Lichen planus is a chronic inflammatory disease that affects the skin and the mucus membrane. Oral lichen planus (OLP), the mucosal counterpart of cutaneous lichen planus, presents frequently in the fourth decade of life. This supports the above-explained hypothesis that the cytokine-mediated lymphocyte homing mechanism plays an important role in the pathogenesis of lichen planus. Attraction of the lymphocytes to the epithelium–connective tissue interface has also been proposed to be due to cytokine-mediated upregulation of adhesion molecules on endothelial cells and concomitant expression of receptor molecules by circulating lymphocytes.
The normal integrity of the basement membrane is maintained by a living basal keratinocyte due to its secretion of collagen 4 and laminin 5 into the epithelial basement membrane zone. In turn, keratinocytes require a basement membrane derived cell survival signal to prevent the onset of its apoptosis. Apoptotic keratinocytes are no longer able to perform this function, which results in disruption of the basement membrane.