Role of nuclear factor kappa-B in phenytoin-induced gingival overgrowth

Objective This study investigates the expression of transcription factor nuclear factor-kappa B (NF-kappa B) and its relation to various cellular mediators that act in the pathogenesis of phenytoin-induced gingival overgrowth. Materials and methods Eighteen epileptic patients had phenytoin-induced gingival overgrowth (PHT-GO), 20 patients with plaque-induced gingivitis (Gingivitis), and 20 periodontally and systemically healthy individuals (Control) were included in this study. The expression of activated NF-kappa B subunits (p50 and p65), IL-1 beta, TNF-alpha and TGF beta-1 levels were examined in the gingival sections obtained from each participant. Results The results demonstrated a significantly higher expression of p65 in fibroblasts in PHT-GO group with respect to Gingivitis (P<0.05) and control groups (P<0.01). However, we found no statistically significant differences between PHT-GO and Gingivitis groups according to the immunohistochemical staining in macrophages (P>0.05). Immune-reactive TGF beta-1 levels in the gingival connective tissue cells were statistically higher in PHT-GO group with respect to Gingivitis group(P<0.05). Statistically significant correlations were found between the HI and activated TGF beta-1 and p65 levels in PHT-GO group. Conclusion The results of this study showed that NF-kappa B is activated in PHT-related gingival overgrowth. This study may provide a basis for future research into specific NF-kappa B inhibition for preventing of the side effects of this drug.