Oral<unk>  is considered to be a T-cell mediated chronic inflammatory tissue reaction that results in a cytotoxic reaction against epithelial basal cells. The inflammatory infiltrate in oral<unk>  is primarily composed of CD8+ T cells. A potential pathway for CD8+ T cell-mediated cytotoxicity in oral<unk>  is described as follows: Antigens presented on MHC 1 molecules activates CD8+ T cells on keratinocytes or by encounters with activated CD4+ helper T cells or cytokines produced by activated CD4+ helper T cells Activated CD8+ T cells induce keratinocyte apoptosis through various mechanisms such as secretion of tumor necrosis factor (TNF)-alpha, secretion of granzyme B, or Fas-Fas ligand interactions. Chemokines are produced by activated CD8+ T cells that attract additional inflammatory cells, thereby promoting continued inflammation. Other mechanisms that have been proposed include: * upregulation of matrix metalloproteinases that disrupt the epithelial basement membrane zone and allow entry of immune cells into the epidermis, * the release of proinflammatory mediators and proteases by mast cells, and * perturbations in the innate immune response that may involve toll-like receptors. Oral<unk>  may also be caused by genetic factor which influence the immune function. A separate study performed in China found an association between a polymorphism in the TNF-alpha gene and risk for oral<unk>  in a subset of patients. An Italian study found a significant increase in a genetic polymorphism of the first intron of the interferon (IFN)-gamma promoter in patients with oral<unk>  compared with controls.
Lichen planus
Geographic tongue
Lichen nitidus
Leukoplakia
Lichen simplex chronicus
Lichen myxedematosus
Lichen sclerosus
Tinea barbae