Oral lichen planus (OLP) tends to present bilaterally as mostly white lesions on the inner cheek, although any mucosal site in the mouth may be involved. Other sites, in decreasing order of frequency, may include the tongue, lips, gingivae, floor of the mouth, and very rarely, the palate.Generally, oral lichen planus tends not to cause any discomfort or pain, although some people may experience soreness when eating or drinking acidic or spicy foodstuffs or beverages. When symptoms arise, they are most commonly associated with the atrophic and ulcerative subtypes. These symptoms can include a burning sensation to severe pain. They may also experience mucosal bleeding in response to mild trauma, such as toothbrushing. Additionally, the Koebner phenomenon (the development of new lesions at sites of trauma) is not only present in cutaneous lichen planus (CLP) but can also occur in the setting of OLP. Residual postinflammatory hyperpigmentation has been reported in association with OLP, manifesting as brown to black pigmentation on the oral mucosa and may most likely occur in dark-skinned individuals.OLP may occur as a sole manifestation of the disease or in conjunction with other clinical manifestations of LP, including cutaneous LP, genital LP, nail LP, and lichen planopilaris (scalp LP). Causes
Cutaneous LP is a self-limiting condition. It usually resolves within 6 to 12 months. Oral LP is a non infectious, chronic inflammatory condition that involves the oral mucosa and may be accompanied by skin lesions.
The etiology of oral LP are unknown.It is not clear whether the mechanisms causing isolated oral LP are different from those causing oral LP with cutaneous LP. An immune-mediated mechanism where basal keratinocytes are being targeted as foreign antigens by activated T cells, especially CD8+ T cells, has been proposed. Upregulation of intercellular adhesion molecule-1 (ICAM-1) and cytokines associated with T-helper 1 immune response, may also play an important role in the pathogenesis of lichen planus.Stress is thought to play a role in the pathogenesis of oral LP. Patients with anxiety and depression are reported more commonly with oral LP if compared to normal healthy individuals. Some studies have indicated that stressful events can induce LP lesions in otherwise healthy individuals. However, a cause effect relationship between stress and the onset of oral LP has not been demonstrated. Autoimmune response to epithelial self-antigens remains a possibility. A single study of cutaneous LP reported evidence in support of autoimmunity by expanding in vitro T cells isolated from the skin lesions of two patients, followed by testing the ability of these T cells to kill autologous keratinocytes (cytotoxicity). Several potential triggers of oral LP have been proposed over the years, mainly

Hypersensitivity reaction
Restorative material (e.g. amalgam and composite) or drugs can cause hypersensitivity reaction and lead to oral LP. Oral LP usually resolve upon removal of the trigger, as is characteristics of oral LP
Viral infection

Pathogenesis
Oral LP is considered to be a T-cell mediated chronic inflammatory tissue reaction that results in a cytotoxic reaction against epithelial basal cells.