Although hyperorthokeratosis and hyperparakeratosis are commonly seen in several oral mucosal lesions, their induced mechanisms are not known. Thus, the aim of this study is to analyze the induced mechanism of hyperkeratinization. We made keratinized oral mucosal epithelium (GE1) system by culturing oral mucosal cells at the air-liquid interface. Then, we analyzed the influence of inflammatory cytokines (TNF-α and IL-6), FGF10, and caspase family inhibitor on the cornified layer in this system. In results, TNF-α significantly thickened the cornified layers (
P < 0.05). Simultaneously TUNEL-positive cells were significantly increased with TNF-α (ANOVA,
P < 0.05) and also BrdU-incorporating cells (ANOVA,
P < 0.05) were increased. Cornified layers were perfectly disappeared when keratinized oral mucosal epithelial cells were cultured with caspase family inhibitor. In conclusion, it is thought that TNF-α enhanced apoptosis and resulted in hyperkeratinization of the oral mucosal epithelium in air-liquid culture.
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