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Abstract

The etiology of oral lichen planus is still uncertain. The most accepted hypothesis currently correlates OLP with an immunological process triggered by an antigen that alters the keratinocytes of the basal layer of the oral mucosa, making them susceptible to an immune cell response. The latter results in the activation of T lymphocytes and the production of cytokines, such as interleukin-2 (IL-2), interferon-γ (INF-γ), and tumor necrosis factor (TNF), leading to apoptosis of keratinocytes. The T lymphocyte-mediated immunopathological response is most likely induced by a series of exogenous triggers responsible for possible alteration of endogenous and surface antigens of oro-mucosal keratinocytes. Currently, endogenic triggers associated with OLP include infectious agents, such as cytomegalovirus (CMV), herpes simplex-1 (HSV-1), Epstein-Barr virus (EBV), herpesvirus human herpesvirus-6 (HHV-6), and papillomavirus (HPV); factors causing lichenoid reactions such as dental restorative materials, medications, and foods; chronic irritative stimuli, including cigarette smoking; and chronic traumatic factors, induced by incongruous prostheses and sharp dental edges. It has been observed how endogenous factors, including genetic predisposition, psychological problems (anxiety, depression, stress), and some systemic diseases such as diabetes mellitus, hypertension, dyslipidemia, and heart disease, could also play a determining role in its development. In conclusion, the inductive mechanisms of potential triggers and the extent of target antigens are currently unknown. However, the resultant dysregulation of the immune response, although never demonstrated exactly, inclines toward the hypothesis of a chronic inflammatory reaction with a pathogenetic basis of an autoimmune type.

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Isola, G., Santonocito, S., Leonardi, R., Polizzi, A. (2023). Aetiology. In: Oral Lichen Planus and Lichenoid Lesions. Springer, Cham. https://doi.org/10.1007/978-3-031-29765-6_3

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