Immunohistochemical detection of BH3-only proteins in ameloblastic tumors.

OBJECTIVE: To evaluate expression of BH3-only proteins in odontogenic tumors, expression of Bid, Bim, Bad, Noxa, and Puma was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: Nine tooth germs, 37 ameloblastomas, and five malignant ameloblastic tumors were examined immunohistochemically with antibodies against Bid, Bim, Bad, Noxa, and Puma. RESULTS: Immunohistochemical reactivity for Bid, Bim, Bad, Noxa, and Puma was detected in the cytoplasm of cellular components in normal and neoplastic odontogenic tissues. Expression of these BH3-only proteins was evident in odontogenic epithelial cells near the basement membrane in tooth germs and ameloblastic tumors. Acanthomatous ameloblastomas showed no reactivity for Bid, Bim, Bad, Noxa, or Puma in keratinizing cells, whereas granular cells in granular cell ameloblastomas reacted with these BH3-only proteins. Basal and desmoplastic ameloblastomas and ameloblastic carcinomas showed immunoreactivity for the BH3-only proteins in most neoplastic cells. CONCLUSION: Expression of Bid, Bim, Bad, Noxa, and Puma in tooth germs and ameloblastic tumors suggests that the BH3-only proteins have a role in apoptotic cell death of normal and neoplastic odontogenic epithelium. Distinctive expression patterns of these BH3-only proteins in ameloblastoma variants suggest that the BH3-only proteins might be involved in tumor cell differentiation of ameloblastomas.

Immunohistochemical detection of phosphorylated JNK, p38 MAPK, and ERK5 in ameloblastic tumors.

BACKGROUND: To evaluate roles of mitogen-activated protein kinases (MAPKs) in oncogenesis and cytodifferentiation of odontogenic tumors, expression of phosphorylated JNK (p-JNK), p38 MAPK (p-p38 MAPK), and ERK5 (p-ERK5) was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: Ten tooth germs, 47 ameloblastomas, and 5 malignant ameloblastic tumors were examined immunohistochemically with the antibodies against p-JNK, p-p38 MAPK, and p-ERK5. RESULTS: Immunoreactivity for p-JNK was detected in epithelial or neoplastic cells detached from the basement membrane in 7 tooth germs and 7 ameloblastomas, and the expression levels of p-JNK in ameloblastic tumors were significantly lower than that in tooth germs. Expression of p-p38 MAPK was found in epithelial or neoplastic cells in tooth germs and ameloblastic tumors except for two ameloblastomas, and increased expression was found in keratinizing cells of acanthomatous ameloblastomas. The expression level of p-p38 MAPK in ameloblastomas was significantly higher than the levels in tooth germs and malignant ameloblastic tumors. Immunoreactivity for p-ERK5 was found predominantly in epithelial or neoplastic cells near the basement membrane in tooth germs and ameloblastic tumors. The expression levels of p-ERK5 in ameloblastic tumors were slightly higher than that in tooth germs, and plexiform ameloblastomas showed significantly higher p-ERK5 expression than follicular ameloblastomas. CONCLUSION: Expression of p-JNK, p-p38 MAPK, and p-ERK5 in tooth germs and ameloblastic tumors suggests that these MAPK signaling pathways contribute to cell proliferation, differentiation, or apoptosis in both normal and neoplastic odontogenic tissues. Altered expression of these phosphorylated MAPKs in ameloblastic tumors may be involved in oncogenesis and tumor cell differentiation.

Immunohistochemical detection of uPA, uPAR, PAI-1, and maspin in ameloblastic tumors.

BACKGROUND: To evaluate the roles of extracellular matrix (ECM)-degrading serine proteinase in progression of odontogenic tumors, expression of urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), plasminogen activator inhibitor-1 (PAI-1), and maspin was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: Tissue specimens of 10 tooth germs, 45 ameloblastomas, and 5 malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against uPA, uPAR, PAI-1, and maspin. RESULTS: Immunohistochemical reactivity for uPA, uPAR, PAI-1, and maspin was detected in normal and neoplastic odontogenic tissues: uPA was recognized predominantly in mesenchymal cells, uPAR was evident in epithelial cells, PAI-1 was found in both epithelial and mesenchymal cells, and maspin was expressed only in epithelial cells. The levels of uPA and uPAR immunoreactivity in ameloblastic tumors were slightly higher than the levels in tooth germs, while PAI-1 reactivity in ameloblastomas tended to be lower than that in tooth germs. The level of maspin immunoreactivity in ameloblastomas was significantly higher than that in tooth germs, and ameloblastic carcinoma showed decreased maspin reactivity. CONCLUSION: Expression of uPA, uPAR, PAI-1, and maspin in tooth germs and ameloblastic tumors suggests that interactions among these molecules contribute to ECM degradation and cell migration during tooth development and tumor progression. Altered expression of the serine proteinase and its associated molecules in ameloblastic tumors may be involved in oncogenesis of odontogenic epithelium.

Immunohistochemical detection of insulin-like growth factors, platelet-derived growth factor, and their receptors in ameloblastic tumors.

BACKGROUND: To evaluate the roles of growth factors in oncogenesis and cytodifferentiation of odontogenic tumors, expression of insulin-like growth factors (IGFs), platelet-derived growth factor (PDGF), and their receptors was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: Tissue specimens of 10 tooth germs, 47 ameloblastomas, and five malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against IGF-I, IGF-II, IGF-I receptor (IGF-IR), PDGF A-chain, PDGF B-chain, PDGF alpha-receptor, and PDGF beta-receptor. RESULTS: Immunohistochemical reactivity for IGFs, PDGF chains, and their receptors was detected predominantly in odontogenic epithelial cells near the basement membrane in tooth germs and in benign and malignant ameloblastic tumors. The expression levels of IGF-II and PDGF chains were significantly higher in ameloblastic tumors than in tooth germs. Malignant ameloblastic tumors showed higher reactivity for PDGF chains than benign ameloblastomas and higher reactivity for platelet-derived growth factor receptors than tooth germs. The expression levels of PDGF chains were significantly higher in follicular ameloblastomas than in plexiform ameloblastomas. Desmoplastic ameloblastomas showed higher expression of IGFs and IGF-IR when compared with other ameloblastoma subtypes. CONCLUSION: Expression of IGFs, PDGF, and their receptors in tooth germs and ameloblastic tumors suggests that these growth factor signals contribute to cell proliferation or survival in both normal and neoplastic odontogenic tissues. Expression of these molecules in odontogenic tissues possibly affects interactions with the bone microenvironment during tooth development and intraosseous progression of ameloblastic tumors. Altered expression of the ligands and receptors in ameloblastic tumors may be involved in oncogenesis, malignant potential, and tumor cell differentiation.

Histomorphometrical study in cavernous lymphangioma of the tongue.

OBJECTIVE: To study the histomorphometrical characteristics of lymphatic vessels in cavernous lymphangiomas of the tongue. MATERIAL AND METHODS: Immunohistochemical stainings were prepared in the 20 specimens with three antibodies [D2-40, CD31 and proliferating cell nuclear antigen (PCNA)]. Three-dimensional (3D) reconstruction and histometrical analysis of the lymphatic vessels was also examined. RESULTS: Distinctly positive staining for D2-40 was found in dilated lymphatic vessels located in the lamina propria beneath the thinned covering epithelium. Small blood vessels stained positively for CD31 were present in the lamina propria. PCNA-positive lymphatic endothelial cells were scattered in both control and lymphangioma. The 3D architecture of lymphatic vessels was characterized by a complex network with irregular branches in the lamina propria. Histometrical analysis showed that the number of lymphatic endothelial cells per lymphatic vessel perimeter in cavernous lymphangioma was significantly higher than that in control. There were no significant differences in the lymphatic density and the ratio of PCNA-positive lymphatic endothelial cell nuclei to the total number of lymphatic endothelial cell nuclei between control and lymphangioma. CONCLUSIONS: These results indicate the absence of excessive endothelial cell proliferation in dilated lymphatic vessels in cavernous lymphangioma. Cavernous lymphangioma may be attributed to the enlargement of lymphatic vessels without the tumorous proliferation of lymphatic endothelial cells.

Immunohistochemical detection of MT1-MMP, RECK, and EMMPRIN in ameloblastic tumors.

BACKGROUND: To evaluate the roles of matrix-degrading proteinase regulators in progression of odontogenic tumors, expression of membrane-bound matrix metalloproteinase (MMP) MT1-MMP, MMP inhibitor RECK and MMP inducer EMMPRIN was analyzed in ameloblastic tumors as well as in tooth germs. METHODS: Tissue specimens of 11 tooth germs, 40 ameloblastomas, and five malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against MT1-MMP, RECK, and EMMPRIN. RESULTS: Immunohistochemical reactivity for MT1-MMP, RECK and EMMPRIN was detected predominantly in odontogenic epithelial cells near the basement membrane in tooth germs and benign and malignant ameloblastic tumors. The level of immunoreactivity for MT1-MMP was slightly higher in benign and malignant ameloblastic tumors than in tooth germs. RECK expression was lower in ameloblastomas than in tooth germs. Follicular ameloblastomas showed significantly lower expression of RECK than plexiform ameloblastomas, and immunoreactivity for RECK in acanthomatous ameloblastomas was slightly lower than that in other cellular variants. CONCLUSION: Expression of MT1-MMP, RECK and EMMPRIN in tooth germs and ameloblastic tumors suggests that these normal and neoplastic epithelial components control MMP-dependent extracellular matrix (ECM) degradation during tooth development and tumor progression via epithelial-mesenchymal interactions.

Expression of bone morphogenetic proteins and their associated molecules in ameloblastomas and adenomatoid odontogenic tumors.

OBJECTIVE: To further clarify the roles of regulators of embryonic development, bone morphogenetic protein (BMPs) and their associated molecules, in oncogenesis and cytodifferentiation of odontogenic tumors, the expression of these regulator molecules were analyzed in epithelial odontogenic tumors as well as in tooth germs. MATERIALS AND METHODS: Tooth germs, ameloblastomas, adenomatoid odontogenic tumors, and malignant ameloblastomas were examined by RT-PCR and immunohistochemistry for detection of BMP-2, -4, -7, BMP receptors I and II (BMPR-I, BMPR-II), core-binding factor alpha1 (CBFA1), and osterix. RESULTS: mRNA expression of BMPs, BMPRs, CBFA1, and osterix was detected in all odontogenic tissues. Immunohistochemical reactivity for BMPs, BMPRs, and CBFA1 was detected in both epithelial and mesenchymal cells of tooth germs and epithelial odontogenic tumors. BMPs and BMPRs were evidently expressed in odontogenic epithelial cells in tooth germs and epithelial odontogenic tumors. Acanthomatous ameloblastomas showed increased BMP-7 reactivity in keratinizing cells. Nuclear CBFA1 expression was detected scatteredly in odontogenic epithelial cells in normal and neoplastic odontogenic tissues, as well as in some mesenchymal cells in tooth germs and in some stromal cells in epithelial odontogenic tumors. Ameloblastic carcinomas showed low reactivity for BMPs, BMPRs, and CBFA1. CONCLUSION: BMPs and their associated molecules might play a role in cytodifferentiation of normal and neoplastic odontogenic epithelium via epithelial-mesenchymal interactions.

Immunohistochemical detection of beta-catenin and adenomatous polyposis coli in ameloblastomas.

BACKGROUND: To clarify the roles of the Wnt signaling pathway in oncogenesis and cytodifferentiation of odontogenic tumors, expression of beta-catenin and adenomatous polyposis coli (APC) was analyzed in ameloblastomas as well as in tooth germs. METHODS: Tissue specimens of 10 tooth germs, 40 benign ameloblastomas, and five malignant ameloblastomas were examined immunohistochemically with the use of antibodies against beta-catenin and APC. RESULTS: Immunohistochemical reactivity for beta-catenin was detected in the cell membrane and cytoplasm of most odontogenic epithelial cells in tooth germs and ameloblastomas. Nuclear beta-catenin expression was recognized in nine of 40 ameloblastomas and two of five malignant ameloblastomas, but not in tooth germs. APC was evidently expressed in odontogenic epithelial cells neighboring the basement membrane in tooth germs and ameloblastomas, and the reactivity was significantly lower in benign and malignant ameloblastomas than in tooth germs. Follicular ameloblastomas and acanthomatous ameloblastomas tended to show high nuclear beta-catenin expression and low APC reactivity, as compared with other ameloblastoma variants. CONCLUSION: Expression of beta-catenin and APC in tooth germs and ameloblastomas suggests that aberration of the Wnt signaling pathway might play a role in oncogenesis and cytodifferentiation of odontogenic epithelium via deregulation of cell proliferation.

Chondroma of the cheek: A case report.

An extremely rare case of soft tissue chondroma occurring in the right cheek of a 47-year-old woman is reported. The localized nodular tumor was encapsulated and composed of hyalinized cartilage with fine calcifications. Most tumor cells were positive for vimentin and S-100 protein, but negative for cytokeratin, factor VIII, and smooth muscle actin. It seems likely that the tumor cells arise from uncommitted mesenchymal stem cells by metaplastic process.

Immunohistochemical analysis of apoptosis-related factors in lining epithelium of radicular cysts.

BACKGROUND: Some studies suggest that apoptosis-related factors are involved in the inflammatory processes of marginal periodontal lesions. However, the role of apoptosis in periapical inflammatory lesions remains unclear. We investigated the possible role of apoptotic cell death in periapical inflammatory lesions by means of immunohistochemical analysis of apoptosis-related factors and use of a cell proliferation marker. METHODS: Paraffin-embedded sections of 19 radicular cysts (RCs), and five residual radicular cysts (RRCs) and control specimens of normal gingivae excised from seven cadavers were prepared and examined immunohistochemically with the use of monoclonal antibodies or polyclonal antisera against single-stranded DNA (ssDNA), p53, Bax, Bcl-2, caspase-3, Fas, Fas ligand (Fas-L), and Ki-67 antigen. RESULTS: Epithelium of gingiva, RCs, and RRCs showed expression of ssDNA in suprabasal and superficial epithelial cells and Ki-67 reactivity in basal and parabasal cells. Expression of Ki-67 and ssDNA in RCs and RRCs was slightly higher than that in gingiva. Both Ki-67 and ssDNA reactivity in RCs with intense inflammatory reactions or with thick lining epithelium were significantly stronger than those in RCs with less inflammatory reactions or with thin lining epithelium. Reactivity for p53 was noted sporadically in epithelium of gingiva, RCs, and RRCs, and p53 expression in RCs was significantly greater than that in gingiva. Ki-67 and ssDNA reactivity in RCs increased parallel to the degree of p53 expression. Bax and Bcl-2 were detected in some basal epithelial cells in RCs and RRCs as well as in gingiva. The ssDNA reactivity significantly increased parallel to Bax expression and slightly decreased parallel to Bcl-2 expression in lining epithelium of RCs. Caspase-3 was detected in superficial epithelial cells of both gingiva and lining epithelium of RCs and RRCs, and the distribution of these cells was compatible with the expression of ssDNA. Expression of Ki-67 and ssDNA in caspase-3-positive fields was significantly higher than that in caspase-3-negative fields in RCs. There was very limited expression of Fas and Fas-L in lining epithelium of RCs and RRCs as well as in gingiva. CONCLUSIONS: These data suggest that apoptosis-related factors are involved in the pathophysiologic activity of periapical inflammatory lesions. Such factors may be affected by the structure of lining epithelium and the degree of inflammatory change.

PTC gene mutations and expression of SHH, PTC, SMO, and GLI-1 in odontogenic keratocysts.

The Patched (PTC) gene is responsible for basal cell nevus syndrome (BCNS) accompanied by multiple odontogenic keratocysts (OKCs), and its product plays a role in the Sonic hedgehog (SHH) signaling pathway involving smoothened (SMO) and GLI-1. To clarify the role of SHH signaling in OKCs, the expression of SHH, PTC, SMO, and GLI-1 and mutations of PTC were examined in 18 sporadic, 4 BCNS-associated OKCs and 7 control gingivae. SHH, PTC, SMO, and GLI-1 were detected in all OKC and gingiva samples by reverse transcriptase-polymerase chain reaction (RT-PCR). Immunoreactivity for SHH and GLI-1 was markedly higher in epithelial components than in subepithelial cells, while immunoreactivity for PTC and SMO was similar in epithelial components and subepithelial cells in OKCs. The positive rate of PTC and SMO expression in subepithelial cells of OKCs was significantly higher than that in gingivae. The positive rate of GLI-1 expression in subepithelial cells of BCNS-associated OKCs was significantly higher than that in primary OKCs. These results suggest that the SHH signaling might be involved in the pathophysiologic nature of OKCs. While mutations of the PTC gene could not be detected in 4 BCNS-associated OKCs by direct DNA sequencing, 3 of 5 primary and 4 of 4 recurrent OKCs had several mutations of this gene. These results suggest that PTC mutations are probably related not only to BCNS-associated OKCs but also to sporadic OKCs.

Sebaceous adenoma in the retromolar region: report of a case with a review of the English literature.

This paper reports a rare case of sebaceous adenoma on the right mandibular retromolar mucosa in a 73-year-old Japanese man, with a review of the English literature of sebaceous adenomas of salivary gland origin. A painless and yellowish polypoid lesion in the retromolar mucosa was histologically a relatively well-circumscribed neoplastic mass composed of well-differentiated sebaceous cells with cystic and duct-like structures, and was considered to be a true sebaceous gland neoplasm arising from the minor salivary gland tissue.

Simplified procedure for augmentation of the sinus floor using a haemostatic nasal balloon.

Perforation of the sinus membrane is the most common complication of sinus lift augmentation. A haemostatic nasal balloon can easily separate the sinus membrane without perforating it. The use of a haemostatic nasal balloon has three major advantages: a low risk of perforation of the sinus membrane even in anatomically complex conditions, a low incidence of infection and bleeding, and a shorter operating time.

A histopathological and lectin-histochemical study of the lining epithelium in postoperative maxillary cysts.

OBJECTIVE: Histopathological and lectin-histochemical characteristics were studied in the lining epithelium of postoperative maxillary cysts (POMC). MATERIALS AND METHODS: Histological (HE, PAS, AB), immunohistochemical (CD3 and L26) and lectin (wheat germ agglutinin, WGA; Ulex europaeus agglutinin I, UEA-I; concanavalin A, ConA) stainings were performed in the 360 POMC specimens. The number of goblet cells and inflammatory cells was counted and statistically analyzed. RESULTS: The lining epithelium was classified into three types based on histopathological characteristics; pseudostratified ciliated epithelium (pSCE), transitional epithelium (TE) and stratified squamous epithelium (SSE). Local infiltration of inflammatory cells into the cyst wall was associated with an increased number of goblet cells in the lining epithelium. The observed association between the infiltration of inflammatory cells and an increase in the number of goblet cells was statistically significant in groups with lining pSCE and TE. Glycoconjugate histochemical analysis revealed that the surfaces of the lining epithelium with squamous metaplasia showed an increased degree of staining reactivity with UEA-I, whereas the staining reactivity with ConA was reduced. Goblet cells were able to be stained with WGA and UEA-I, but showed extremely low reactivity with ConA. CONCLUSION: Changes in the glycoconjugate expression of the metaplastic lining epithelium and goblet cell development play an important role in the local defense mechanisms against inflammatory factors in POMC.

Intramucosal naevus with pseudoepitheliomatous hyperplasia in the gingiva: a case report.

This article describes the unusual case of an intraoral pigmented naevus with pseudoepitheliomatous hyperplasia of the gingiva. A 62-year-old man presented with an almost coal-black pigmented and partly white, spotted, dome-shaped swelling on the lingual gingiva of the mandible. Histologically, the lesion consisted of clusters of round-shaped naevus cells containing melanin granules, reactive with both S-100 immunohistochemical stain and Masson-Fontana silver stain, and pseudoinvasive squamous nests, reactive with cytokeratin. The pathogenesis of the present lesion and problems encountered in its differential diagnosis are discussed.

Histopathological and immunohistochemical analysis of calcifying odontogenic cysts.

METHOD AND RESULTS: Calcifying odontogenic cysts (COCs) were examined histopathologically and immunohistochemically to characterize the histological and cytological properties of these lesions. Histopathologically, COCs showed thin or thick lining epithelium with ghost cells. COCs were classified according to proliferative type or nonproliferative type lining epithelium, the presence or absence of ameloblastomatous appearance, and the presence or absence of odontoma in the cyst walls. Immunohistochemically, amelogenin protein was expressed chiefly in ghost cells, whereas cytokeratin 19 (CK19) and bcl-2 proteins were expressed chiefly in lining epithelial cells. The proportion of cases positive for bcl-2 protein was slightly higher in COCs with odontoma than in those without odontoma. Lining epithelial cells sporadically showed positive reactions for Ki-67 antigen. Mean Ki-67 labeling index was slightly greater in COCs with proliferative type lining epithelium, COCs with ameloblastomatous appearance of the cyst walls, and COCs with odontoma of the cyst walls than in COCs without these histological features. Our results suggest that ghost cells or lining epithelial cells show ameloblastic cytodifferentiation or odontogenic epithelial characteristics, that bcl-2 protein is associated with survival of lining epithelial cells in COCs, and that high proliferation potential is associated with ameloblastomatous proliferation or combined odontoma. COCs exhibited various histological features with several transitional forms, and immunohistochemical examinations revealed little or no difference in cytodifferentiation and cellular activity among COCs. CONCLUSION: We conclude that COCs with various histological features have neoplastic potential and may not be separate entities within the same histological spectrum.

Immunohistochemical analysis of apoptosis-related factors (Fas, Fas ligand, caspase-3 and single-stranded DNA) in ameloblastomas.

BACKGROUND: To clarify the possible role of apoptotic cell death in oncogenesis and cytodifferentiation of odontogenic epithelium, apoptosis-related factors--Fas, Fas ligand (FasL), caspase-3 and single-stranded DNA (ssDNA)--were analyzed in ameloblastomas as well as in tooth germs. METHODS: Specimens of 5 tooth germs, 29 benign ameloblastomas and 5 malignant ameloblastomas were examined by immunohistochemistry using anti-Fas, FasL, caspase-3 and ssDNA polyclonal antibodies. RESULTS: Immunoreactivity for Fas and FasL was detected in normal and neoplastic odontogenic epithelial cells. Fas expression in ameloblastomas was slightly lower than that in tooth germs, whereas FasL expression was similar in tooth germs and ameloblastomas. Malignant ameloblastomas showed downregulation of Fas expression and upregulation of FasL expression, as compared with benign ameloblastomas, indicating escape from cell death attack by immune cells. Immunoreactivity for caspase-3 was detected chiefly in cells neighboring the basement membrane in tooth germs and ameloblastomas. Expression of caspase-3 and Fas tended to be low in basal cell ameloblastomas and high in desmoplastic ameloblastomas, as compared with other variants of ameloblastomas. Caspase-3 expression was more intense in malignant ameloblastomas than in tooth germs and benign ameloblastomas. Apoptotic bodies reactive with anti-ssDNA antibody were detected in normal and neoplastic odontogenic epithelial cells detached from the basement membrane. Keratinizing cells in acanthomatous ameloblastomas and granular cells in granular cell ameloblastomas showed increased numbers of apoptotic bodies and increased expression of Fas and caspase-3, as compared with other neoplastic cells. Apoptotic reactions in malignant ameloblastomas were less frequent than in benign ameloblastomas, indicating abnormal regulation of cell turnover in odontogenic epithelial cells. CONCLUSION: These apoptosis-related factors were detected in various patterns in normal and neoplastic odontogenic epithelium, suggesting that these factors might be associated with oncogenesis and cytodifferentiation of epithelial odontogenic tumors.

Immunohistochemical detection of amelogenin and cytokeratin 19 in epithelial odontogenic tumors.

OBJECTIVE: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: Diverse types of epithelial odontogenic tumors express amelogenin and CK19, suggesting that these tumors have ameloblastic differentiation or odontogenic epithelial properties.

Immunohistochemical analysis of cell-cycle- and apoptosis-related factors in lining epithelium of odontogenic keratocysts.

We examined the immunohistochemical expressions of cell-cycle- and apoptosis-related factors to investigate the possible role of these factors in odontogenic keratocyst (OKC). Expression of cyclin D1 and p16 protein was detected in the basal and parabasal cells in lining epithelium of OKCs and was found more frequently in basal cell nevus syndrome (BCNS)-associated OKCs than in primary or recurrent OKCs. Positivity for p21 protein was detected in basal to superficial cells, whereas that for p27 protein was detected in parabasal to superficial cells in lining epithelium of OKCs. DNA topoisomerase IIalpha reacted with nuclei in basal and parabasal cells of the lining epithelium of OKCs, and positive cells were observed in BCNS-associated OKCs significantly more frequently than in primary or recurrent OKCs. Expression of Fas in suprabasal to superficial cells and expression of Fas-L in basal and parabasal cells were detected in lining epithelium of OKCs. Immunoreactivity for caspase-3 was detected in basal to suprabasal or superficial cells in lining epithelium of OKCs. Single stranded (ss)DNA-positive nuclei were detected in superficial cells in lining epithelium of OKCs. Fas was more broadly distributed in BCNS-associated OKCs than in primary OKCs, and ssDNA-positive cells were observed in BCNS-associated OKCs significantly more frequently than in primary or recurrent OKCs. These results suggest that BCNS-associated OKCs might be a distinguishable entity from solitary OKCs.