Lichen planus: molecular pathway and clinical implications in oral disorders

Stem cells play a role in many mucosal disorders characterised by abnormal proliferation and differentiation of keratinocytes, such as oral lichen planus (OLP). In OLP there were changes in stem cell markers as component of integrin complexes α6 and β1 integrin increased along with increase of melanoma-associated chondroitin sulphate proteoglycan (MCSP) and decreased of notch1 (N1) and keratin 15 (K15). Stem cell marker expression may be altered by pathological signalling in these lesions. Cadherins are transmembrane receptors that provide cell-cell contact and communication function through calcium-dependent homophilic and heterophilic interactions. In actively diseased areas of OLP lesions, basal keratinocytes downregulate CD40 and were focally E-cadherin-negative, in contrast to non-diseased areas and normal oral mucosa. This loss of E-cadherin expression may contribute to epithelial basal cell destruction and T-cell migration into the epithelial compartment in OLP. In addition, Growth factor pathways as a role in OLP and has been analyzed in this review