Peripheral Columnar Cells Research Articles

ADENOID AMELOBLASTOMA: A CASE REPORT

Adenoid ameloblastoma is a rare variant of ameloblastoma that exhibits adenoid characteristics, resembling an adenomatoid odontogenic tumor. Despite few studies, the clinical, histopathologic, and behavioral aspects of this lesion are still unknown. A 57-year-old White female patient presented with a well-defined unilocular radiolucency between the roots of the right mandibular premolars, without intraoral changes. After an excisional biopsy, microscopic examination revealed islands of odontogenic epithelium surrounded by fibrous stroma. The peripheral columnar cells showed ameloblast-like differentiation with nuclear palisading and reverse polarization. A cribriform pattern was observed, as well as large duct-like spaces lined by columnar or cuboid cells and filled with eosinophilic mucoid material. A diagnosis of adenoid ameloblastoma was made and the patient is currently being followed up. Adenoid ameloblastoma is a rare variant of ameloblastoma that exhibits adenoid characteristics, resembling an adenomatoid odontogenic tumor. Despite few studies, the clinical, histopathologic, and behavioral aspects of this lesion are still unknown. A 57-year-old White female patient presented with a well-defined unilocular radiolucency between the roots of the right mandibular premolars, without intraoral changes. After an excisional biopsy, microscopic examination revealed islands of odontogenic epithelium surrounded by fibrous stroma. The peripheral columnar cells showed ameloblast-like differentiation with nuclear palisading and reverse polarization. A cribriform pattern was observed, as well as large duct-like spaces lined by columnar or cuboid cells and filled with eosinophilic mucoid material. A diagnosis of adenoid ameloblastoma was made and the patient is currently being followed up.

Immunolocalization of IP3R and V-ATPase in Ameloblastomas.

The goal of this study was to investigate the immunolocalization of inositol 1,4,5-trisphosphate receptor (IP3R) and vacuolar ATPase (V-ATPase) in ameloblastomas with special attention to the invasive front. Thirty-seven cases of previously diagnosed formalin-fixed paraffin-embedded (FFPE) human ameloblastoma samples were selected for this study. The samples were grouped according to the predominant histologic pattern and comprised twelve plexiform, eighteen follicular, and seven unicystic ameloblastomas. Of the unicystic variants, six demonstrated purely luminal and intraluminal growth, and one displayed mural extension. One granular cell variant was included in the follicular ameloblastoma group. All specimens were evaluated for IP3R and V-ATPase expression by immunohistochemistry (IHC). IP3R was positive in columnar cells, similar to ameloblasts, and non-peripheral cells in all samples. In the area of tumor protrusion and front of invasion, membranous and cystoplasmic IP3R expression was observed. In contrast, areas adjacent to tumoral protrusion demonstrated only membranous staining patterns. V-ATPase was not expressed in peripheral columnar cells of the unicystic and granular cell variants of ameloblastoma; however, strong staining was present in these cells in plexiform ameloblastomas, follicular ameloblastomas, and areas of mural growth of unicystic ameloblastomas. In areas of tumor protrusion, reactivity for V-ATPase was observed with both membranous and cytoplasmic staining, while other areas showed only membranous V-ATPase. These findings suggest that concomitant immunolocalization of IP3R and V-ATPase, with both cytoplasmic and membranous expression in the peripheral columnar cells, may indicate the invasive potential of ameloblastomas. Furthermore, these results suggest the tumoral spread of ameloblastomas may be correlated with the autophagy process and channelopathy. The expression of these proteins could establish a baseline for future research and provide therapeutic targets for treatment of ameloblastomas.

Cell proliferation proteins and aggressiveness of histological variants of ameloblastoma and keratocystic odontogenic tumor

ABSTRACTTumors that originate from the epithelium of the odontogenic apparatus are classified as benign or malignant. The proliferative activity could provide a basis for differences in the biologic behavior among the histological variants of ameloblastoma (AM) and keratocystic odontogenic tumor (KCOT). We examined 32 solid AM and 18 KCOT cases. The AM sample comprised 16 cases of follicular AM, six cases of unicystic AM, eight cases of plexiform AM and two cases of acanthomatous AM. Sections were stained with the Ki-67 antibody. Ten representative fields were selected randomly in each section. For AM, peripheral tall columnar cells of tumor islands/nests/cords were selected. For KCOT, fields were selected in the basal and the suprabasal region of the epithelial lining. We counted the average number of Ki-67 positive cells/field for AM and KCOT. AM exhibited Ki-67 expression in peripheral tall columnar cells, whereas KCOT exhibited Ki-67 expression in the basal and suprabasal layer. No significant difference between AM and KCOT was observed; the cellular proliferative activity varied among the subtypes. No significant difference in Ki-67 expression in acanthomatous, cystic and follicular types of AM was observed, although the plexiform type exhibited significantly higher levels than the other three types. High expression of Ki-67 could be a useful prognostic marker for proliferative activity and a prognostic indicator for recurrence rate of AM and KCOT.

UNUSUAL CASE OF MANDIBULAR AMELOBLASTOMA THAT HAS EXCEEDED THE MIDLINE: A CASE REPORT

This study reports a case of mandibular ameloblastoma that has exceeded the midline. A 62-year-old female patient presented with painless swelling complaint in body region and left mandibular symphysis. The clinical examination showed intact mucosa and normal color; facial asymmetry left and dysphagia. The panoramic radiographies suggested image circumscribed radiolucent unilocular in the left mandible body with a length exceeding symphysis and parasymphysis to the opposite side. CT (CT) scan showed hypodense image in the region was to break the buccal bone plate. The incisional biopsy generated histologic sections that revealed odontogenic tumor fragments in the form of nests and strands with peripheral columnar cells similar to ameloblasts, confirming the diagnosis of ameloblastoma unicystic. Marsupialization was performed for tumor decompression in progress, preservation and preparation for subsequent enucleation surgery. Bilateral involvement that goes beyond the midline is unusual in odontogenic tumors, especially in ameloblastoma.

Evaluation of epithelial cell proliferation in Ameloblastoma and Keratocystic Odontogenic tumor: A comparative study

Background: Ameloblastoma (AM) and keratocystic odontogenic tumor (KCOT) are the most common odontogenic tumors which exhibit aggressive clinical behavior. The aggressive behavior of the AM and KCOT can be correlated with the degree of proliferation of the epithelium. Objective: The objective of the study was to determine the proliferation potential of AM and KCOT to correlate with the aggressive clinical behavior. Materials and Methods: The study material consisted of 10 solid AMs, 10 KCOTs, and 5 oral squamous cell carcinomas (SCCs). Sections were immunohistochemically stained with the Ki-67 antibody. Representative fields were randomly selected in each immunohistochemically stained section. Counting was done under Olympus compound microscope fitted with an eyepiece ×10 magnification and objective ×40 magnification. Ten fields were chosen for each section. In AM, peripheral tall columnar cells of tumor islands/nests/cords were selected. In KCOT fields were selected in the basal and the suprabasal region of the epithelial lining. Differences in the average number of Ki-67-positive cells per field among all the three groups (AM, KCOT, and SCC) were analyzed by using the Kruskal–Wallis test. Results: AM showed expression of Ki-67 in peripheral tall columnar cells and the count was 10.83 ± 1.76, whereas in KCOT Ki-67-positive cells were present in the basal and suprabasal layer with a positive cell count of 9.4 ± 0.45. There was no statistical difference between AM and KCOT ( P > 0.005). The value obtained indicates the equal aggressive nature of the above lesion in consideration. Conclusion: The proliferative potential of the epithelium in odontogenic tumors is quite significant for their clinical behavior. Similar expression count of Ki-67 in AM and KCOT explains their aggressive clinical behavior and a high recurrence rate.

Immunohistochemical Expression of Cytokeratins in Central and Peripheral Odontogenic Fibromas

This study investigated the immunohistochemical expression of cytokeratins (CK) 5/6, 7, 8, 10, 13, 14, 18, and 19 in five cases of central odontogenic fibromas (COF), nine peripheral odontogenic fibromas (POF), and three dental follicle specimens. Study Design: Paraffin-embedded sections were obtained for the immunohistochemical evaluation of CK monoclonal antibodies. Results: CK 14 expression was positive in the epithelial islands of all cases. In four OF cases (28.57%) a weak positivity to CK 19 was observed in some central stellate cells (three POF and one COF). Of these four cases, three were WHO type and one simple type. Strong expression of CK 7 was detected in some central stellate cells and peripheral columnar cells of three cases of POF (21.43%). Conclusion: CK expression in OFs suggested a variable degree of epithelium maturation, demonstrating a possible difference in COF and POF origin.

Wnt signaling as a possible promoting factor of cell differentiation in pleomorphic adenomas.

There are well known that Wnt signaling was some roles of cell differentiation at the development tissues, especially the oral and maxillofacial regions of some developmental stages. Therefore, to determine Wnt signaling in the pleomorphic adenoma tissues, we examined. The expression of Wnt1 and β-catenin as well as the distribution of various cytoskeletal proteins CK7 and CK13 was examined in 30 cases of pleomorphic adenoma by immunohistochemistry. Wnt1 was detected in almost all tumor cells. The peripheral columnar cells in squamous metaplasia and small cuboidal cells in duct-like structures were strongly positive to Wnt1. Although β-catenin was clearly localized on the cell membrane of tumor cells, nuclear translocation was observed in small cuboidal cells and in some basaloid cells. The immunofluorescent staining pattern of Wnt1 and CK7 as well as Wnt1 and CK13 was consistent with IHC results. Thus, in pleomorphic adenoma, Wnt is involved in tumor cell differentiation of peripheral columnar cells forming solid nests and small peripheral columnar cells forming duct-like structures. Moreover, among the three currently known Wnt pathways, β-catenin is the suggested pathway working during cell differentiation. Furthermore, peripheral columnar cells in solid tumor nests and in squamous metaplasia are governed by another Wnt pathway other than β-catenin. Therefore, Wnt signaling through β-catenin pathway may be involved in the 'mixed' differentiation characteristic of pleomorphic adenoma although another pathway may also be possibly working in other parts of the tumor tissue.

CD44 expression in Dentigerous cyst, Radicular cyst and Ameloblastoma, by immunohistochemical analysis

The expression of cell adhesion molecule CD44s was analyzed immunohistochemically in 20 odontogenic lesions. CD44s was detected in almost all the cells on the cell membrane in basal and parabasal cells of the odontogenic cystic lining of the dentigerous cysts and the radicular cysts sparing the superficial layer of the cystic lining. CD44s was expressed on the cell membrane of the peripheral columnar cells and in the stellate cells, but were very negligible in the keratinizing areas.

Rare giant granular cell ameloblastoma: a case report and an immunohistochemical study.

Aims. The aim is to present a case of rare giant granular cell ameloblastoma and to review the pertinent literature highlighting the molecular aspects of its pathogenesis by analyzing the expression of CD-68, Bcl-2, and β-catenin. Methods. H and E stained sections showed large odontogenic islands showing peripheral ameloblast-like cells and central stellate reticulum-like cells with extensive granular cell transformation surrounded by fibrous stroma. Polyclonal rabbit anti-CD 68, anti-Bcl2, and anti-β-catenin were stained immunohistochemically. Results. CD-68 showed a moderate to strong staining intensity in granular cells. Moderate staining of Bcl-2 was expressed by the peripheral columnar cells of tumor islands and negative in the granular cells. Expression of β-catenin was generally weak, except for only the focal areas that showed a moderate staining intensity and weak in peripheral cells. Conclusion. The present case of giant granular cell ameloblastoma is a rare entity. Development of monstrous size is indicative of ameloblastomas persistent growth. Granular cell transformation in ameloblastomas probably occurs as a consequence of extensive molecular changes. Immunohistochemical studies help us to know the pathogenesis of this granular cell ameloblastoma. Therefore, an effort has been made here to study the expression of Bcl-2, CD-68, and β-catenin.

Round Blue Cell Tumor arising in the Background of Ameloblastic Fibrosarcoma

ABSTRACTWorld Health Organization (WHO) blue book of head and neck tumors reports 64 cases of ameloblastic fibrosarcoma and 14 cases of ameloblastic fibrodentinosarcoma/fibro-odontosarcoma. We present a unique case that does not fit into any of the WHO classified odontogenic sarcomas. The patient presented in 2006 with a densely sclerotic lesion arising from the left sphenoid bone, displacing the orbital contents and extending up to the inferior margin of the maxillary sinus. He was treated with left maxillectomy orbital exenteration. He relapsed 6 years later, salvage surgery was unsuccessful and subsequent care was supportive. Histologically the malignant neoplasm showed follicles comprising of peripheral columnar cells lined up in palisaded fashion with hyperchromatic nuclei displaced away from basement membrane. Center of the follicles comprised of spindle-shaped cells resembling stellate reticulum. Intervening areas showed fibrosarcomatous areas. Other areas revealed predominant sheets of round cells having hyperchromatic nuclei, inconspicuous nucleoli and scant cytoplasm. These round cells revealed strong membranous positivity for CD99.How to cite this articleHussain R, Hassan U, Jamshed A, Loya A. Round Blue Cell Tumor arising in the Background of Ameloblastic Fibrosarcoma. Int J Head Neck Surg 2013;4(2): 83-85.

Immunohistochemical expression of thymosin β4 in ameloblastomas and odontomas.

Ameloblastoma is regarded to be a benign odontogenic tumor, but it is destructive, locally invasive and presents a high rate of recurrence. Thymosin β4 (Tβ4) is closely associated with tooth germ development. Tβ4 also plays a role in malignant progression and invasion. However, little is known about the function of Tβ4 in odontogenic tumors. Thus, we investigated Tβ4 expression in ameloblastomas and compared it with odontomas. We immunohistochemically evaluated the expression of Tβ4, ameloblastin (AMBN), amelogenin (AMEL) and enamelin (ENAM) in 57 samples of ameloblastomas from 40 patients, and also assessed the expression of these molecules in 11 cases of odontomas, two of ameloblastic fibro-odontomas and one of tooth germ-like structures without the formation of enamel and dentin. Tβ4 signals were observed in almost all of the ameloblastomas. The signals were observed in both peripheral columnar cells and central polyhedral/angular cells. Similar findings were observed in tooth germ-like structures, and in the ameloblastomatous nests in the ameloblastic fibro-odontomas. These samples had negative results for AMBN, AMEL and ENAM. Meanwhile, Tβ4 signals were not seen in the odontomas, although immunolabeling for AMBN, AMEL and ENAM was observed in the enamel matrix and in some ameloblasts. Ectomesenhymal regions in the odontomas were negative for staining with the antibodies for AMBN, AMEL and ENAM. These results suggest that Tβ4 could be associated with morphogenesis and tumor invasion in the ameloblastoma, and that Tβ4 may play a role in the behavior of ameloblastoma.

Immunohistochemical expression of cyclin D1 in ameloblastomas and adenomatoid odontogenic tumors

Background:Cyclin D1, a member of G1 cyclins, controls the cell-cycle transit from the G1 to S phase. The deregulation and overexpression of cyclin D1 has been revealed in many tumors of diverse histogenesis. Ameloblastoma is the most frequently encountered odontogenic tumor known for its local invasiveness and a high tendency to recur. The adenomatoid odontogenic tumor is a benign, nonaggressive tumor with a limited growth and no tendency to recur.Aim:The aim was to investigate whether the immunohistochemical expression of cyclin D1 as a proliferation marker in ameloblastoma and adenomatoid odontogenic tumor correlates with the known clinical behavior of these two benign neoplasms.Materials and Methods:Ameloblastoma cases consisted of follicular, plexiform, and unicystic subtypes. The positive staining was assessed based on intensity of staining, localization of staining, and in different cell types in both the tumors. Two cases of follicular ameloblastoma and one case of plexiform ameloblastoma showed intense staining, but the predominant staining intensity was overall mild in both ameloblastoma and adenomatoid odontogenic tumors. The immunoreactivity was found both in nucleus and cytoplasm in ameloblastoma and only nuclear in adenomatoid odontogenic tumors. The peripheral columnar and central stellate reticulum-like cells of ameloblastoma showed immunoreactivity with squamous and granular cells being negative. In adenomatoid odontogenic tumors, the whorls showed predominant localization of staining. Statistical comparison with a Mann–Whitney U-test showed no significant difference in staining intensities between different histologic subtypes of ameloblastomas and also between ameloblastoma and adenomatoid odontogenic tumors (P>0.005).Conclusion:The marked expression of cyclin D1 in these tumors suggested its participation in proliferation of both the tumors and its expression patterns were irrespective of their known biologic behavior.

Expression of heparanase: a possible role in invasiveness and aggressive clinical behavior of ameloblastomas

Heparanase is an endoglycosidase that cleaves heparan sulfate (HS), thus participating in degradation and remodeling of the extracellular matrix (ECM). Heparanase up-regulation is correlated with lymph node and distant metastasis, microvessel density and reduced postoperative survival of cancer patients. In the present study, we carried out an immunohistochemical investigation of heparanase to extend and confirm present knowledge regarding its expression in ameloblastomas (AMs), which are characterized by locally aggressive behavior. Paraffin-embedded tissue specimens of 53 AMs were stained using an antibody against heparanase. Immunohistochemical reactivity for heparanase was detected in 94.3% of the AMs examined. Heparanase was expressed strongly in peripheral columnar cells and slightly in central stellate reticulum-like cells. Small tumor nests and budding epithelial branches showed a stronger staining pattern. Stromal cells were negative for heparanase, or showed diffuse expression. However, an enhanced positive immunoreaction was present specifically near osseous tissue and adjacent to the invasive front of tumor nests. Areas of cystic degeneration showed intense heparanase immunoreactivity. The enzyme may facilitate the function of HS-binding growth factors that elicit an angiogenic response and favor osteoclastogenesis in AM.

Enhanced expression of podoplanin in ameloblastomas

Podoplanin, a mucin-type transmembrane glycoprotein, is specifically expressed by lymphatic but not blood vascular endothelial cells, and is also widely expressed in various specialized cell types throughout the body. Recent studies have demonstrated that it mediates a pathway leading to collective cell migration and invasion in vivo and in vitro. In the present study, we carried out an immunohistochemical investigation of podoplanin to clarify whether it is expressed in human ameloblastomas (AMs), which are characterized by locally aggressive behavior with a high rate of recurrence. In addition, we examined the localization of the epithelial marker E-cadherin and the mesenchymal marker vimentin to clarify whether AMs show epithelial-mesenchymal transition (EMT). Paraffin-embedded tissue specimens of 38 AMs were examined immunohistochemically using antibodies against podoplanin, E-cadherin, and vimentin. Immunohistochemical reactivity for podoplanin was detected in the cell membrane and cytoplasm of most odontogenic tumor epithelial cells in AMs. Podoplanin was expressed strongly in peripheral columnar cells and slightly in central stellate reticulum-like cells. E-cadherin was expressed in central stellate reticulum-like cells and showed decreased expression in peripheral columnar cells. Immunoreactivity for E-cadherin was weak or negative in keratinizing cells of acanthomatous AMs, suggesting terminal differentiation of the tumor cells. Immunohistochemical reactivity for vimentin was found in stromal cells, but partial or no reaction was observed in neoplastic cells. Expression of podoplanin in AMs is considered to be associated with neoplastic odontogenic tissues; this molecule might play a role in the collective cell migration of tumor nests in AMs. The pattern of expression of E-cadherin and vimentin suggests that invasion in AMs occurs in the absence of EMT. The migration and invasion mediated by podoplanin in AMs could be related to cytoskeletal reorganization.

Mutational analysis of Wnt signaling molecules in ameloblastoma with aberrant nuclear expression of β‐catenin

To clarify the genetic background of ameloblastoma, expression of beta-catenin, and mutational status of genes involved in Wnt signaling pathway were investigated. We analyzed beta-catenin and cyclin D1 in 18 cases of ameloblastoma by immunohistochemical staining, and searched for mutations in CTNNB1 (gene for beta-catenin), APC, AXIN1, and AXIN2 by polymerase chain reaction (PCR) and direct sequencing method. We detected membranous and occasionally cytoplasmic expression of beta-catenin in 16 of 18 cases (89%), and nuclear expression of beta-catenin principally in the peripheral columnar cells in 11 of 18 cases (61%). In nine of the 18 cases (50%), we detected the expression of cyclin D1 principally in the peripheral columnar cells. However, there was no correlation between nuclear expressions of beta-catenin and cyclin D1. No missense mutations were found in CTNNB1, APC, AXIN1, and AXIN2 in all cases except for silent mutation and already-known single nucleotide polymorphism. Mutations in CTNNB1, APC, AXIN1, and AXIN2 are not implicated in nuclear accumulation of beta-catenin, and that the expression of cyclin D1 is accelerated independently of beta-catenin in ameloblastomas. Other Wnt signaling members or alternative pathways involved in the degradation of beta-catenin should be subject of further investigation.

Midkine expression correlating with growth activity and tooth morphogenesis in odontogenic tumors

Midkine (MK; a low molecular weight heparin-binding growth factor) is a multifunctional cytokine. MK plays a role in morphogenesis of many organs including teeth through epithelial-mesenchymal interactions. We immunohistochemically examined MK expression in various human odontogenic tumors. There was no difference in positive rate and intensity of MK between benign odontogenic tumors and their malignant counterparts. Ameloblastoma showed MK localization in the peripheral columnar cells in budding processes from the parenchyma, which frequently expressed proliferating cell nuclear antigen. MK was also preferentially expressed in keratinized cells in acanthomatous ameloblastoma and keratocystic odontogenic tumor. In odontogenic mixed tumors except for odontoma, intense immunoreactivity to MK was found in epithelial follicles, the surrounding odontogenic ectomesenchymal tissue, and the basement membrane between them. Intensity in the odontogenic ectomesenchyme decreased in relation to distance from the epithelial follicles. No expression was found in tumor cells associated with production of dental hard tissues in odontogenic mixed tumors including odontoma. These findings suggested that MK is involved in the reciprocal interaction between odontogenic epithelium and odontogenic ectomesenchymal tissue in areas without dental hard tissue formation in odontogenic mixed tumors. Coexpression of MK and proliferating cell nuclear antigen was also observed in epithelial follicles and highly cellular nodules in the ectomesenchyme of odontogenic mixed tumors. MK is considered to mediate growth activity of odontogenic tumors and cell differentiation of odontogenic mixed tumors through molecular mechanisms similar to those involved in morphogenesis of the tooth.

Expression of Sonic hedgehog (SHH) signaling molecules in ameloblastomas.

To clarify the roles of Sonic hedgehog (SHH) signal transduction in oncogenesis and cytodifferentiation of odontogenic tumors, expression of SHH, Patched (PTC), Smoothened (SMO), and GLI1 was analyzed in ameloblastomas as well as in tooth germs. Tissue specimens of 9 tooth germs, 36 benign ameloblastomas, and 1 malignant ameloblastoma were examined by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry for the expression of SHH, PTC, SMO, and GLI1. Expression of SHH, PTC, SMO, and GLI1 mRNA was detected in all tooth germ and ameloblastoma samples. Immunohistochemical reactivity for SHH, PTC, SMO, and GLI1 was detected in both normal and neoplastic odontogenic tissues. Expression of SHH, PTC, and GLI1 was more evident in epithelial cells than in mesenchymal cells, whereas SMO reactivity was marked in both epithelial and mesenchymal components in tooth germs and ameloblastomas. In ameloblastomas, these SHH signaling molecules were expressed more intensely in peripheral columnar or cuboidal cells than in central polyhedral cells; keratinizing cells and granular cells showed no or little reactivity. Expression of SHH, PTC, SMO, and GLI1 in tooth germs and ameloblastomas suggests that these SHH signaling molecules might play a role in epithelial-mesenchymal interactions and cell proliferation in tooth development as well as in growth of these epithelial odontogenic tumors.

Expression of parathyroid hormone-related protein (PTHrP), osteoclast differentiation factor (ODF)/receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoclastogenesis inhibitory factor (OCIF)/osteoprotegerin (OPG) in ameloblastomas.

To clarify the roles of osteoclast regulatory factors in progression of odontogenic tumors, expression of parathyroid hormone-related protein (PTHrP), osteoclast differentiation factor (ODF)/receptor activator of nuclear factor-kappaB ligand (RANKL), and osteoclastogenesis inhibitory factor (OCIF)/osteoprotegerin (OPG) were analyzed in ameloblastomas as well as tooth germs. Tissue specimens of nine tooth germs and 36 benign and one malignant ameloblastomas were examined by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry for the expression of PTHrP, ODF/RANKL, and OCIF/OPG. Expression of PTHrP, ODF/RANKL, and OCIF/OPG mRNA was detected in all tooth germ and ameloblastoma samples. Immunohistochemical reactivity for PTHrP was recognized in both normal and neoplastic odontogenic epithelial cells. In ameloblastomas, PTHrP reactivity in peripheral columnar or cuboidal cells was stronger than that in central polyhedral cells, and keratinizing cells showed increased PTHrP reactivity. ODF/RANKL and OCIF/OPG were expressed predominantly in mesenchymal cells rather than in odontogenic epithelial cells in both tooth germs and ameloblastomas. Epithelial ODF/RANKL and OCIF/OPG expression was slightly lower in ameloblastomas than in tooth germs. Tumor cells in plexiform ameloblastomas showed slightly higher reactivity for PTHrP and ODF/RANKL than tumor cells in follicular ameloblastomas. Expression of PTHrP, ODF/RANKL and OCIF/OPG in tooth germs and ameloblastomas suggests that these factors might locally regulate bone metabolism and dynamics in tooth development as well as in progression of ameloblastomas. These factors might also be involved in tumor cell differentiation and/or tumor tissue structuring in ameloblastomas.

Neural cell adhesion molecule and neurothelin expression in human ameloblastoma

Purpose: The objective of the present study was to determine whether neural cell adhesion molecules (NCAM; CD56) and neurothelin (CD147) are expressed by adontogenic cells in the ameloblastoma. Materials and Methods: Frozen sections from ameloblastoma specimens (n = 7) were stained with monoclonal antibody-recognizing CD56 and CD147 molecules using indirect immunoperoxidase and indirect immunofluorescent techniques. Results: CD56 and CD147 molecules were strongly expressed by the peripheral columnar cells of the tumor nests. Neurothelin reactivity was also present in the stellate reticulum of the nests and in some stromal components. Conclusions: The presence of these antigens in ameloblastoma supports the classic view about the neural crest origin of cells giving use to this tumor. © 2001 Ameriacn Association of Oral and Maxillofacial Surgeons

Immunohistochemical detection of amelogenin and cytokeratin 19 in epithelial odontogenic tumors

Epithelial odontogenic tumors exhibit considerable histological variation and are classified into several benign and malignant entities. Expression of amelogenin and cytokeratin 19 (CK19), that are potentially useful polypeptides for identification of odontogenic epithelial components, was evaluated in various types of epithelial odontogenic tumors. Specimens of 33 ameloblastomas, three calcifying epithelial odontogenic tumors (CEOTs), two clear cell odontogenic tumors (CCOTs) and five malignant ameloblastomas were examined by immunohistochemistry using anti-amelogenin and anti-CK19 antibodies. Immunohistochemical reactivity for amelogenin was detected in many peripheral columnar or cuboidal cells and some central polyhedral cells in ameloblastomas, and histological variants showed various degrees of amelogenin expression. Expression of CK19 was diffusely present in neoplastic cells in ameloblastomas, and decreased expression was found in keratinizing cells of acanthomatous variants and some neoplastic cells of desmoplastic variants. In CEOTs, immunohistochemical reactivity for amelogenin was detected in neoplastic cells and intercellular amyloid-like materials, whereas CK19 was expressed in neoplastic cells. CCOTs showed positive reactivity for amelogenin and CK19 in neoplastic cells. Malignant ameloblastomas exhibited various degrees of amelogenin expression with constant CK19 expression in neoplastic cells. Diverse types of epithelial odontogenic tumors express amelogenin and CK19, suggesting that these tumors have ameloblastic differentiation or odontogenic epithelial properties.