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Due to the frequent presence of inflammation in cases of carcinoma and its use as a parameter for the assessment of tumor aggressiveness, the role of inflammation in oral carcinogenesis was investigated. This was performed by evaluating the expression of cellular markers, cytokines and nuclear transcription factors that identify the cells that participate in the antitumor defense in cases of oral epithelial dysplasia (OED) and oral squamous cell carcinoma (OSCC). A semi-quantitative immunohistochemical analysis was performed for the transcription factors cluster of differentiation 8 (CD8), forkhead box P3 (FOXP3), transforming growth factor (TGF)-β, tumor necrosis factor (TNF)-α and nuclear factor κ-light chain enhancer of activated B-cells (NF-κB), in cases of OED and OSCC. CD8, TGF-β, TNF-α and NF-κB participated in the processes of tumor transformation and progression. The presence of inflammatory infiltrate in cases of OED favors the transformation and invasion process when stromal TNF-α and NF-kB are overexpressed, as NF-kB activated by TNF-α during inflammation predisposes the lesion to transformation, functioning as a link between inflammation and cancer. The control of these inflammatory mediators may prevent malignant transformation in the oral cavity.

Role of inflammation in oral carcinogenesis (Part II): CD8, FOXP3, TNF-α, TGF-β and NF-κB expression