FreeFlap in Mandibular Reconstruction. Ferri J,Piot B, Ruhin B, Mercier J. J Oral MaxillofacSurg 55440-448, 1997.

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Emotional woes : A strain to the periodontiumAnju Samuel1, Nithin Mathew Cherian2

CASE REPORT

Birth of stress

Stress has become such an ingrained part ofour vocabulary and daily existence, that it is difficultto believe that our current use of the termoriginated only a little more than 50 years ago, whenit was essentially “coined” by Hans Selye. Selyeobserved that patients suffering from differentdiseases often exhibited identical signs andsymptoms. They just “looked sick”. Thisobservation may have been the first step in hisrecognition of “stress”1.

Psychological disturbances can lead patientsto neglect oral hygiene with resultant unfavorableeffects on the periodontal tissues. The associationof stress with periodontal disease is difficult toprove as there are many factors influencing theincidence and severity of periodontal disease, someof which are assumed and have not been identified.Nevertheless, more recent studies indicate thatpsychosocial stress represents a risk indicator for

periodontal disease and should be addressed beforeand during the treatment2.

Definition of stress and stressor

The term stress is used loosely, in laymanterms, to describe adverse emotions or reactionsto unpleasant experiences. However, the termstress has a precise physiological definition. It is“a state of physiological or psychological straincaused by adverse stimuli, physical, mental, oremotional, internal or external, that tend to disturbthe functioning of an organism and which theorganism naturally desires to avoid”. Thus,stresscan be viewed as a process with both psychologicaland physiological components3.

A stressor is any stimulus, situation or circumstancewith the potential to induce stress reactions3.

Pathophysiology of the stress response

In response to a variety of stressful stimuli,an elegant sequence of events is initiated.Activation of the hypothalamic–pituitary–adrenalaxis by stress results in the release of an increasedconcentration of corticotropin-releasing hormonefrom the hypothalamus. The pituitary gland isconnected to the hypothalamus by theinfundibulum, a stalk of tissue that contains nervefibersand small blood vessels. Corticotropin-releasing hormone, in turn, acts on theanteriorpituitary, resulting in the release ofadrenocorticotropic hormone (corticotropin). The

1. Senior Lecturer, Dept: of Periodontology &Implantology,ST.Gregorios Dental College, Kothamangalam, ErnakulamDistrict, India.

2. Senior Lecturer, Dept: Of OMFS, Mar Baselios Dental College,Kothamangalam, Ernakulam District, India.

Adress for correspondence :Dr. Anju Samuel, MDSSenior Lecturer, Dept: of Periodontology &Implantology,ST.Gregorios Dental College, Kothamangalam,Ernakulam District, India.Email: [email protected]

Samuel A, Cherian N M

Abstract

Stress poses as a health risk to all individuals in day today life. It affects the immune and inflammatoryresponses. They have got an impact on oral diseases, wound healing and alter the management ofperiodontal diseases.

Keywords : Stress, Perodontal disease

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adrenocorticotropic hormone then acts on theadrenal cortex and causes the production andrelease of glucocorticoid hormones into thecirculation. The glucocorticoids then produce amyriad of effects throughout the body, such assuppressing the inflammatory response, modifyingcytokine profiles, elevating blood glucose levels,and altering levels of certain growth factors .Importantly, it has been established thatproinflammatory cytokines, such as interleukin-1,can also activate the hypothalamic–pituitary–adrenal axis, leading to a feedback loop . Immunefunction plays a critical role early in the woundhealing cascade. Pro-inflammatory cytokines, suchas interleukin-1 and tumor necrosis factor, are justtwo of the essential cytokines in this regard. It hasbeen speculated that success in the later stages ofhealing is critically dependent on these earlyevents3.

The second major pathway to be activatedis thesympathetic nervous system. A well-knownexampleof this is the so-called flight or Figurehtresponse to potentially harmful stimuli. Stressactivates the nerve fibers of the autonomic nervoussystem, which innervate the tissues of the immunesystem. The adrenal medulla is actually a modifiedsympathetic ganglion. Its nerve bodies, instead ofpossessing axons, secrete their products directlyinto the bloodstream. The release ofcatecholamines results in the hormonal secretionof norepinephrine and epinephrine from theadrenal medulla, which results in a range of effectsthat may act to modulate immune responses.Catecholamines, released during stress, contributeto the development of hyperglycemia by directlystimulating glucose production and interfering withthe tissue disposal of glucose . In addition, thesympathetic nervous system has a role in regulatingimmune cell activities3.

Cases for PeriodontalDestruction Due to Stress

Neglect of oral hygiene

It is obvious that proper oral hygiene is partiallydependent on the mental health status of thepatient. It has been reported that psychological

disturbances can lead patients to neglect oralhygiene and that the resultant accumulation ofplaque is detrimental to the periodontal tissue.Academic stress was reported as a risk factor forgingival inflammation with increasing crevicularinterleukin-b levels and a diminution of quality oforal hygiene.

Changes in dietary intake

Emotional conditions are thought to modifydietary intake, thus indirectly affecting periodontalstatus. Psychological factors affect the choice offoods, the physical consistency of the diet, and thequantities of food eaten. This can involve, forinstance, the consumption of excessive quantitiesof refined carbohydrates and softer diets requiringless vigorous mastication and thereforepredisposing to plaque accumulation at theapproximal risk site.

Smoking and other harmful habits

Circulating nicotine results in (i)vasoconstriction, produced by the release ofadrenaline and noradrenaline, which is supposedto result in a lack of nutrients for the periodontaltissue; (ii) suppression of in vitro secondaryantibody responses and (iii) inhibition of oralneutrophil function.

Gingival circulation

The tonus of the smooth muscle of bloodvessels may be altered by the emotions by way ofthe autonomic nervous system. Furthermore, inlong or continued emotions, a constant constrictionof blood vessels could alter the supply of oxygenand nutrients to the tissues.

Alteration in salivary flow and components

It is assumed that both increase and decreasein salivary flow, induced by emotional disturbance,may affect the periodontium adversely. Emotionaldistress may also produce changes in saliva pH andchemical composition like IgA secretion. Theserelationships between salivary physiology andpsychological status do not necessarily demonstratecausation of periodontal disease, but they show apathway in which periodontal health is influencedby salivary changes.


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Oral habits

Neurotic needs find oral expression. The mouthmay be used to obtain satisfaction, to expressdependency or hostility, and to inflict or receivepain. Sucking, biting, sensing, and feeling maybecome habitual as in thumb sucking, tonguethrusting, infantile swallowing, and biting oftongue, lip, cheek or fingernail. These actions alsoFigure in bruxing, clenching, tooth doodling, andsmoking. Such habits may lead to tooth migration,occlusal traumatism, and occlusal wear.

Lowered host resistance

Under stress, the release of adrenaline andnoradrenaline may not only induce a decrease inblood flow, but possibly also in those bloodelements necessary for maintaining resistance todisease-related microbes. It may be thatglucocortiocoids, released during the stress prolongthis vascular response.

Bruxism

Evaluations from psychometric and healthinventories suggest that stress bruxists have moremuscular symptoms and seemed more emotionallydisturbed. Bruxism has been considered ofetiological importance in chronic inflammatoryperiodontal disease. However, it is difficult to findscientific evidence to substantiate this claim, whichseems to be basically supported only by clinicalobservations.

Clinical Implications

1. Studies have demonstrated that individualsunder psychological stress are more likelytodevelop clinical attachment loss and loss ofalveolar bone.One possible link in this regardmay be increases in production of IL-6 inresponse toincreased psychological stress.Perhaps the relationship is simply due to thefact that individuals under stress areless likelyto perform regular good oral hygiene andprophylaxis4.

2. Recent studies were well-designed and confirmpositive correlations between stress, depressionand periodontal disease by demonstratingconvincing linkages between depression and

tooth loss; stress and attachment loss; stress/depression and neglect of oral hygiene; andelevated cortisol levels and pocket depth/toothloss.These studies firmly support both thebiological and behavioural mechanisms for thisperio–systemic connection. These findingshave important clinical implications becausethey suggest that addressing psychologicalfactors such as stress and depressionrepresents an important part of overallpreventive periodontal maintenance and, moreimportantly, may also prevent oralinflammation from developing into systemicinflammation in susceptible individuals. Thesimple stress profile and depression scale usedin one recent study4 provides information onthe psychological status of a patient (stresslevels related to employment, domestic andhealth environments; attitudes and personalitytraits related to relaxation, anxiety, hostility,obsessive compulsiveness and positive/negative perceptions of life events) and maybe valuable tools in a modern periodontalpractice that emphasizes individualizeddiagnosis, treatment planning andmaintenance5.

3. Studies conducted by RadafsharG,Zarabi.H,on relationship of stress and coping styles toperiodontal disease;a case control study cameto a conclusion that psychological stressassociated with various ife events is asignificant risk indicator for periodontaldisease6.

References

1. Paul J. Rosch, M.D., F.A.C.P. Reminiscencesof Hans Selye, and the birth of “Stress”. TheAmerican Institue of Stress.

2. Sachin Goyal, GarimaGupta,Betsy Thomas, K.M. Bhat, and G. S. Bhat.Stress and periodontaldisease: The link and logic!! . Ind Psychiatry J.2013 Jan-Jun; 22(1): 4–11

3. Lakshmi Boyapati & Hom-Lay Wang. The roleof stress in periodontal disease and woundhealing.Periodontology 2000, Vol. 44, 2007,195–210.


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4. Matthew Locke Consultant in RestorativeDentistryCardiff University School ofDentistry. Periodontal Disease Risk Factors

5. Relationship Between Stress, Depression andPeriodontal Disease; Anthony M. Iacopino,DMD, PhD; JCDA, June 2009, Vol. 75, No. 5

6. Radafshar G., Zarrabi H., Jalayer S.Relationships of Stress and Coping Styles to



Periodontal Disease: A Case-Control Study. JDent Shiraz Univ Med Scien 2012; 13(4): 169-175

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Zygomatic implants - A case report with review of literatureSherin.A.Khalam1, Surej Kumar L K2, Nikhil Mathew Kurien3, Kannan Venu Gopal4

CASE REPORT

Introduction

Introduced by Brånemark in 1988, zygomaticimplants were designed to rehabilitate atrophicupper maxilla, or upper jaws subjected to resectionfor oncological reasons or with bone loss secondaryto trauma. Their use has made it possible to reducebone grafting procedures in patients seeking apermanent solution with a minimum number ofsurgical operations and the shortest treatment timepossible - without losing the expectations forsuccessful treatment.The insertion of standarddental implants and the preparation of a prosthesisare limited in patients with atrophic upper jaws,due to the limited amount and quality of theavailable bone, as well as because of the presenceof highly pneumatized maxillary sinuses. In thesecases it is necessary to resort to advanced bone graft

1. Senior Lecturer2. Prof& HOD3. Reader4. Junior ResidentPMS College Of Dental Science & Research, Golden HillsVattappara, Trivandrum, India.

Adress For CorrespondenceDr.Sherin.A.Khalam, MSc(PSY), MDS (OMFS), FICOIPMS College Of Dental Science & Research,Golden Hills Vattappara, Trivandrum, India.

Khalam SA, Kumar SLK, Kurien NM, Gopal KV

surgery, such as the bloc iliac crest Le Fort Iosteotomy, onlay-type bone grafting techniques, ormaxillary sinus lift procedures in the posteriorsectors of the maxilla1-4. These techniques pose aseries of inconveniences, such as the need formultiple surgical interventions, the use of extraoralbone donor sites (e.g., iliac crest or skull) - withthe morbidity involved in surgery of these zones -and the long time for which patients remainwithout rehabilitation during the graftconsolidation and healing interval5. These factorscomplicate patient acceptance of the restorativetreatment and limit the number of procedurescarried out. Zygomatic implants are an effectivetreatment alternative that reduces the use of bonegraft procedures, employing the zygomatic boneas anchorage. When contemplating zygomaticimplant rehabilitation, the patient must present notonly posterior alveolar crest reabsorptionprecluding the placement of additional fixationsfor supporting the prosthesis, but also sufficientbone volume in the anterior zone of the upper jaw- with a minimum height of 10 mm and a width of4 mm - to allow the placement of 2-4 conventionalfixations. If the bone volume in the anterior uppermaxillary zone is insufficient, there must be ideal

Abstract

Zygomatic implants are a good rehabilitation alternative for upper maxilla with severe bonereabsorption.These implants reduce the need for onlay-type bone grafting in the posterior sectors andfor maxillary sinuslift procedures - limiting the use of bone grafts to the anterior zone of the upper jawin those cases where grafting isconsidered necessary. Zygomatic implants are designed for use incompromised upper maxilla. They allow theclinician to shorten the treatment time, affording an interestingalternative for fixed prosthetic rehabilitation. Thisstudy confirms that zygomatic bone offers predictableanchorage and acceptable support function for prostheses in atrophic jaws. However, these implants arenot without complications. Longer-term evaluations are needed of zygomatic implant survival in orderto establish a correct clinical prognosis.

Key words: Zygomatic implants, atrophic upper maxilla, edentulism, dental implants.

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Journal of MaxilloFacial Science & Research - 2014, Volume-1, Issue-1 Khalam SA, Kumar SLK, Kurien NM, Gopal KV

conditions for onlay-type bone grafting and guidedbone regeneration (GBR) techniques.Differenttherapeutic options are available for therehabilitation of atrophic upper maxilla6-12.Maxillary sinus lift procedures are accepted and arepredictable for implant placement. In order to applythis technique, a bone donor site must be available.This site can be intraoral (chin, ascendingmandibular ramus, retromolar trigone, etc.) orextraoral (iliac crest, skull, tibia, etc.), dependingon the size of the maxillary sinus and on whethersinus lifting is to be uni- or bilateral.

Description of the zygomatic implant

The zygomatic implants (Figure. 1) are self-tappingscrews in c.p. titanium with a well-defined machinedsurface. They are available in eight different lengthsranging from 30 to 52.5 mm. They present a unique458 angulated head to compensate for theangulation between the zygoma and the maxilla.The portion that engages the zygoma has a diameterof 4.0 mm, and the portion that engages the residualmaxillary alveolar process a diameter of 4.5 mm.At the maxillary level the angulated implantplatform extremity offers the possibility to screwany kind of abutmentfrom the Brainemark system1.However, for the newest generation of abutmentsa separate slightly shorter abutment screw must beutilized for the construction of conventionalscrewed prosthesis.

Figure 1. Zygoma implant ® (Nobel Biocare, Götenborg, Sweden).

Case report

A 45 year old male patient reported with atrophicmaxilla and partially edentulous area in relation to35, 36 and 37 region. Due to severe ridge resorptionauthors planned for zygomatic implants in maxillaunder general anaesthesia.

Surgical procedure

The zygomatic implant surgical procedure shouldinvolve atraumatic surgery, avoiding overheatingin the zygoma bone as well as in the maxilla understerile circumstances with what is in reality still atwo-stage approach. Although the operation can

be carried out underlocal anesthesia, for thepatient’s comfort, it has beendone up to now undertotal anesthesia or neuroleptic deconnection13.After a palatal incision of the soft tissue along theentire maxillary crest, the soft tissue is completelyreflected from maxillary crest to zygomatic buttressand the suborbital nerve identified. A window isthen made by drilling at the upperlimit betweenthe zygoma and the sinus to determine theorientation of the zygoma and to reflect theSchneidarian membrane. This window will also behelpful during the surgical procedure

for cooling the drills to avoid overheating . Differentdrills are used with increasing diameters

ending with the insertion at low speed of theself-tapping zygomatic implant. Thelength of thisis carefully chosen by means of a special gauge.After insertion of the implant, a cover screw isplaced on the top of the zygomatic implant andthe soft tissue closed. There are no evidence-basedarguments that advocate the use of a membraneto cover the hole made in the sinus. The otherimplants are placed during the same surgicalprocedure. At the second stage surgery 6 monthslater, the abutments are screwed on the implantsand an immediate (same day) provisional prosthesisis provided for the patient.

Prosthetic procedure

The prosthesis is made of gold and acrylic or goldand porcelain routinely like a standard screwedreconstruction on standard implants. Althoughscrewed bridges allow a better adjustment of theocclusion, overdentures retained by rigid bars arealso considered sometimes because of theimportant cantilever due to the palatal emergenceof the zygomaticimplants and to the distancebetween the two maxillas or simply the resorptionof the maxilla. Considering the biomechanicalaspects of the prosthetic reconstructions onzygomatic implants, it is well known that whenmasticatory load is applied to a rigid semicirculararch connectingfour anterior implants and twozygomatic ones, the masticatory load in theposterior region is transferred to the bony supportsituated in the zygoma. Occlusal view of a bridgemade of gold and porcelain on topof twozygomatic implants and four standard implants.

30


Figure-2. Postoperative panoramic X-ray viewof rehabilitation withtwo zygomatic implants and three standard implants in the anteriorzone of the upper maxilla.

Review of literature

Depending on the remnant bone volumeand quality as established by the classification ofLekholm and Zarb 1985(7), maxillary sinus lift andimplant placement are carried out in one or twophases.When the bone height is insufficient tosecure the necessary primary implant stability (type4 bone with type D or Ereabsorption), bonegrafting is performed in a first phase, followed 6months later by implant placement(2). Lekholm etal.(8)conducted a multicenter retrospectivestudywith a follow-up period of three years, involving150 patients with edentulous upper jaws that weretreated with different bone grafting techniques(onlay, inlay, or using the Le fort I osteotomy plusbone grafting). These authors reported a 23%failure rate when placing the implants in the samesurgical step as bone grafting, and a 10% failurerate when two surgical phases were used. Thesuccess rate of prosthetic rehabilitation in thepatients was 85%. Keller et al.(9) presented thelong-term results (with 12 years of follow-up)corresponding to 118 inlay autologous bone graftsplaced in the nasal and sinusal zones in patientswith compromised upper maxilla. The survival ratewas 87%, while the correct prosthetic function ratewas 95%. These procedures may require severalsurgical interventions, and the duration oftreatment associated with such bone graftingprocedures, plus the time needed to prepare thedefinitive dental rehabilitation, is considerable.Nevertheless, the end results usually offer highpercentage success rates. Zygomatic implants havebeen proposed to facilitate thetreatment of atrophicupper maxilla, since they reduce the need for arange of surgical interventions, and moreover

shorten the overall treatment time (10,11).Differentauthors (8-13) have described the use of zygomaticimplants for the functional and estheticreconstruction of palatal deformities, post-maxillectomy defects or other mutilating disorders,and in developmental anomalies of the craniofacialskeletal components (e.g., ectodermal dysplasia) -with satisfactory results in all cases.

Summary

The management of the posterior maxilla withimplant placement, including zygomatic implants,can be planned using the zones of available boneconcept as a guideline. The use of anteriortilted orposterior-tilted implants allows for stablishingposterior implant support for a fixed prosthesis. Theuse of 2 premaxillary implants in onjunction with2 posterior-tilted implants accomplishes thisobjective in a predictable manner. However, anyof the implants may fail, interfering with the abilityto continue use of the prosthesis. resented here isthe expanded use of the zygoma implant asa“rescue implant”. The removal of a failed implantis immediately replaced with a zygoma implant toreestablish support needed for continuation of theprosthesis. In cases of rare, usually unilateral sinusinfection associated with zygomatic implants, thephysiologic drainage of the osteomeatal complexmust evaluated and be attended to, including thepossible need for a FESS procedure.

Conclusion

The zygomatic implant – the zygomaticus fixture -appears to be a promising development in implanttechnology. It offers an interesting alternativesolution to heavy bone grafting in the severelyresorbed posterior maxilla. It has been in use formore than

10 years and gives a predictable outcome in therehabilitation of totally as well as partiallyedentulous patients. More published reports areneeded and more follow-up has to be provided toassess its final goal and predictability.

References

1. Aparicio C, Brainemark PI, Keller EK, Olive´J. Reconstruction of the premaxillawithautogenous iliac bone with


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osseointegrated implants. Int J Oral MaxillofacImplants 1993: 8:61–67.

2. Bahat O. Brainemark System Implants in theposterior maxilla:clinical study of 660 implantsfollowed for 5 to 12 years. Int J Oral MaxillofacImplants 2000: 15: 646–653.

3. Balshi TJ, Wolfinger GJ. Treatment ofcongenital ectodermal dysplasia withzygomatic implants: a case report. Int J OralMaxillofac Implants 2002; 17: 277–281.

4. Bedrossian E, Stupel L. Immediate stabilizationat stage II of zygomatic implants: rationale andtechnique. J Prosthet Dent 2001: 86: 10–14.

5. Bedrossian E, Stumpel L III, Beckely M,Indersano T. The zygomatic implant:preliminary data on treatment of severelyresorbed maxillae. A clinical report. Int J OralMaxillofac Implants 2002: 17: 861–865.

6. Bra°nemark PI. An experimental and clinicalstudy of osseointegrated implants penetratingthe nasal cavity and maxillary sinus. J OralMaxillofac Surg 1984: 42:497–505.

7. Carmagnola D, Berglund T, Araujo M,Albrektsson T, Lindhe J. Bone healing aroundimplants placed in a jaw defect augmented withBio-Oss. An experimental study in dogs. J ClinPeriodontol 2000: 27: 799–805.

8. Champy M, Lodde JP, Kahn JL Kielwasser P.Attempt at systematization in the treatmentof isolated fractures of the zygomatic bone:techniques and results. J Otolaryngol 1986: 39–43.

9. Esposito M, Grusovin MG, Worthington HV,Coulthard P. Interventions for replacingmissing teeth: bone augmentation techniquesfor dental implant treatment. CochraneDatabase Syst Rev. 2006 Jan25;(1)

10. Gosain AK, Song L, Capel CC, Corrao MA,Lim TH. Biomechanical and histologicalteration of facial recipient bone afterreconstruction with autogenous bone graftsand alloplastic implants: a 1-year study. PlastReconstr Surg 1998: 101: 1561–1571.

11. Higuchi KW. The zygomaticus fixture: analternative approach for implant anchorage inthe posterior maxilla. Ann R Australas CollDent Surg 2000: 15: 28–33.

12. Izzo SR, Berger JR, Joseph AC, Iazow SK.Reconstruction after total maxillectomy usingan implant-retained prosthesis: a case report.Int J Oral Maxillofac Implants 1994: 9: 593–595.

15. Kahnberg KE, Ekestubbe A, Gro¨ndahl K,Nilsson P, Hirsch JM. Sinuslifting procedure.I. One-stage surgery with bone transplant andimplants. Clin Oral Implants Res 2001: 12:479–487.

13. Langer B. What are the clinical limitations ofwide-diameter(4 mmor greater) rootformendosseous implants? Int J Oral MaxillofacImplants 2000: 15: 293–296.



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Intraoral nevi - A reviewResmi .K . Raman1, Nayana .S. Raj2, Anna P. Joseph3, Vinod Mony4, Bindu .J. Nair5

CASE REPORT

Introduction

Nevi are benignnon-neoplastic proliferations ofnevus cells within the epithelium or the connectivetissue and are categorized as hamartoma ordevelopmental malformation.1 The term “Nevus”is Latin for “maternal impression” or“birthmark.”2Most lesions are distributed above thewaist,with head and neck region being a commonsite of involvement.Although nevi are commonlesions that are seen on the skin in the large majorityof the population, they are rare intraorally.3 In 1943,Field and Ackermann reported the firstdocumented case of an intraoral nevus.Later Kinget al adopted the termintramucosal nevus.4

Pathologically oral nevi present asjunctional,compound, intramucosal or blue nevi.

Nevogenesis

The origin of nevus cells has been postulated tobe from cells that migrate from the neural crest to

1 - Post graduate student2 - Post graduate student3 - Reader4 - Senior Lecturer5 - Professor and Head Department, Dept. of Oral Pathology, PMS College of Dental Science &Research

Adress for correspondence :Resmi K. RamanPost graduate student, Dept. of Oral Pathology,PMS College of Dental Science &Research, Vattappara, India.

Raman RK, Raj NS , Joseph AP, Mony V, Nair BJ

the epithelium and dermis, or to be from alteredresident melanocytes.5 Nevus cellare large ovoid,rounded, or spindle shaped cells with palecytoplasm; and may contain granules of melaninpigment in their cytoplasm.4 The nevus progenitorcells are known as nevoblats.

Among the various theories of origin, Masson’stheory of dual origin of melanocytes was widelyaccepted. He believed that the nevus cells in theupper dermis developed from epidermalmelanocytes, whereas the nevus cells in the lowerdermis develop from schwann cells.TheAbtropfung hypothesis states that nevi arise fromproliferation of intraepidermal melanocytes withingrowth centers termed junctional nests or theques.An alternate hypothesis states that nevus cells arisefrom a pluripotential cell of nerve sheath origin.6

Abstract

Nevi are benign, non-neoplastic proliferations of nevus cells within the epithelium or theconnective tissue. Intraoral nevi are uncommon relative to those in the skin. The most common intraoral nevus is theintramucosal type characterized by a benign, unencapsulated proliferation of small,ovoid cells nevus cells organized into small, round aggregatescalled thèques. In this article we reviewthe pathogenesis, clinical features and histopathological features of intra oral nevi.

Key Words : Intraoral nevi, Melanocytic nevus, Theques, Blue nevus, Nevogenesis.

Table - 1 Classification

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Journal of MaxilloFacial Science & Research - 2014, Volume-1, Issue-1 Raman RK, Raj NS , Joseph AP, Mony V, Nair BJ

Current models of nevogenesispropose thatmelanocytic neoplasms arise from a single cell oforigin.One possibility is that an immaturemelanocytic stem cell serves as the nevusprogenitor cell, on acquiring mutations secondaryto UV light exposure or other mutagenicprocesses.Alternatively, the nevogenic mutationoccurs in a dierentiated melanocyte, with themutation causing the cell to regain proliferativecapacity.7

Melanocytic lesions follow a characteristic lifecyclethat consists of four stages: initiation,promotion, senescence,and involution. Initiationoccurs when a nevus progenitor cell acquires amutation. Promotion occurs when the mutated cellis activated and proliferation begins. After a periodof proliferation, nevi stop proliferating through theactivation of senescence pathways. This allowsthem to remain stable for extended periods of timebefore undergoing involution.7

Clinical Presentation

Most oral nevi are asymptomatic, and the lesionsare usually detected as an incidental finding onroutine dental examination.4The most commonmelanocytic nevi encountered in the oral cavity arethe intramucosal type (63%), followed by blue nevi(19%), compound nevi (9%), junction nevi (5%),and combined nevi (4%).8

Oral nevi are found in all races and more frequentlyin whites, in whom 55 percent of reported oral nevioccurred.4 Studies have revealed that oral mucosalnevi are slightly predominant in women rather thanmen,at a ratio of 1.5:1. The incidence of oral neviwas highest in patients aged 20-40 years, whoaccounted for almost one half of thepatients.8When seen intraorally they are mostcommonly observed on the hard palate.9

Melanocytic nevi can be brown, bluish-gray, oralmost black and occasionally non-pigmented. Itcan be congenital or acquired. Congenitalmelanocytic nevi sre classified into two typesaccording to their size: giant congenital melacyticnevi( also called as ‘ garment nevus’ , ‘bathingtrunk nevus’ or ‘ giant hairy nevus’ ) are greater 20cm in diameter and small congenital nevi, whichare usually less than 1.5 cm in their greatestdimension.1

Junctional nevi are dark brown in colour becausethe nevus cells proliferate at the tips of the retepegs, close to the surface. Intramucosal (Figure.1)and compound nevi are typically light brown domeshaped lesions.1

Blue nevus was first described by Tièche in 1906as small, sharply defined, blue to blue-black spotsmostly seen on the face and extremities11. Theyoccur almost equally among males and females8.Intraoral blue nevi (Figure 2) present asasymptomatic, slightly raised, blue-black, well-circumscribed lesions.The blue color of the nevusis due to the presence of melanin deep within thedermal melanocytes and the Tyndall effect. Mostblue nevi are present at an early age. The mostcommon location of the intraoral blue nevus is thehard palate10. Blue nevus is a frequent componentof a combined nevus and is usually associated withacommon compound or dermal nevus, or, muchless frequently, Spitz nevus.Sclerosing blue nevus,also known as a desmoplastic blue nevus, is animportant morphologic variant. Clinically, it

Figure 2. Blue nevus of hard palate

Figure 1. Intramucosal nevus on the gingiva

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Journal of MaxilloFacial Science & Research - 2014, Volume-1, Issue-1 Raman RK, Raj NS , Joseph AP, Mony V, Nair BJ

appears as a firm, solitary, variably pigmentedpapule or nodule.11

The cellular blue nevus, established as adistinct entity by Allen and Spitz et al presentsclinically as a firm bluish black to bluish gray dome-shaped nodule. Large, long-standing lesions candegenerate, ulcerate, and become painful.RareCBN can be unexpectedly amelanotic orhypomelanotic.The term atypical cellular blue nevushas been applied to rare lesions that show atypicalhistologic features and raise histologic differentialdiagnosis of malignant blue nevus.11

The Spitz nevus, also known as benign juvenilemelanoma or a nevus of epitheloid and spindlecells, was first described by Sophie Spitz in 19481and is most common in children andadolescents.12Other synonyms include juvenilemelanoma, Spitz tumor, nevus of large spindleand/or epithelioid cells, and spindle cell andepithelioid nevus.12,13A Spitz nevus can arise denovo or in association with an existing melanocyticnevus. 13They can present in three different ways:solitary nodular, multiple grouped, and multipledisseminated.The occurrence of the intra-oral Spitznevus is very rare.12

Halo nevus or Sutton’s nevus is a melanocytic nevustypically appear as a central pigmented papule ormacule surrounded by a pale hypopigmentedborderor “halo” of the surrounding epithelium. The halodevelopsapparently as a result of nevus celldestruction bythe immune system. It is mostcommon on the skin of the trunk during the seconddecade of life.6,14

The clinical differential diagnosis for oral neviinclude localized lesions such as amalgamtattoo,oral melanotic macule,melanoacanthoma,melanocytic hyperplasia, post inflammatoryhyperpigmentation, malignant melanoma anddiffuse lesions such as smoker’s melanosis, druginduced pigmentation and melasma. Oral nevi canalso be associated with certain syndromes like basalcell nevus syndrome, blue rubber bleb syndromeand B-K mole syndrome.

Histopathology

The melanocytic nevus is characterized by a benign,unencapsulated proliferation of small, ovoid cells

callednevus cells.A characteristic microscopicfeature is that the superficial nevus cellstend to beorganized into small, round aggregates(thèques).Melanocytic nevi are classifiedhistopathologically according to their stage ofdevelopment, which is reflected by the relationshipof the nevus cells to the surface epithelium andunderlying connective tissue.14Based on this oralnevi are classified asjunctional, compound andintramucosal nevi.

Injunctional nevus (Figure 3-a) there is proliferationnevus cell along the epithelial mesenchymaljunction.The zone of demarcation is absent andthe nevus cells contact and seem to blend into thesurface epithelium.15

Migration of nevus cells into the connective tissuecompartment is seen in compound nevus (Figure3-b). The cells cross the epithelialmesenchymaljunction and grow down into theconnective tissue- the so-called abtropfung or‘dropping of f ’ effect.15 In the intramucosal(intradermal) nevus (Figure3-c), the nevus cells aresituated within the connective tissue and areseparated from the overlying epithelium by a welldefined band of connective tissue.4

Histological variants of acquired melanocytic nevisuch as neural, balloon cell (Figure 4-b) and halonevi occur. Only the halo nevus isclinicopathologically distinctive. The neural andballoon cell nevi are histologic variants ofintradermal or compound nevi.4

Blue nevus is characterized by a variety ofhistologic subtypes, although most are classifiedas either “common”, “cellular” or combined.Thecommon blue nevus, which is the most frequentsubtype seen in the oral cavity is characterized byan intramucosal proliferation of elongated, bipolar,spindle-shaped melanocytes that are often grouped

Figure 3- a- Junctional nevus showing nevus cells within the base ofreteridges, b- Compound nevus showing theques in both epithelium andconnective tissue, c- Intramucosal nevus showing theques within theconnective tissue.

35


in short fascicles parallel arranged to the overlyingepithelium.In contrast, a cellular blue nevus isusually characterized by an intramucosal, nodularproliferation of dendritic spindle-shaped,pigmented melanocytes, in addition to tightly-packed aggregates of larger oval-to-roundmelanocytes with pale cytoplasm and little or nomelanin.16

Sclerosing blue nevus shows features typical bluenevi,but is associated with exaggerated dermalfibrosis.Amelanotic BN shows a dermalproliferation of spindle cells associated withvariably desmoplasticstroma. Diagnosis rests onobserving architectural features of BN, such asinverted wedge shape and extension into deepreticular dermis along adnexal structures.11

Depending on the location and the size of thecellular areas, cellular blue nevi have differentarchitectural outlines.Melanocytes forming thecellular areas of CBN show a characteristic ovalto spindle cells, with moderate amounts of clearor lightly pigmented cytoplasm. The nuclei areusually vesicular with finely stippled chromatin andinconspicuous nucleoli.In amelanocytic CBN,Cellular component is essentially indistinguishablefrom that of conventional CBN but lackspigmentation.Most malignant blue nevi arise inassociation with a preexisting benign BN orCBN.Atypicalcytologic features, abnormal mitosisand tumor necrosis have emerged as the featuresmost specific for malignant blue nevus.11

The spitznevus (spindle cell and or epitheloid cellnevus) is basically composed of pleomorphic cellsof three basic types: spindle cells, oval orepithelioid cells and both mononuclear andmultinucleated giant cells. These are arranged inwell circumscribed sheets and there is generallyconsiderable junctional activity.4

Histopathologically, a Spitz nevus is very similarto a melanoma due to the large size of the spindleor polygonal cells, frequently containingconsiderable cellular and nuclear pleomorphisms,the presence of inflammatory infiltrate, and, on thebase of the lesion, a diminished cell size and spreadamong the collagen fibers of the connective tissue.12

An atypical Spitz nevus shares histologic featureswith the classic Spitz nevus, but it may have oneor more atypical features, which can becharacteristic of malignancy. These includepleomorphism, increased cellularity, loss of cellularcohesion, epidermal pagetoid spread, high basalmitotic rate; pushing deep margins into the dermisand nests variable in size, shape, and orientation.17

Histopathologically, the halo nevus differs from theroutine acquired melanocytic nevus only inthepresence of an intense chronic inflammatory cellinfiltrate, which surrounds and infiltrates thenevuscell population.14

The special stains used for the demonstation ofnevus cells include Masson Fontana, Shmrol’sreaction, Churukian’sammonical silver method andDOPA reaction.Immunohistochemical markerssuch asHMB45 (Figure 5-a), S100 protien, MelanA, MiTF, Tyrosinase, PGP 9.5 and Neuron specificenolaseshows positivity for the nevus cells.

Treatment & Prognosis

Surgical excision is recommended for intraoral nevias a prophylactic measure becauseoral melanocyticnevi clinically can mimic an early melanoma.Recurrence is rare after surgical excision.4Congenitalnevi, cellular blue neviand junctional nevi havehighest chances for malignant transformation.Although transformation of oral pigmented nevito melanoma has not been well documented, it isbelieved that nevi represent precursor lesions tooral mucosal melanoma.1 Variation is symmetry,border,colour,diameter, evolving and elevation

Figure 5- a-HMB 45 positivity , b-S100 positivity in intraoral nevi

Figure 4- a- Epitheloid blue nevus, b-Balloon cell nevus


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(ABCDE rule) are considered as alarming orwarning signs of malignant transformation of nevi.

References

1. Sabrinath B, Sivapathasundharam B,GauravGhosh, Dhivy. Pigmentation:IJDA2009;1(1):38- 43.

2. Hiroshi Shimizu. Nevus and neurocutaneoussyndrome.In: Hifoshi Shimizu, Shimizu’sTextbook of dermatology. Nakayama:Hokkaido university press;2007.p-327-331.

3. V.T Beena, IshaChauhan R, Heera et al .Oralmelanotic nevi: a case report and review ofliterature. Oral & Maxillofacial PathologyJournal 2010.

4. Rajendran R. Benign and malignant tumors ofthe oral cavity. In: Rajendran R,Shivapathsundharam B, editors. Shafer’sTextbook Of Oral Pathology. 7th ed. Delhi:Reed elsevier; 2012.p.81-222.

5. Regezi, Sciubba, Jordan. Oral pathologyclinicopathological correlation. 6thed.

6. Elder DE, Elenitsas R, Johnson B, MurphyG, editors. Lever’s histopathology of theskin.9th ed. Philadelphia: JB Lippincott; 2005.

7. Andrew L. Ross,Margaret I. Sanchez et al.Molecular Nevogenesis. DermatologyResearch and Practice 1-9.

8. www.medscape.com.

9. Craig L. Hatch. Pigmented lesions of the oralcavity. Dental Clinics of North America2005;49(1):185-220.

10. JunuOjha, Jesse L. Akers, John O. Akers.Intraoral Cellular Blue Nevus: Report of aUnique Histopathologic Entity and Review ofthe Literature.Cutis 2007;80:189-192.

11. ArturZembowicz, Pushkar A. Phadke. BlueNevi and Variants- An Update . Arch PatholLab Med 2011; 135:327- 336.

12. Ruth Lopes, G Marcelo, C G Hébel et al.Intra-oral spitznaevus: a case report:Clinics2008;63(1):140-142.

13. Daryl J. Sulit, MD. Spitz nevus: DermatologyReview.com journal; june 2005;1-6.

14. C.Angela .Epithelial pathology.In: Neville,Damm, Allen, Bouquot. Oral andMaxillofacial pathology, 3rded.Saunders; p-362-452.

15. Surej Kumar L.K, Varun Menon . Oral Nevipresenting as a kissing lesion on Lip: A casereport .IOSR Journal of Dental and MedicalSciences 2013; 5(2): 16-18.

16. Rogério-Oliveira Gondak, Rogério da Silva-Jorge et al. Oral pigmented lesions:Clinicopathologic features and review of theliterature. Med Oral Patol Oral Cir Bucal.2012; 17 (6):919-924.

17. LT Daryl J. Classic and Atypical Spitz Nevi:Review of the LiteratureCuti .2007;79:141-146.



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Inclusion bodies : A significant clue in pathologic diagnosisSaira Elizabeth Denny1, Archana Nair1, T.T Sivakumar2, Varun B.R3, Bindu J Nair3

CASE REPORT

Introduction

Inclusion bodies are abnormal structures seen inhistopathology and haematology, which aids inarriving at proper diagnosis of certain pathologicconditions. They show peculiar morphologicalalterations giving rise to specific patterns andstaining characteristics which make them easy toidentify. These bodies can be aggregates ofproteins, viral, bacterial or fungal organisms, alteredcellular structure or calcifications which areidentified either intracellularly or extracellularly.Intracellular inclusion bodies can be seen either inthe cytoplasm, in the nucleus or in both.1 Theinclusion bodies seen in specific pathologicconditions are listed (Table I).

1. Inclusion bodies seen in infectious diseasesa. Viral infections: i) Intra cytoplasmic inclusionsNegri bodies

Negri bodies are intra cytoplasmic, eosinophilic,sharply outlined, pathognomonic inclusion bodies1. Postgraduate student2. Professor3. Senior lecturer4. Professor and HeadDepartment of Oral and Maxillofacial Pathology.PMS College of Dental Sciences and Research,Trivandrum.

Adress For CorrespondenceDr. Bindu J. NairProf. & HOD, Department of Oral and Maxillofacial PathologyPMS College of Dental Sciences and Research,Trivandrum.

Denny SE, Nair A, Sivakumar TT, Varun B.R, Nair BJ

found in certain nerve cells of the brain in patientsinfected with rabies. They are formed by theaccumulation of viral nucleoproteins and cellularorganelles and measure around 2–10 µm indiameter.2 These inclusion bodies were firstdetected by Adelchi Negri and reported it officiallyin 1903.3 Staining with Giemsa can differentiateNegri bodies from other intracellular inclusions bytheir characteristic magenta colour with dark-bluegranules.4 (Figure 1a)

Guarnier bodies

Guarnier bodies are intra cytoplasmic, round tooval, eosinophilic bodies, which was named afterthe Italian physician Giuseppe Guarnieri.5 They arelocated adjacent to the nucleus and appear as pinkblobs and are found in virtually all poxvirusinfections. They are formed by the aggregation ofviral particles.6 (Figure 1b)

Henderson Petterson bodies

Henderson–Patterson bodies, also calledMolluscum bodies(Figure 1c), are large, roundcytoplasmic inclusions, and is the characteristiccytologic feature of molluscum contagiosum.7,8

These bodies appear about 1-2 layers above thebasal cell layer of the epidermis as pink to redinclusions, in hematoxylin and eosin stain. Theyincrease in size as the infected cells move towardsthe surface. As it reaches the upper layers of theepidermis, it compresses the nucleus appearing as

Abstract

One of the specific and interesting features during histopathologic and hematologic analysis is theobservation of certain intracellular and extracellular structures, which show peculiar morphologic andstaining characteristics. These are called inclusion bodies, which can be aggregates of proteins, viral,bacterial or fungal organisms, altered cellular structure or calcifications. In this article we have discussedsome of the inclusion bodies seen in various pathologic conditions with their microscopic appearanceand staining characteristics.

Key words: Inclusion bodies, diagnosis, pathology

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Journal of MaxilloFacial Science & Research - 2014, Volume-1, Issue-1 Denny SE, Nair A, Sivakumar TT, Varun B.R, Nair BJ

a thin crescent at the periphery of the cell. At thegranular layer, the staining reaction of themolluscum body changes from eosinophilic tobasophilic.9 They are regarded as the cellularresponse to the presence of living foreign body.7,8

Ultrastructure shows each inclusion is composedof brick shaped viruses with dumbbell shapednucleoids surrounded by the amorphous layer ofcapsids.10

ii) Intra nuclear inclusion bodies

Cowdry type A and Cowdry type B bodies

Cowdry Type-A inclusion bodies are seen in viralinfections caused by herpes simplex virus andvaricella zoster virus. In routine histopathology,they appear as droplet-like masses of acidophilicmaterial surrounded by clear halos within nuclei,with margination of chromatin on the nuclearmembrane 1,11 measuring 3-8 micrometre indiameter.12 (Figure 1d)

PATHOLOGIC CONDITIONS INCLUSION BODIES

1. Infectious diseases:a. Viral infections.

b. Bacterial infections.

c. Fungal infections

2. Neoplasm.

3. Inflammatory conditions

4. Immune mediated disorders

5. Reactive lesions

6. Cystic lesions

7. Blood dyscrasias

i. Intra cytoplasmicNegri bodiesGuarnier bodiesHenderson Petterson bodies

ii. Intra nuclearCowdry type A bodiesCowdry type B bodiesMitosoid bodiesOwl’s eye bodies

iii. Both intra cytoplasmic and intra nuclearWarthin Finkeldey cellLeishman-Donovan bodiesBabes-Ernst bodiesDohle bodiesAsteroid bodies

Psammomatoid BodiesVerocay bodiesKamino BodiesWagner Meissner bodiesPustulo-ovoid bodies

Russel bodies

L E Body

Civatte and colloid bodiesToto bodiesRushton bodies

Basophilic stipplingsHowell jolly bodiesPappenheimer bodiesCabot ringsHeinz bodiesFessas bodies

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Cowdry Type-B inclusion bodies(Figure 1e) are theeosinophilic amorphous or droplet like bodiessurrounded by clear halo without any associatednuclear changes seen in adenovirus and poliovirusinfections.1,11

Mitosoid bodiesMitosoid bodies (mitosoid cells, mitosoid Figures)

are the hallmark of focal epithelial hyperplasia.These are cells in which the nucleus containsfragmented DNA and has coarsely clumpedheterochromatin, resembling a mitotic Figure.14

They are seen in the middle spinous layer of theepithelium.13(Figure 1f)

Owl’s eye inclusion bodies

Owl’s eye inclusion bodies(Figure 1g) are seen inhodgkin’s lymphoma and cytomegalo viralinfections. Cytomegalo virus causes cytopathiceffects in the affected cells thus giving rise tobasophilic nuclear inclusions. There is visiblemargination of the chromatin around the nuclearinclusion resulting in a halo effect or the owl’s eyeappearance.15

ii) Both Intracytoplasmic and Inranuclearinclusions

Warthin–Finkeldey cell

A Warthin–Finkeldey cell is a type ofmultinucleated giant cell found in hyperplasticlymph nodes. It is seen in the early course ofmeasles, HIV-infected individuals, Kimura disease,and rarely in a number of neoplastic (e.g.lymphoma) and non-neoplastic lymph nodedisorders. It consists of fused lymphocytes and canbe seen in a lymph node biopsy after a measlesvaccination.Under the light microscope, these cellsconsist of a large, grape-like cluster of nuclei. Thecharacteristic Warthin-Finkeldey syncytial giant cellmay have 50 nuclei, many with intra nuclearinclusions. Hyaline-like cytoplasmic inclusions mayalso be seen.16(Figure 1h)

b. Bacterial infections

Leishman-Donovan bodies

They are dull blue grey, small, round to ovalbodies(Figure 2a) of 2� 4 ìm in diameter withindistinct cytoplasm, round basophilic nucleus anda small, rod-shaped paranuclear kinetoplast seenin leishmaniasis.17 Leishman’s or Giemsa’s stainscan be used for the demonstration of these bodies.They are non flagellated form of the parasiticprotozoan Leishmania donovani and occur once theparasite has invaded the cells of the reticuloendothelial system.18

Babes-Ernst bodies

The cells of cornybacterium diphteriae containsgranules composed of polymetaphosphate. These

Figure 2. Bacterial inclusion bodies:a: Leishman-Donovan bodies,b: Babes-Ernst bodies, c: Dohle bodies

Figure 1.Viral inclusion bodies:a :Negri bodies, b: Guarnier bodies, c: Henderson Petterson bodies, d:Cowdry type A bodies, e: Cowdry type B bodies, f: Mitosoid bodies,g:Owl’s eye bodies, h: WarthinFinkeldey cell


Figure 3. Fungal inclusion bodies: Asteroid bodies

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granules when stained with loeffler’s methyleneblue, take up bluish purple colour, hence calledmetachromatic granules. They are called volutinor babes ernst granules(Figure 2b). They are oftensituated at the poles of the bacilli and are calledpolar bodies. Special stains such as Albert’s,Neisser’s and Ponder’s have been diviced fordemonstrating these granules clearly.19

Dohle bodies

Dohle bodies(Figure 2c) are small, one micron sizepale irregular light blue grey, basophilic, roundedoval or rod shaped structures seen chiefly in theperiphery of neutrophils in patients infected withinfections like tuberculosis, diphtheria, andtyphoid.6,4 These cells are seen in the peripheralblood smear and reflect the defective cellproduction and maturation of neutrophils. Specialstains like Leishman-Giemsa stain andRomanowsky stain can be used for thedemonstration of Dohle bodies.1

c. Fungal infections:

Asteroid bodies

Asteroid bodies(Figure 3), also known as cigarbodie appear as stellate inclusions with numerousrays radiating from the central core. They are foundin the disease sporotrichosis. 6,20

2. Inclusion bodies seen in neoplasms

Psammoma Bodies

Psammoma bodies are seen in numerous benignand malignat epithelial and connective tissuetumours. They are seen in psammomatoid juvenileossifying fibroma, psammomatoid melanoticschwannoma, cystadenocarcinoma andpsammomatoid meningoma. These bodies showsmineralized collagenous foci that vary from small,smoothly contoured round to oval patterns to largerirregularly shaped ossicles like pattern withconcentric layering similar to that of psammomabodies(Figure 4a). The ossicles are identified withinbony trabeculae as well as within the adjacentcellular stroma. The ossicles are rimmed by aprominent marginal osteoid and may also containosteocytes.21

Wagner Meissner bodies

Wagner Meissner bodies are oval aggregates ofeosinophilic globules. (Figure 4b) containingparallel slits and bordered by nuclei, observed

within the cellular sheets of neurofibroma.1,22,23.

These bodies are identical to the tactile corpuscle-like Meissner bodies

Kamino Bodies

Kamino bodies are eosinophilic hyaline globuleswith scalloped borders commonly located at thedermoepidermal junction.24 They are found to beassociated with Spitz nevus and pigmented spindlecell nevus. Kamino bodies(Figure 4c) are composedof laminin, fibronectin, type IV collagen and typeVII collagen and therefore, they give a positivereaction to periodic Acid- Schiff ’s and trichromestains.25

Pustulo-ovoid bodies of Milian

Figure 4. Inclusion bodies seen in neoplasms:a: Psammomatoid bodies, b:Kamino bodies, c:Wagner Meissner bodies,d:Pustulo-ovoid bodies.

Figure 5. Inclusion bodies seen in inflammatory conditions:

Russel bodies


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Pustulo-ovoid bodies (bangle bodies)26 are largeeosinophilic intra-cytoplasmic inclusionscomposed of coalescing granules, representinglysosomes and are surrounded by a clear halo(Figure4d). They are seen in granular cell tumour oftongue.6,27. These granules were diastase-resistantand PAS-positive.28

3. Inclusion bodies seen in inflammatoryconditions

Russell bodies

Russell bodies(Figure 5) are eosinophilic, large,homogenous immunoglobulin-containinginclusions usually found in a plasma cell undergoingexcessive synthesis of immunoglobulincharacteristized by distended endoplasmicreticulum. They are found in pathologic conditionssuch as plasmocytoma, multiple myeloma andrhinoscleroma.29 They measure about 20- 40 µm indiameter.6 They are named for William Russell(1852-1940), a Scottish Physician.30

4. Inclusion bodies seen in immune mediateddisorders

LE body

LE bodies(hematoxylin bodies) are seen in systemiclupus erythematosus. Immunologically this disease

is associated with an enormous array ofautoantibodies, classically including the antinuclearantibodies. The serum of the patient showsexposed nucleus of the damaged cell which reactwith ANAs resulting in the formation of ahomogenous mass of nuclear chromatin material.These appear as basophilic round bodies called theLE body or haematoxylin body. LE cell is aphagocytic leukocyte commonly PMNs andmacrophages which engulf the homogenousnuclear material of the injured cell 31,32,33(Figure 6a)

Civatte or Colloid bodies

Civatte or Colloid bodies are also called as Cytoid,Hyaline or Sabaroud bodies. These bodies arecharacteristic finding in skin lesions of patientswith various dermatoses, particularly lichen planus(LP) and discoid lupus erythematosus(DLE). Theyare generated by damaged basal keratinocytesthrough apoptotic cell death, consist largely ofkeratin intermediate filaments, and are almostinvariably covered with immunoglobulins, mainlyIgM. Citoid bodies appear as rounded, homogenous,eosinophilic masses on routine H and E staininglying in the deeper parts of epidermis/epitheliumand more frequently in dermis/connective tissue.They are known as Civatte bodies (in epithelium/epidermis) (Figure 6b), colloid bodies or hyalinebodies (in connective tissue) (Figure 6c). They are10-25 ìm in diameter and situated mostly withinor above the inflammatory cell infiltrate.34

5. Inclusion bodies seen in reactive lesions

Toto bodies

Toto bodies are homogeneous, eosinophilic poolsof material in the superficial spinous layer of thesurface epithelium. The epithelial cells of thegingiva in inflammatory fibrous hyperplasia (epulisfissuratum) exhibit mucopolysaccharide keratindystrophy which replaces individual cells. This isreferred to as plasma pooling and this alteredappearance is termed as toto bodies.1, 4(Figure 7)

6. Inclusion bodies seen in cystic lesions

Rushton bodies

Rushton bodies appear as eosinophilic, linear,straight or curved or hairpin shaped, circular orpolycyclic forms, often with a granular core andsometimes concentrically laminated(Figure 8).They occur almost exclusively within odontogeniccysts particularly radicular cyst, residual cyst and

Figure 6. Inclusion bodies seen in immune mediated disorders:a : LE bodies, b:Civatte bodies, c: Colloid bodies

Figure7. Inclusion bodies seen in reactive lesions: Toto bodies


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plexiform ameloblastoma and are found almostalways within the epithelial lining and only rarelyin the fibrous capsule. Electron microscopic studiesshow the lamellar variant to be composed ofalternating electron dense and electron lucentlayers, whereas the granular form consists ofamorphous material in which fragments of redblood cells are seen. They stain strongly withorcein, Mallory aldehyde fuschin, Papanicolaou andGomori.6,35

7. Inclusion bodies seen in blood discrasias:

Basophilic stipplings

Basophilic stipplings are round or irregularly shapedgranules of variable size seen in erythrocytes whenstained with giemsa.36 These stipplings representthe spontaneous aggregation of ribosomal RNAin the cytoplasm of erythrocytes.37 They arefrequent in anemias as a result of lead or otherheavy metals poisoning.36(Figure 9a)

Figure 8. Inclusion bodies seen in cystic lesions: Rushton bodies

Pappenheimer bodies

Pappenheimer bodies are abnormal granules of ironfound inside red blood cells on routine blood stain.They are a type of inclusion body formed byphagosomes that have engulfed excessive amountsof iron. They appear as dense, blue-purple granuleswithin the red blood cell and there is usually onlyone or two, located in the cell periphery. They areseen in iseases such as sideroblastic anemia,hemolytic anemia, and sickle cell disease .Pappenheimer bodies are visible with a Wright and/or Giemsa stain. Confirmation of non-heme ironin the granules is made with a Perls’ Prussian bluestain.38

Howell jolly bodies

Howell–Jolly bodies are small round basophilicinclusions that are nuclear remnants of DNA incirculating erythrocytes(Figure 9b). Duringmaturation in the bone marrow erythrocytesnormally expel their nuclei, but in some cases asmall portion of DNA remains. Its presence usuallysignifies a damaged spleen. It is named for WilliamHenry Howell and Justin Marie Jolly. They are veryrarely seen in normal people but common after theremoval of the spleen, in some haemolytic anemiasand in megaloblastic anemia.39

Figure 9. Inclusion bodies seen in blood dyscrasias: a : Basophilicstippling, b: Howell jolly bodies, c: Cabot rings, d: Heinz bodies

Figure 10. Inclusion bodies seen in granulomatous diseases:a :Schaumann bodies, b: Hamazaki-wesenberg bodies, c: Lafora bodies

Figure 11. Inclusion bodies seen in foreign body reactions: Parent bodies


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Cabot rings

Cabot rings were first described in 1903 byAmerican physician, Richard Clarke Cabot. Theyare thin, red-violet staining, thread like strands inthe shape of a loop or Figure 8 that are found onrare occasions in red blood cells(Figure 9c). Theyare believed to be microtubules that are remnantsfrom a mitotic spindle, and their presence indicatesan abnormality in the production of red blood cells.Cabot rings stains red or purple with a Wright’sstain. Cabot’s rings have been described inpernicious anemia, lead poisoning, leukemia,alcoholic jaundice, and in some forms of severeanemia. They can also be seen in patients takingcytostatics.40

Heinz bodies

They are small irregular deep purple granules inred blood cells. They are found in glucose-6-phosphate dehydrogenase deficiencies but alsofound in congenital haemolytic anaemias and inpremature infants. They are named after RobertHeinz (1865-1924), a German physician. Alsoknown as Ehrlich or Heinz-Ehrlich bodies4 theyoccur as a result of damaged DNA componentusually through oxidation or due to change in theinternal morphology of the amino acid residuewithin the red blood cells.6 They are best seen whenblood films are stained with dyes such as crystalviolet or methylene blue.4 (Figure 9d)

Fessas bodies:

Fessas P., 1963noticed the spontaneous formationof precipitated Hb like material within theimmature and/or mature erythroid cells of patientswith severe or intermediate â- thalassemia. Theseinclusion bodies were attributed to an excess of á-Hb chains. 41

8. Inclusion bodies seen in granulomas

Schaumann (conchoidal) bodies:

Large basophilic concentric lamellar calcificationsof 100 µm in size, often containing centralbirefringent calcium oxalate crystals. They are seenin sarcoidosis, and other granulomatous disorderslike tuberculosis, leprosy etc. They are composedof lipo mucoglycoproteins impregnated withcalcium and iron. Although usuallyintracytoplasmic they may, if numerous or verylarge, be extruded into the extracellularspace.1,42(Figure 10a)

Hamazaki-wesenberg (H-W) bodies:They are oval or spindle-shaped, range up to severalmicrons in size, and appear yellow-brown withH&E stain(Figure 10b). They are found insarcoidosis. The pigment appears to be lipofuscin.Ultrastructural studies have shown that H-W bodiesare giant lysosomes and residual bodies. They areacid-fast and stain with silver stains as well as avariety of other stains. When visualized with silverstains H-W bodies can be easily mistaken forbudding yeasts due to clustering of individualbodies.42

Lafora bodies:

Lafora bodies are cytoplasmic, basophilic andmetachromatic inclusions having a concentric targetlike lamination(Figure 10c). They are found innerve cells but may also be found in the liver,muscle and skin of patients with Lafora bodydisease. The bodies are Alcian blue and PASpositive but resistant to diastase.4 These inclusionbodies are also seen in the excretory ducts ofeccrine and apocrine sweat ducts of clinicallynormal skin.6

9. Inclusion bodies seen in foreign bodyreactionsParent bodyParent bodies are seen in a condition calledmyospherulosis, which is a complication of healingof an extraction wound or soft tissue wound intowhich was placed antibiotic ointment with apetrolatum base. This treatment results in theformation of multiple cyst like spaces that containnumerous brown-black within the connectivetissue within the connective tissue. The collectionof spherules sometimes are surrounded by an outermembrane known as parent body (Figure 11),forming structures that resemble a ‘bag of marbles’.The spherules represent red blood cells that havebeen altered by the medication. The unusual darkcolouration is due to degradation of haemoglobin.43

ConclusionInclusion bodies appear as a result of anydisharmony to the normal homeostasis of the bodyand therefore their appearance is pathognomonic.These bodies can be due to the altered cellular andnuclear changes in response to any biochemicalprocess during the course of the disease. Thereforethese bodies, if present, are an important aid indiagnosing various pathologic conditions.


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ABOUT THE JOURNALThe Journal of Maxillofacial Science & Research, the official publication of PMS College of Dental Science andResearch, Vattappara, Trivandrum, is intended to be a research periodical that aims to inform its readers of ideas,opinions, developments and key issues in dentistry - clinical, practical and scientific - stimulating interest, debateand discussion and an opportunity for life long learning ,amongst dentists of all disciplines. All papers publishedin the JMFSR are subject to rigorous peer review by our excellent review board. We have tried to design thejournal in such a way that the readers can find the relevant information fast and easily.

The journal is intended for dentists, dental undergraduates, members of the dental team, hospital, community,academic and general practitioners.SectionsGuest Editorials : by eminent researchers and authors on their subject.

Messages : by eminent personalities, researchers and authors.

Review articles: scientific peer-reviewed papers with a focus on clinical research to enable researchers and scientiststo communicate their findings to the rest of the community.

Case reports: articles, and papers on the latest developments and information relevant for those in dental practice.This section contains essentially case reports and general articles about clinical matters.

Practice section:. to include clinical guide , how-to-do-it papers, dental business articles ,and the latest developmentsand information relevant for those in dental practice.

Abstracts: a selection of abstracts from dental journals.

Opinion section: intended to keep the readers aware of what people are thinking in dentistry today, andintroduce differing views for debate by including letters and articles expressing the views and opinions of peoplethat are open to debate and discussion.

Education section: any type of paper, article or report that is relevant to the vital subject of dental education,whether it is undergraduate, postgraduate, specialist or lifelong learning

Summaries: this section acts as a bridge between the practice and research sections, providing a summary of theresearch papers in this issue. Besides the abstract and ‘in brief ’ box, in this page, we plan to includes a comment oneach paper by a specialist in the field, emphasizing the relevance of the paper , to ensure that the informationfrom the research is easily available to both practitioners and researchers.

The Cover Photograph :Fusion of TEETH

Photo courtsey Dr. (Capt) Vivek .V.

About the Journal

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