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Calcifying epithelial odontogenic tumors (CEOTs) and ghost cell odontogenic tumors (GCOTs) are characteristic odontogenic origin epithelial tumors which produce calcifying materials from transformed epithelial tumor cells. CEOT is a benign odontogenic tumor composed of polygonal epithelial tumor cells that show retrogressive calcific changes, amyloid-like deposition, and clear cytoplasm. Differentially, GCOTs are a group of transient tumors characterized by ghost cell presence, which comprise calcifying cystic odontogenic tumor (CCOT), dentinogenic ghost cell tumor (DGCT), and ghost cell odontogenic carcinoma (GCOC), all derived from calcifying odontogenic cysts (COCs). There is considerable confusion about COCs and GCOTs terminology, but these lesions can be classified as COCs or GCOTs, based on their cystic or tumorous natures, respectively. GCOTs include ameloblastomatous tumors derived from dominant odontogenic cysts classified as CCOTs, ghost cell-rich tumors producing dentinoid materials as DGCTs, and the GCOT malignant counterpart, GCOCs. Many authors have reported CEOTs and GCOTs variably express keratins, β-catenin, BCL-2, BSP, RANKL, OPG, Notch1, Jagged1, TGF-β, SMADs, and other proteins. However, these heterogeneous lesions should be differentially diagnosed to allow for accurate tumor progression and prognosis prediction.
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Peripheral ameloblastoma (PA) in gingiva is rare and often confused with oral basal cell carcinoma (OBCC). The tissues of one case of PA and one case of OBCC with the same mandibular molar area affected were compared via an immunohistochemical examination using 50 antisera. The PA and OBCC showed similar proliferation of basaloid epithelial strands, but toluidine blue staining revealed that the PA had pinkish juxta-epithelial myxoid tissue, whereas the OBCC was infiltrated by many mast cells. Immunohistochemical comparisons showed that the PA was strongly positive for ameloblastin, KL1, p63, carcinoembryonic antigen, focal adhesion kinase, and cathepsin K, and slightly positive for amelogenin, Krox-25, E-cadherin, and PTCH1, whereas the OBCC was not. On the other hand, the OBCC was strongly positive for EpCam, matrix metalloprotease (MMP)-1, α1-antitrypsin, cytokeratin-7, p53, survivin, pAKT1, transforming growth factor-β1, NRAS, TGase-1, and tumor nescrosis factor-α, and consistently positive for β-catenin, MMP-2, cathepsin G, TGase-2, SOS-1, sonic hedgehog, and the β-defensins-1, -2, -3, while the PA was not. These data suggest that the tumorigeneses of PA and OBCC differ, and that PAs undergo odontogenic differentiation and generate oncogenic signals for infiltrative growth and bone resorption, whereas OBCCs undergo basaloid epidermal differentiation as a result of growth factor/cytokine-related oncogenic signals.
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Ameloblastomas and adenomatoid odontogenic tumors (AOTs) are common epithelial tumors of odontogenic origin. Ameloblastomas are clinico-pathologically classified into solid/multicystic, unicystic, desmoplastic, and peripheral types, and also divided into follicular, plexiform, acanthomatous, granular types, etc., based on their histological features. Craniopharyngiomas, derived from the remnants of Rathke's pouch or a misplaced enamel organ, are also comparable to the odontogenic tumors. The malignant transformation of ameloblastomas results in the formation of ameloblastic carcinomas and malignant ameloblastomas depending on cytological dysplasia and metastasis, respectively. AOTs are classified into follicular, extrafollicular, and peripheral types. Ameloblastomas are common, have an aggressive behavior and recurrent course, and are rarely metastatic, while AOTs are hamartomatous benign lesions derived from the complex system of the dental lamina or its remnants. With advances in the elucidation of molecular signaling mechanisms in cells, the cytodifferentiation of epithelial tumor cells in ameloblastomas and AOTs can be identified using different biomarkers. Therefore, it is suggested that comprehensive pathological observation including molecular genetic information can provide a more reliable differential diagnosis for the propagation and prognosis of ameloblastomas and AOTs. This study aimed to review the current concepts of ameloblastomas and AOTs and to discuss their clinico-pathological features relevant to tumorigenesis and prognosis.
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Peripheral Adenomatoid Odontogenic Tumor — A Rare Cause of Gingival Enlargement: A Case Report with CBCT Findings
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