Exploratory Expression Analysis of Stem Cell and Epithelial–Mesenchymal Transition Markers in Ameloblastoma

Ameloblastoma is a common benign odontogenic tumor. Its etiology has been associated with dysregulation of the MAPK and SHH pathways, and new theories suggest that tumor stem cells (TSCs) and the epithelial–mesenchymal transition (EMT) are participants in their pathogenesis. Objective: To determine the immunohistochemical expression of SOX2 and CD44 as indicators of TSCs and the gene expression of vimentin, smooth muscle actin, and FGFR1 as indicators of the EMT in conventional, unicystic, and peripheral ameloblastoma. Materials and Methods: Conventional, unicystic, and peripheral ameloblastomas and dental follicles, as a control group, were analyzed by peroxidase immunohistochemistry assays for SOX2 and CD44 as TSC-related markers, and the EMT relationship was determined by RT-qPCR expression for vimentin (VIM), alpha smooth muscle actin (ACTA2), fibroblast growth factor receptor 1 (FGFR1), and GAPDH as a control. Results: The most affected anatomical site was the mandible, with an average age of 38.03 (±20.95) years. SOX2 and CD44 immunoexpression were significantly higher in conventional ameloblastoma. RT-qPCR results showed predominant non-significant expression of VIM, ACTA2, and FGFR1 in unicystic ameloblastoma compared to other ameloblastoma types. Conclusion: The significantly higher immunoexpression of SOX2 and CD44 in conventional subtypes could suggest a greater presence of TSCs, and predominant VIM, ACTA2, and FGFR1 gene expression in unicystic ameloblastoma could suggest the possibility of EMT processes related to cystic formation. More research on TSCs and the EMT is necessary to elucidate this finding.