Oral lichen planus (OLP) is a chronic inflammatory disease that causes bilateral white striations, papules, or plaques on the buccal mucosa, tongue, and gingivae. Erythema, erosions, and blisters may or may not be present. Note the images below.
The dense sub-epithelial mononuclear infiltrate in oral lichen planus is composed of T cells and macrophages, and there are increased numbers of intra-epithelial T cells. Most T cells in the epithelium and adjacent to the damaged basal keratinocytes are activated CD8+ lymphocytes. Therefore, early in the formation of oral lichen planus lesions, CD8+ T cells may recognize an antigen associated with the major histocompatibility complex (MHC) class I on keratinocytes. After antigen recognition and activation, CD8+ cytotoxic T cells may trigger keratinocyte apoptosis. Activated CD8+ T cells (and possibly keratinocytes) may release cytokines that attract additional lymphocytes into the developing lesion. 
Oral lichen planus lesions contain increased levels of the cytokine tumor necrosis factor (TNF)–alpha. [4, 5] Basal keratinocytes and T cells in the subepithelial infiltrate express TNF in situ. [6, 7] Keratinocytes and lymphocytes in cutaneous lichen planus express elevated levels of the p55 TNF receptor, TNF-RI.  T cells in oral lichen planus contain mRNA for TNF and secrete TNF in vitro.  Serum and salivary TNF levels are elevated in oral lichen planus patients. [10, 11, 12, 13] TNF polymorphisms have been identified in patients with oral lichen planus, and they may contribute to the development of additional cutaneous lesions.  Oral lichen planus has been treated successfully with thalidomide, [15, 16] , while thalidomide is known to suppress TNF production. [17, 18] Together, these data implicate TNF in the pathogenesis of oral lichen planus.
The lichen planus antigen is unknown, although it may be a self-peptide (or altered self-peptide), in which case lichen planus would be a true autoimmune disease. The role of autoimmunity in the pathogenesis is supported by many autoimmune features of oral lichen planus, including its chronicity, onset in adults, predilection for females, association with other autoimmune diseases, occasional tissue-type associations, depressed immune suppressor activity in patients with oral lichen planus, and the presence of autocytotoxic T-cell clones in lichen planus lesions. The expression or unmasking of the lichen planus antigen may be induced by drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), viral infection, or other unidentified agents. [19, 20, 21]
The prevalence of oral lichen planus in the United States is unknown.
Oral lichen planus affects approximately 1-2% of the general adult population, although the prevalence of the disease is unknown in many areas.  Oral lichen planus is a common noninfectious oral mucosal disorder among adult patients who attend oral pathology and oral medicine clinics.
Oral lichen planus affects all racial groups.
The female-to-male ratio for oral lichen planus is 1.4:1.
Oral lichen planus predominantly occurs in adults older than 40 years, although younger adults and children can be affected.
Oral lichen planus is a chronic inflammatory disease. The lesions of cutaneous lichen planus typically resolve within 1-2 years, whereas the lesions of oral lichen planus are long lasting and persist for 20 years or longer. Resolution of the white striations, plaques, or papules is rare. Symptomatic oral lichen planus (ie, atrophic or erosive disease) characteristically waxes and wanes, although the associated white patches do not resolve. Patients with atrophic (erythematous) or erosive (ulcerative) disease commonly have significant local morbidity. Oral lichen planus can have a significant negative impact on quality of life. 
Current immunosuppressive therapies usually control oral mucosal erythema, ulceration, and symptoms in patients with oral lichen planus with minimal adverse effects. However, a range of therapies may need to be tried.
Advise patients that oral lichen planus lesions may persist for many years with periods of exacerbation and quiescence.
Follow up patients with oral lichen planus at least every 6 months for clinical examination and repeat biopsy as required, although patients should be advised to seek medical care whenever the symptoms are exacerbated or the presentation of the lesions change.
In the context of appropriate medical care, the prognosis for most patients with oral lichen planus is excellent.
Patient education is important. Many patients with oral lichen planus are concerned about the possibilities of its malignancy and contagiousness. Many patients are frustrated by the lack of available patient education concerning oral lichen planus. 
Inform patients with oral lichen planus of the following:
The chronicity of oral lichen planus and the expected periods of exacerbation and quiescence
The aims of treatment, specifically the elimination of mucosal erythema, ulceration, pain, and sensitivity
The lack of large randomized controlled therapeutic clinical trials
The possibility that several treatments may need to be tried
The potentially increased risk of oral cancer
The possibility of reducing the risk of oral cancer (see Complications)
Information about oral lichen planus is currently available online. For instance, an oral lichen planus chat room is available at the homepage of the International Lichen Planus Support Group Web.
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