Ameloblastoma ex calcifying odontogenic cyst (dentinogenic ghost cell tumor)

Calcifying odontogenic cyst (COC) has shown to be of extensive diversity in its clinical and histopathological features, as well as in its biological behavior. In this report, a rare case is described of ameloblastoma ex COC (dentinogenic ghost cell tumor) and the relevant literature is briefly reviewed.     

K-Ras gene status and expression of Ras/mitogen-activated protein kinase (MAPK) signaling molecules in ameloblastomas

BACKGROUND: To clarify the roles of rat sarcoma (Ras)/mitogen-activated protein kinase (MAPK) signaling pathway in oncogenesis and cytodifferentiation of odontogenic tumors, K-Ras gene status and expression of Ras, Raf1, MAPK/extracellular signal-regulated kinase (ERK) kinase (MEK)1, and ERK1/2 proteins were analyzed in ameloblastomas as well as in tooth germs. METHODS: Paraffin sections of 10 tooth germs and 46 benign and 6 malignant ameloblastomas were examined immunohistochemically for the expression of K-Ras, Raf1, MEK1, and ERK1/2. Frozen tissue samples of 22 benign ameloblastomas and 1 malignant (metastasizing) ameloblastoma were analyzed by direct DNA sequencing to detect K-Ras gene alteration. RESULTS: Immunohistochemical reactivity for K-Ras, Raf1, MEK1, and ERK1/2 was detected in both normal and neoplastic odontogenic epithelium, and these molecules were reactive chiefly with odontogenic epithelial cells neighboring the basement membrane. Plexiform ameloblastomas showed slightly stronger expression of these Ras/MAPK signaling molecules than follicular ameloblastomas. Keratinizing cells and granular cells showed decreased reactivity for the signaling molecules. Basal cell ameloblastomas showed slightly stronger reactivity for the signaling molecules than did the other subtypes. K-Ras immunoreactivity in malignant ameloblastomas was lower than that in dental lamina of tooth germs. Direct DNA sequencing showed a GGT to GCT point mutation at codon 12 of K-Ras gene in one ameloblastoma. Conclusion: Expression of K-Ras, Raf1, MEK1, and ERK1/2 in tooth germs and ameloblastomas suggests that Ras/MAPK signaling pathway functions to regulate cell proliferation and differentiation in both normal and neoplastic odontogenic epithelium. K-Ras gene status implied that K-Ras mutations might play a minor role in oncogenesis of odontogenic epithelium.     

Immunohistochemical analysis of inducible nitric oxide synthase (iNOS) and heat shock proteins (HSPs) in ameloblastomas

BACKGROUND: To clarify the possible role of nitric oxide (NO) and stress proteins in oncogenesis and cytodifferentiation of odontogenic epithelium. Inducible NO synthase (iNOS) and heat shock proteins (HSPs) were analyzed in ameloblastomas as well as in tooth germs. METHODS: Specimens of seven tooth germs, 36 benign ameloblastomas and five malignant ameloblastomas were examined by immunohistochemistry using antibodies against iNOS and 27-, 60- and 70-kDa HSPs (HSP27, HSP60 and HSP70). RESULTS: Immunoreactivity for iNOS was detected in normal and neoplastic odontogenic epithelial cells and was higher in malignant ameloblastomas than in tooth germs and benign ameloblastomas. HSP27 was expressed constitutively in all odontogenic epithelial cells in tooth germs and benign and malignant ameloblastomas. Expression of HSP60 and HSP70 was detected in normal and neoplastic odontogenic epithelial cells and was prominent in cells neighboring the basement membrane. HSP60 reactivity showed no apparent difference between normal and neoplastic odontogenic epithelium, whereas HSP70 expression was slightly higher in benign and malignant ameloblastomas than in tooth germs. CONCLUSIONS: Activation of iNOS might be associated with malignant potential of epithelial odontogenic tumors. Elevated expression of HSP70 is considered to be involved in neoplastic transformation of odontogenic epithelial cells.     

细胞外基质黏附分子表达与成釉细胞瘤生物学特性的关系

 【目的】探讨细胞外基质黏附分子层粘连蛋白（LN）和纤黏连蛋白（FN）与成釉细胞瘤复发和侵袭的关系。【方法】采用免疫组织化学LABC方法检测28例成釉细胞瘤组织中LN和FN的表达。【结果】在28例成釉细胞瘤中，LN和FN在基底膜的阳性表达率分别为46．4％和39．3％，复发性成釉细胞瘤LN和FN在基底膜的阳性表达率明显低于原发性成釉细胞瘤（P〈0．01）。LN和FN的表达形式相似，阳性着色部位均位于基底膜及部分肿瘤细胞的胞浆，在基底膜连续着色的部位，靠近基底膜的肿瘤外周细胞胞浆染色较强，中央内层细胞胞浆染色弱或无，而在基底膜着色缺失的部位，靠近基底膜的肿瘤外周细胞胞浆染色弱或缺失。【结论】LN和FN在基底膜表达缺失与成釉细胞瘤的复发密切相关，可能是成釉细胞瘤局部侵袭的机制之一。     

Expression of tenascin and nucleolar organizer region in ameloblastoma and ameloblastic fibroma

J Oral Pathol Med (2010) 39 : 223–229 Background: The aim of this study was to assess the expression, distribution and comparison of tenascin, a glycoprotein of the extracellular matrix in ameloblastoma and ameloblastic fibroma, both odontogenic neoplasms with diverse biological behavior and to understand the proliferative activity by using the morphometric analysis. Methods: Paraffin embedded tissue from 25 cases of odontogenic tumors i.e., ameloblastoma (n = 15) and ameloblastic fibroma (n = 10) were used. The expression of tenascin was evaluated using immunohistochemistry. Morphometric analysis of nucleolar organizer regions (NORs) from ameloblastoma and ameloblastic fibroma was carried out by silver staining. Results: A heterogeneous expression of tenascin was found in ameloblastoma which was mainly localized at the epithelial–mesenchymal interface and a patchy distribution was observed in the stroma (80%), while strong positivity was observed in the stroma and at the basement membrane zone of ameloblastic fibroma (100%). argyrophilic nucleolar organizer regions (AgNORs) revealed higher mean counts in ameloblastoma (3.093 ± 0.902) when compared with those of ameloblastic fibroma (1.553 ± 0.250). Ameloblastoma presented more than two NORs (two to five) per nucleus in majority of the cells, while ameloblastic fibroma exhibited only one NORs per nucleus. Conclusions: Expression of tenascin in these neoplasms suggest that it could play a role in epithelial‐ mesenchymal interaction, while AgNORs reveal that ameloblastomas are more aggressive when compared with ameloblastic fibromas.     

Pseudomalignancies of the head and neck

Pseudomalignancies are benign or reactive lesions that mimic malignant neoplasms either clinically or histologically. In the head and neck region there are a number of pseudomalignancies that may present to a histopathologist, including soft tissue lesions, benign odontogenic tumours and salivary gland pathology. In this review we discuss common pseudomalignant lesions that may present in the head and neck, including their clinical presentation, histopathological features and differential diagnosis.