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The discovery and characterization of genes and molecules involved in oral carcinogenesis have contributed to the diagnosis, assessment of prognosis and survival of patients with oral cancer. The knowledge of etiological and biological mechanisms involved in cancer allows important advances in diagnosis and therapeutics. Numerous parameters are used to measure the aggressiveness of a tumor, among which cell proliferation stands out, an important phenomenon related to the behavior of lesion and that is linked to dysregulation of the cell cycle machinery in various cancers. Scientific researches have been conducted to investigate these events. This review discusses the use of cell proliferation markers in oral cancer, particularly oral squamous cell carcinoma, emphasizing those related to cell proliferation rate, such as PCNA, Ki-67, AgNORs, cyclins, MCM and geminin. Criteria used for diagnostic and prognostic such as clinical stage, size and location of lesions, margin of lesions, associated with the use of these biomarkers offer valuable opportunities to evaluate the behavior of the disease and, moreover, are of great prognostic value.

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Purpose: Studies on odontogenic tumors have identified various molecular dysfunctions involved on their development, and some mechanisms such as angiogenesis and matrix modulation, are useful means of investigating the differences in biologic behavior of these tumors. Some important markers to identify tumor aggressiveness by immunohistochemistry are VEGF, TGF-β and MMP-9 proteins. This study aimed to compare the immunohistochemical expression of VEGF, TGF-β, and MMP-9 in ameloblastoma and adenomatoid odontogenic tumor (AOT). Methods: Immunoexpression of VEGF, TGF-β, and MMP-9 was studied in 15 solid ameloblastomas, and 15 AOTs. A semi-quantitative analysis of the immunostained cells was performed, and the statistical analysis was made using the Mann-Whitney nonparametric and Spearman correlation test, with significance level at .05 (P<.05). Results: A higher epithelial immunoexpression of VEGF and TGF-β was observed in ameloblastoma and AOT, respectively, and the stromal reactivity to VEGF was statistically higher in ameloblastoma (P<.05). No statistical difference was observed for MMP-9 (P>.05). Conclusion:The results suggest the involvement of angiogenesis in tumor progression of ameloblastomas, and the inductive effect of stromal cells in AOT, hence justifying its lower growth potential.

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