case report a histopathological and immunohistochemical … · 2019. 7. 31. · ameloblastic bromas...

Hindawi Publishing CorporationCase Reports in PathologyVolume 2013 Article ID 604560 7 pageshttpdxdoiorg1011552013604560

Case ReportA Histopathological and Immunohistochemical Analysis ofAmeloblastic Fibrodentinoma

Ronell Bologna-Molina12 Sirced Salazar-Rodriacuteguez3 Ana Mariacutea Bedoya-Borella4

Ramoacuten Gil Carreoacuten-Burciaga1 Gabriel Tapia-Repetto2 and Nelly Molina-Frechero5

1 Oral Pathology Research Department School of Dentistry Universidad Juarez del Estado de Durango (UJED)34000 Durango DGO Mexico

2 School of Dentistry Universidad de la Republica (UDELAR) 19200 Montevideo Uruguay3 Pathology Department Instituto Nacional de Oncologıa y Radiobiologıa (INOR) 10400 Havana Cuba4Biology Department CBC Universidad de Buenos Aires (UBA) 8000 Buenos Aires Argentina5Health Care Department Universidad Autonoma Metropolitana Xochimilco 04960 Mexico City DF Mexico

Correspondence should be addressed to Ronell Bologna-Molina ronellbolognahotmailcom

Received 14 December 2012 Accepted 7 January 2013

Academic Editors Y L Choi I Meattini T Tot and D Vlachodimitropoulos

Copyright copy 2013 Ronell Bologna-Molina et alThis is an open access article distributed under the Creative Commons AttributionLicense which permits unrestricted use distribution and reproduction in any medium provided the original work is properlycited

Ameloblastic fibrodentinoma (AFD) is considered a mixed odontogenic tumor that is characterized by conserved epithelialand ectomesenchymal neoplastic components AFD is composed of long narrow cords and islands of odontogenic epitheliumthe epithelial strands lie in a myxoid cell-rich ectomesenchymal tissue with stellate-shaped fibroblasts that exhibit long slendercytoplasmic extensions that resemble dental papilla The lesions show the presence of dysplastic dentin Although AFD is arare entity and its very existence is not completely accepted based on the extent of histodifferentiation it is considered torepresent a stage between ameloblastic fibroma and ameloblastic fibroodontoma This study aimed to provide a histopathologicaland immunohistochemical characterization of this infrequent tumor A large panel of antibodies including amelogenin Ck 19calretinin syndecan-1 E-cadherin MSH2 histone H3 and Ki-67 was used to illustrate the nature of the tumor

1 Introduction

Odontogenic tumors (OT) are lesions that are derived fromthe tooth-producing tissues or their remnants that remainentrapped either within the jawbones or within the adjacentsoft tissues From a biological standpoint some of theselesions represent hamartomas that exhibit varying degreesof differentiation whereas others are benign or malignantneoplasms that exhibit variable aggressiveness and a potentialto develop metastasis [1]

Ameloblastic Fibrodentinoma (AFD) is considered asldquovery low frequencyrdquo tumor This rare neoplasm representsless than 1 of all odontogenic tumors in most of thepublished literature worldwide [1]

Histopathologically AFD is comprised of an odonto-genic ectomesenchyme that resembles the dental papilla and

epithelial strands and nests that resemble the dental laminaand enamel organ with the presence of dentin formation

Occasionally this odontogenic tumormight be associatedwith an unerupted tooth presenting as a slow-growingasymptomatic swelling in the posterior mandible The age atdiagnosis generally falls within the first two decades of life [2]

Treatment consists of enucleation and curettageAlthough recurrence is a possibility it does not justify initialaggressive treatment AFD rarely progresses to malignancyas ameloblastic fibrodentinosarcoma [3]

The aim of this study was to histopathologically andimmunohistochemically characterize this rare tumor using alarge panel of antibodiesWe furthermore discuss the possibleimplications or functions that each protein might contributeto the biological behavior of this uncommon tumor

2 Case Reports in Pathology

Figure 1 Computed tomography of the mandible showing theextension of the tumor area

Figure 2 Front view of stereolithography in order to plan surgicaltreatment

2 Case Report

Female patient one year and six months old showed evi-dent facial asymmetry and increased volume in the rightmandibular body region In the intraoral examination thepatient showed increased volume in the posterior molarregion of 6 cmwithout pain on palpation andwithout changeof color Computed tomography (CT) showed an expansivelesion extending from the condyle covering the ramus andmandibular body (Figure 1) Before conducting the enucle-ation of the lesion stereolithography to plan surgical man-agementwas conducted (Figure 2) Treatment performedwastumor enucleation and curettage under general anesthesiaThe tumor was diagnosed histopathologically as AFD

3 Materials and Methods

The immunohistochemical study conducted two samplesfrom the same patient Paraffin blocks were sliced into

2mm thick sections which were mounted onto polylysine-coated glass slides and were air-dried overnight at roomtemperature After deparaffinization and rehydration thetissue sections were treated with 01M sodium citrate (pH62) and Tween-20 to expose the epitopes The endogenousperoxidases were blocked with 09 hydrogen peroxidefollowed by incubation in 1 bovine serum albumin dilutedin PBS for 5min to eliminate nonspecific binding Thesections were incubated with primary antibodies for 45minThe monoclonal antibodies used are shown in Table 1 Afterincubation with the primary antibodies the sections wereincubated with biotinylated anti-mouserabbit antibodiesand with the streptavidinperoxidase complex for 30mineach (LSAB thorn labeled streptavidin biotin Dako) To visualizethe reaction a 331015840-diaminobenzidine H2O (Dako) substratewas applied Then the sections were counterstained withMayerrsquos hematoxylin solution For the negative controls theprimary antibody was substituted with PBS

4 Results

The antibodies used to detect the expression of the indicatedproteins in the epithelial andmesenchymal cells are shown inTable 1

5 Discussion

Ameloblastic fibromas ameloblastic fibrodentinomas(AFDs) ameloblastic fibroodontomas and odontomas arelesions that exhibit similar histopathological clinical andradiographical features resulting in a controversial debateover whether they can be delineated as distinct pathologicalentities or as developmental stages of the same lesion Someresearchers and clinicians consider them as separate entitieswhereas others view them as chronological stages of thesame lesion with ameloblastic fibromas at one extremeand odontomas at the other extreme and with ameloblasticfibroodontomas and AFDs in an intermediate stage [4]

The ameloblastic fibromas AFDs and ameloblasticfibroodontomas are considered mixed odontogenic tumorsthat are characterized by conserved epithelial and ectomes-enchymal neoplastic components They are distinguishedby the fact that AFDs exhibit dysplastic or tubular dentinwhereas the ameloblastic fibroodontomas exhibit enamelmatrix deposits or mature enamel and ameloblastic fibromasexhibit any type of dental hard tissue deposits AFD is arare entity and its very existence is not completely acceptedIndeed AFDhas been considered to represent a histologicallydistinct stage between ameloblastic fibroma and ameloblasticfibroodontoma based on the extent of histodifferentiation [5ndash7]

Currently whether this lesion represents a separate entityremains unclear Notably in the revised WHO classificationof odontogenic tumors ameloblastic fibromas and AFDs aresynonymously used terms and are categorized together [3]

Ameloblastic fibromas and AFDs have been suggestedto occur in two histologically indistinguishable variantsThe first is a neoplastic lesion which if left in situ does

Case Reports in Pathology 3

Table 1 The antibodies used to detect the expression of the different proteins in the epithelial and mesenchymal cells of the AFD samples

Antibody Sourceclone Dilution Antigen retrieval Epithelial cells Mesenchymal cellsAmelogenin Santa CruzSC-33109 1 100 Mw + NegCK19 Genetexpolyclonal 1 100 Mw +++ NegCalretinin DAKODAK-CALERET 1 1 100 Mw + NegE-cadherin DAKONCH-38 1 100 Mw ++ NegSyndecan-1 DAKOMI15 1 100 Mw +++ ++Histone H3 GeneTexE107 1 100 Mw +++ +++Ki-67 DAKOMIB1 1 100 Mw + +MSH-2 GenetexEPR3943 1 100 Mw +++ +++Neg negative + weak ++ moderate +++ strong immunoexpression and Mw microwave

not appear to differentiate further The second variant is anonneoplastic hamartomatous lesion which appears to becapable of developing into an ameloblastic fibroodontomaand then differentiating further into a complex odontoma[2 8]

When analyzed microscopically we observed long nar-row cords and islands of odontogenic epitheliumThe epithe-lial strands resided in a myxoid cell-rich stroma with stellate-shaped fibroblasts exhibiting long slender cytoplasmic exten-sions that resembled dental papilla The lesions exhibitedcalcifying elements (dentin matrix and dentinoid material)

In the immunohistochemical findings of this study thecords and islands of epithelial cells were also strongly positivefor antihuman cytokeratin 19 (CK19) (Figure 3) Cytokeratins(CKs) are the specific intermediate filaments of epithelialcells They comprise a complex family of at least 20 differentpolypeptides The immunoexpression patterns of CKs differaccording to cell type developmental stage differentiationstatus and anatomical site [9] Various CKs are expressed intooth germ tissue However CK19 is expressed in all types ofodontogenic epithelial cells in the developing tooth germ [10]and in neoplastic epithelial cells in some odontogenic tumors[11ndash13]

The strong immunopositivity that we found for CK19 inthe epithelial cells confirms the odontogenic nature of thislesion

Amelogenins (AMELs) represent the main family ofproteins secreted by ameloblasts during amelogenesis (90of enamel proteins) [14] AMELs are cell adhesion proteinsthat play a role in the biomineralisation of teethThey regulatethe formation of crystallites during the secretory stage oftooth enamel development and are thought to play a majorrole in the structural organization and mineralization of thedeveloping enamel [15]

In young or immature enamel amelogenin antibodiesimmunostain 90ndash95 of the enamel protein This proteinis biosynthesized in young ameloblasts is secreted into theextracellular enamel matrix [16] and is eventually almostcompletely removed by extracellular enzymatic degradationduring enamel maturation [17]

Mori et al [16] reported that epithelial cells stainedpositively for AMEL and recently Crivelini et al found astrong positive immunoreactivity for AMEL within the distalends of the epithelial cells of the ameloblastic fibromas and a

weaker immunoreactivity in the stellate reticulum-like cellsConsistently we found immunopositivity for AMEL withinthe peripheral layer of columnar epithelial odontogenic cellsof AFDs confirming the ameloblastic component of thesetumors (Figure 4)

Calretinin is a 29 kDa calcium-binding protein thatbelongs to the family of E-F hand proteins which includes S-100The E-F hand proteins are characterized by a helix-loop-helix structure which functions as the calcium-binding site[18]

A study byAlaeddini et al [19] evaluated the expression ofcalretinin in different odontogenic tumors and did not detectany calretinin expression in ameloblastic fibromas In con-trast we observed weak immunopositivity for calretinin inthe columnar epithelial odontogenic cells of the AFD samples(Figure 5) Mistry et al [20] demonstrated that calretinin isweakly expressed within the tooth germs of developing ratmolars during the early cap stage They further showed thatas the teeth develop the intensity of the immunoreactivityincreases from weak to intense during the late bell stagesindicating that the expression of calretinin in AFD correlateswith progressively advanced stages of maturation Takentogether these data support the theory that all ameloblasticfibromas AFDs and ameloblastic fibroodontomas merelyrepresent various progressive stages of the same lesionultimately resulting in the formation of odontomas Howeverthis concept has not been widely accepted for several reasonsFor example a number of cases of recurrent or residualameloblastic fibromas have demonstrated no evidence offurther maturation into a more differentiated odontogeniclesion such as an ameloblastic fibroodontoma or an odon-toma Moreover ameloblastic fibromas are known to occurin patient age groups beyond what has been observed forodontogenesis [4 19 21] However in some studies forexample in work conducted by Alaeddini et al [19] theyfound that ameloblastic fibroma occurred mostly in the thirddecade this data also demonstrated that ameloblastic fibromaoccurred at a much older age than did the ameloblasticfibroodontoma

Cadherins (named for ldquocalcium-dependent adhesionrdquo)are a class of type-1 transmembrane proteins They playimportant roles in cellular adhesion ensuring that the cellswithin tissues are bound together They have been shownto be involved in many biological processes morphogenesis


100 120583m

(a)

100 120583m

(b)

Figure 3 Strong expression for CK19 in the islands and strands of odontogenic epithelium magnification 400x (a) and 600x (b)

100 120583m

Figure 4 Weak immunopositivity for amelogenin within theperipheral layer of columnar epithelial odontogenic cells 400x

100 120583m

Figure 5 Weak immunopositivity for calretinin antibody in thecolumnar epithelial odontogenic cells 600x

cytoskeletal organization and cell migration as well as inpathological conditions such as cancer [22] In cancer theloss of E-cadherin function through genetic or epigeneticmechanisms has been implicated in the progression andmetastasis of numerous malignancies [23] In our study we

100 120583m

Figure 6 Strong expression for E-cadherin in the islands and thestrands of odontogenic epithelium magnification 400x

found that the expression of E-cadherin is well conservedamong some benign neoplasms and is strong in epithelialodontogenic cells (Figure 6)

Syndecan-1 is a cell surface proteoglycan that facilitatescellular attachment to the extracellular matrix Its expressionis downregulated in many transformed cellular modelsThe loss of syndecan-1 expression decreases intercellularadherence as well as attachment to the extracellular matrixThe loss of syndecan-1 expression in ameloblastomas andameloblastic carcinomas has been demonstrated to correlatewith more aggressive biological behaviors (invasion andmetastasis) [24ndash26]

In this study we detected strong membranousimmunopositivity for syndecan-1 in the cords and theislands of epithelium and in the central areas resembling thestellate reticulum (Figure 7) The preservation of syndecan-1expression suggests a cohesion and conservation of theepithelial architecture Notably when we evaluated theprimitive connective tissue stroma that resembled dentalpapilla it exhibited moderate expression levels of syndecan-1(Figure 7) Beyond its key role as a cell adhesion moleculesyndecan-1 also participates with the extracellular matrix to


100 120583m

Figure 7 Strong membranous immune positivity for syndecan-1 in the cords and the islands of epithelium and in the centralareas resembling the stellate reticulum and moderate positivity inmesenchymal cells magnification 200x

100 120583m

Figure 8 Strong nuclear expression of MSH2 in epithelial andmesenchymal cells magnification 100x

promote and to regulate cellular proliferation and growth byinteracting with families of growth factors that are linked toheparin [27]

The MSH2 gene encodes for an essential DNA repairprotein that facilitates the repair of DNA during replicationImmunohistochemical analysis of the expression of MSH2 intumors indicates that its expression is generally lost in tumorsfrom hereditary nonpolyposis colorectal cancer patients andthe reduced expression of MSH2 has been reported in othertypes of carcinomas [28] Leach et al [29] demonstratedthat MSH2 is a ubiquitously expressed protein exhibitingan exclusively nuclear localization in the normal tissuesWe observed strong nuclear expression of MSH2 in ADFs(Figure 8) consistent with a previous study by Castrilli et al[30] whodetectedMSH2 expression in all 25 ameloblastomasthat they evaluated These data suggest that the developmentand progression of these tumors do not depend on a defect inthe human DNA mismatch repair system

Analysis of cell proliferation indices in situ providesimportant insight into the rate of cellular turnover in varioustissues or tumors We evaluated two such cell cycle-related

100 120583m

Figure 9 Strong nuclear positivity for the antibody histone H3 inboth epithelial and mesenchymal cells magnification 200x

100 120583m

Figure 10 Weak expression of Ki-67 protein in the cords and theislands of epithelium and the mesenchymal cells magnification600x

factors histone H3 and Ki-67 and found that the positivelystaining cells were distributed in both the epithelial andthe mesenchymal compartments When we compared theimmunopositivities of histone H3 and Ki-67 we found thathistone H3 exhibited significantly more immunoreactivityin more than half of all epithelial and mesenchymal cells(Figures 9 and 10) These findings suggest that Ki-67 is amore specific proliferation marker for AFD Moreover theweak expression of Ki-67 illustrates the low proliferative rateof this tumor further substantiating the benign nature ofthis neoplasm This is consistent with a study by Sano etal which suggests that the evaluation of growth potential inameloblastic fibromas and related lesions might enhance ourunderstanding of tumor aggressiveness [31]

6 Conclusion

In summary we have described here a histopathologicaland immunohistochemical characterization of AFD In thisstudy we demonstrated for the first time the presence ofthese proteins (calretinin syndecan-1 MSH2 and histoneH3) in AFD some of which can serve as useful markers for


understanding the histogenesis and biological behavior ofthis rare odontogenic tumor

It is important to keep inmind that due to the rarity of thisneoplasm we have only included one case report Thereforethe interpretation of our results might be limited to a trend ora singular description future studies should involve a moreextensive series of tumor cases to confirm our observations

Conflict of Interests

The authors do not have direct or indirect financial relationswith the commercial identity mentioned in this paper Theauthors declare that they have no conflict of interests

Acknowledgments

Theauthors thankDr Jorge Tellez andDr Ruby Lopez for thesurgical information the CT images and stereolithography

References

[1] A M Taylor ldquoNew findings and controversies in odontogenictumorsrdquoMedicina Oral Patologia Oral y Cirugia Bucal vol 13no 9 pp E555ndashE558 2008

[2] H P Philipsen P A Reichart and F Praeligtorius ldquoMixedodontogenic tumours and odontomas Considerations on inter-relationship Review of the literature and presentation of 134new cases of odontomasrdquo European Journal of Cancer B OralOncology vol 33 no 2 pp 86ndash99 1997

[3] L Barnes J W Eveson P Reichart and D Sidransky EdsWorld Health Organization Classification of Tumors Pathologyand Genetics Head and Neck Tumors IARC Press Lyon France2005

[4] Y Chen T J Li Y Gao and S F Yu ldquoAmeloblastic fibromaand related lesions a clinicopathologic study with reference totheir nature and interrelationshiprdquo Journal of Oral Pathologyand Medicine vol 34 no 10 pp 588ndash595 2005

[5] I R Kramer J J Pindborg and M ShearHistological Typing ofOdontogenic Tumours (International Histological Classificationof Tumours) Springer Berlin 2nd edition 1992

[6] D G Gardner ldquoThe mixed odontogenic tumorsrdquo Oral SurgeryOral Medicine and Oral Pathology vol 58 no 2 pp 166ndash1681984


[8] H P Philipsen and P A Reichart ldquoRevision of the 1992-editionof the WHO histological typing of odontogenic tumours Asuggestionrdquo Journal of Oral Pathology and Medicine vol 31 no5 pp 253ndash258 2002

[9] R Moll W W Franke D L Schiller B Geiger and R KreplerldquoThe catalog of human cytokeratins patterns of expression innormal epithelia tumors and cultured cellsrdquo Cell vol 31 no 1pp 11ndash24 1982

[10] A Pelissier J P Ouhayoun M H Sawaf and N ForestldquoEvolution of cytokeratin expression in developing humantooth germrdquo Journal de Biologie Buccale vol 18 no 2 pp 99ndash108 1990

[11] K Heikinheimo M Hormia G Stenman I Virtanen and RP Happonen ldquoPatterns of expression of intermediate filamentsin ameloblastoma and human fetal tooth germrdquo Journal of OralPathology and Medicine vol 18 no 5 pp 264ndash273 1989

[12] M M Crivelini V C de Araujo S O M de Sousa and N S deAraujo ldquoCytokeratins in epithelia of odontogenic neoplasmsrdquoOral Diseases vol 9 no 1 pp 1ndash6 2003

[13] H Kumamoto M Yoshida and K Ooya ldquoImmunohistochem-ical detection of amelogenin and cytokeratin 19 in epithelialodontogenic tumorsrdquo Oral Diseases vol 7 no 3 pp 171ndash1762001

[14] M M Crivelini R C Felipini G I Miyahara and S Cde Sousa ldquoExpression of odontogenic ameloblast-associatedprotein amelotin ameloblastin and amelogenin in odonto-genic tumors immunohistochemical analysis and pathogeneticconsiderationsrdquo Journal of Oral Pathology amp Medicine vol 41pp 272ndash280 2012

[15] J Catalano-Sherman R Laskov A Palmon S David and DDeutsch ldquoProduction of a monoclonal antibody against humanamelogeninrdquoCalcified Tissue International vol 54 no 1 pp 76ndash80 1994

[16] M Mori K Yamada T Kasai T Yamada H Shimokawa andS Sasaki ldquoImmunohistochemical expression of amelogenins inodontogenic epithelial tumours and cystsrdquo Virchows ArchivmdashA Pathological Anatomy and Histopathology vol 418 no 4 pp319ndash325 1991

[17] S F Zalzal C E Smith and A Nanci ldquoAmeloblastin andamelogenin share a common secretory pathway and are co-secreted during enamel formationrdquo Matrix Biology vol 27 no4 pp 352ndash359 2008

[18] J Rogers M Khan and J Ellis ldquoCalretinin and other CaBPsin the nervous systemrdquo Advances in Experimental Medicine andBiology vol 269 pp 195ndash203 1990

[19] M Alaeddini S Etemad-Moghadam and F Baghaii ldquoCompar-ative expression of calretinin in selected odontogenic tumoursa possible relationship to histogenesisrdquo Histopathology vol 52no 3 pp 299ndash304 2008

[20] D Mistry M Altini H G Coleman H Ali and E MaioranoldquoThe spatial and temporal expression of calretinin in developingratmolars (Rattus norvegicus)rdquoArchives of Oral Biology vol 46no 10 pp 973ndash981 2001

[21] Y Kabasawa K Nagumo Y Takeda et al ldquoAmelogenin positivecells scattered in the interstitial component of odontogenicfibromasrdquo Journal of Clinical Pathology vol 61 no 7 pp 851ndash855 2008

[22] B D Angst C Marcozzi and A I Magee ldquoThe cadherinsuperfamily diversity in form and functionrdquo Journal of CellScience vol 114 no 4 pp 629ndash641 2001

[23] U H Frixen J Behrens M Sachs et al ldquoE-cadherin-mediatedcell-cell adhesion prevents invasiveness of human carcinomacellsrdquo Journal of Cell Biology vol 113 no 1 pp 173ndash185 1991

[24] R Bologna-Molina A Mosqueda-Taylor E Lopez-Corella etal ldquoSyndecan-1 (CD138) and Ki-67 expression in differentsubtypes of ameloblastomasrdquo Oral Oncology vol 44 no 8 pp805ndash811 2008

[25] R Bologna-Molina A Mosqueda-Taylor E Lopez-Corellaet al ldquoComparative expression of syndecan-1 and Ki-67 inperipheral and desmoplastic ameloblastomas and ameloblasticcarcinomardquo Pathology International vol 59 no 4 pp 229ndash2332009

[26] R Bologna-Molina A Mosqueda-Taylor P de Almeida-OsleiV Toral-Rizo and G Martınez-Mata ldquoPeripheral desmoplastic


ameloblastoma histopathological and immunohistochemicalprofile of a caserdquoMedicina Oral Patologia Oral y Cirugia Bucalvol 15 no 6 pp e846ndashe849 2010

[27] R Bologna-Molina R Gonzalez-Gonzalez A Mosqueda-Taylor N Molina-Frechero P Damian-Matsumura and HDominguez-Malagon ldquoExpression of syndecan-1 in papillarycarcinoma of the thyroid with extracapsular invasionrdquo Archivesof Medical Research vol 41 no 1 pp 33ndash37 2010

[28] S N Thibodeau A J French P C Roche et al ldquoAlteredexpression of hMSH2 and hMLH1 in tumors withmicrosatelliteinstability and genetic alterations in mismatch repair genesrdquoCancer Research vol 56 no 21 pp 4836ndash4840 1996

[29] F S Leach K Polyak M Burrell et al ldquoExpression of thehumanmismatch repair gene hMSH2 in normal and neoplastictissuesrdquo Cancer Research vol 56 no 2 pp 235ndash240 1996

[30] G Castrilli M Piantelli L Artese et al ldquoExpression ofhMSH2 and hMLH1 proteins of the human DNA mismatchrepair system in ameloblastomardquo Journal of Oral Pathology andMedicine vol 30 no 5 pp 305ndash308 2001

[31] K Sano S I Yoshida HNinomiya et al ldquoAssessment of growthpotential by MIB-1 immunohistochemistry in ameloblasticfibroma and related lesions of the jaws compared withameloblastic fibrosarcomardquo Journal of Oral Pathology andMedicine vol 27 no 2 pp 59ndash63 1998

Submit your manuscripts athttpwwwhindawicom

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Hindawi Publishing Corporationhttpwwwhindawicom Volume 2014


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Evidence-Based Complementary and Alternative Medicine

Volume 2014Hindawi Publishing Corporationhttpwwwhindawicom


Figure 1 Computed tomography of the mandible showing theextension of the tumor area

Figure 2 Front view of stereolithography in order to plan surgicaltreatment

2 Case Report

Female patient one year and six months old showed evi-dent facial asymmetry and increased volume in the rightmandibular body region In the intraoral examination thepatient showed increased volume in the posterior molarregion of 6 cmwithout pain on palpation andwithout changeof color Computed tomography (CT) showed an expansivelesion extending from the condyle covering the ramus andmandibular body (Figure 1) Before conducting the enucle-ation of the lesion stereolithography to plan surgical man-agementwas conducted (Figure 2) Treatment performedwastumor enucleation and curettage under general anesthesiaThe tumor was diagnosed histopathologically as AFD

3 Materials and Methods

The immunohistochemical study conducted two samplesfrom the same patient Paraffin blocks were sliced into

2mm thick sections which were mounted onto polylysine-coated glass slides and were air-dried overnight at roomtemperature After deparaffinization and rehydration thetissue sections were treated with 01M sodium citrate (pH62) and Tween-20 to expose the epitopes The endogenousperoxidases were blocked with 09 hydrogen peroxidefollowed by incubation in 1 bovine serum albumin dilutedin PBS for 5min to eliminate nonspecific binding Thesections were incubated with primary antibodies for 45minThe monoclonal antibodies used are shown in Table 1 Afterincubation with the primary antibodies the sections wereincubated with biotinylated anti-mouserabbit antibodiesand with the streptavidinperoxidase complex for 30mineach (LSAB thorn labeled streptavidin biotin Dako) To visualizethe reaction a 331015840-diaminobenzidine H2O (Dako) substratewas applied Then the sections were counterstained withMayerrsquos hematoxylin solution For the negative controls theprimary antibody was substituted with PBS

4 Results

The antibodies used to detect the expression of the indicatedproteins in the epithelial andmesenchymal cells are shown inTable 1

5 Discussion

Ameloblastic fibromas ameloblastic fibrodentinomas(AFDs) ameloblastic fibroodontomas and odontomas arelesions that exhibit similar histopathological clinical andradiographical features resulting in a controversial debateover whether they can be delineated as distinct pathologicalentities or as developmental stages of the same lesion Someresearchers and clinicians consider them as separate entitieswhereas others view them as chronological stages of thesame lesion with ameloblastic fibromas at one extremeand odontomas at the other extreme and with ameloblasticfibroodontomas and AFDs in an intermediate stage [4]

The ameloblastic fibromas AFDs and ameloblasticfibroodontomas are considered mixed odontogenic tumorsthat are characterized by conserved epithelial and ectomes-enchymal neoplastic components They are distinguishedby the fact that AFDs exhibit dysplastic or tubular dentinwhereas the ameloblastic fibroodontomas exhibit enamelmatrix deposits or mature enamel and ameloblastic fibromasexhibit any type of dental hard tissue deposits AFD is arare entity and its very existence is not completely acceptedIndeed AFDhas been considered to represent a histologicallydistinct stage between ameloblastic fibroma and ameloblasticfibroodontoma based on the extent of histodifferentiation [5ndash7]

Currently whether this lesion represents a separate entityremains unclear Notably in the revised WHO classificationof odontogenic tumors ameloblastic fibromas and AFDs aresynonymously used terms and are categorized together [3]

Ameloblastic fibromas and AFDs have been suggestedto occur in two histologically indistinguishable variantsThe first is a neoplastic lesion which if left in situ does
















100 120583m

(a)

100 120583m

(b)


100 120583m


100 120583m



100 120583m






100 120583m


100 120583m





100 120583m


100 120583m



6 Conclusion







Acknowledgments


References







































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of































100 120583m

(a)

100 120583m

(b)


100 120583m


100 120583m



100 120583m






100 120583m


100 120583m





100 120583m


100 120583m



6 Conclusion







Acknowledgments


References







































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of

















100 120583m


100 120583m





100 120583m


100 120583m



6 Conclusion







Acknowledgments


References







































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of





















Acknowledgments


References







































of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of




























of






Disease Markers



OncologyJournal of





PPAR Research



Journal of

ObesityJournal of
















case report a histopathological and immunohistochemical … · 2019. 7. 31. · ameloblastic bromas...

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