[Expressions of NF--kappaBp65, TRAF2, cyclinD1 and their association with cell apoptosis in oral lichen planus].

Objective: To examine the expression and distribution of NF-kappaBp65, TRAF2, and cyclinD1 and their association with cell apoptosis in oral lichen planus (OLP).

Methods: Sixty OLP patients were divided into erosion-atrophy group (n=30) and non-erosion group (n=30) according to their clinical features. Immunohistochemistry with SP method was used to detect the expressions of NF-kappaBp65, TRAF2, cyclinD1 in the 60 OLP and 40 normal oral mucosa (control) specimens. TUNEL assay of randomly selected specimens from 10 normal and 15 OLP cases was performed to detect the cell apoptotic index (AI).

Results: Compared with the control group, OLP group showed significantly increased AI of the epithelial cells (67.32-/+18.99) and decreased AI of the lymphocytes (34.12-/+9.89) (P<0.05). In the OLP group, the positivity rates for NF-kappaBp65, TRAF2, and cyclin D1 in the epithelial cells (85.00%, 76.67% and 71.67%, respectively) and in the lymphocytes (91.67%, 86.67% and 70.00%, respectively) were all significantly higher than those in the control group (P<0.05). NF-kappaBp65 expression was significantly increased in the lamina propria in the non-erosion OLP group as compared to the erosion-atrophy group. A positive correlation was noted between lymphocyte NF-kappaBp65 expression and AI of the epithelial cells, but an inverse correlation found between lymphocyte NF-kappaBp65 expression and the AI of the lymphocytes. Lymphocyte TRAF2 and cyclin D1expressions were also inversely correlated to lymphocyte AI. There was a positive correlation between TRAF2 and cyclin D1 expressions and the expression NF-kappaBp65 in the epithelial cells and lymphocytes in OLP.

Conclusions: Accelerated apoptosis of the keratinocytes and inhibition of lymphocyte apoptosis may coexist to contribute to the formation and progression of OLP. NF-kappaBp65 expression, particularly its abnormal nuclear expression, may play a partial role in the pathogenesis of OLP.