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.
Thorough examination may lead to the detection of extraoral manifestations of LP that provide additional support for the diagnosis or the identification of clinical findings that suggest another diagnosis. Tissue biopsies of oral LP help to confirm the diagnosis and are particularly of value for erythematous and erosive LP, which share features with multiple other mucosal disorders, including oral malignancy. Biopsies to confirm oral LP are less essential in patients who present with classic reticular LP, particularly in patients in whom a diagnosis of LP has already been confirmed through biopsy of an extraoral manifestation of this disorder. Differential diagnosis
Skin
Lichenoid drug eruption
The cutaneous manifestations resemble idiopathic lichen planus. Chronic graft-versus-host disease
The history of preceding hematopoietic cell transplant is helpful for diagnosis
Psoriasis
Atopic dermatitis
Cutaneous lupus erythematosus
Discoid lupus erythematosus

Mouth
Oral lichenoid drug reaction
Lichenoid drug eruptions may be caused by a variety of systemic medications and share clinical features with oral LP. Histologic findings of a deep mixed infiltrate with lymphocytes, plasma cells, and neutrophils (with or without eosinophils) and perivascular inflammation favor this diagnosis. Oral lichenoid contact reaction (allergic contact mucositis)
Oral lichenoid contact reactions may be caused by a variety of substances. The clinical and histologic features of oral lichenoid contact reactions are similar to oral LP. Patch testing and recognition of the proximity of an offending substance to the eruption can aid with diagnosis. Autoimmune blistering diseases
Mucous membrane pemphigoid and other autoimmune blistering diseases may present with oral erosions and desquamative gingivitis similar to that seen in erosive LP.