The Pathogenesis of Oral Lichen Planus

Abstract

Both antigen-specific and non-specific mechanisms may be involved in the pathogenesis of oral lichen planus (OLP). Antigen-specific mechanisms in OLP include antigen presentation by basal keratinocytes and antigen-specific keratinocyte killing by CD8 + cytotoxic T-cells. Non-specific mechanisms include mast cell degranulation and matrix metalloproteinase (MMP) activation in OLP lesions. These mechanisms may combine to cause T-cell accumulation in the superficial lamina propria, basement membrane disruption, intra-epithelial T-cell migration, and keratinocyte apoptosis in OLP. OLP chronicity may be due, in part, to deficient antigen-specific TGF-␤1-mediated immunosuppression. The normal oral mucosa may be an immune privileged site (similar to the eye, testis, and placenta), and breakdown of immune privilege could result in OLP and possibly other autoimmune oral mucosal diseases. Recent findings in mucocutaneous graft-versus-host disease, a clinical and histological correlate of lichen planus, suggest the involvement of TNF-␣, CD40, Fas, MMPs, and mast cell degranulation in disease pathogenesis. Potential roles for oral Langerhans cells and the regional lymphatics in OLP lesion formation and chronicity are discussed. Carcinogenesis in OLP may be regulated by the integrated signal from various tumor inhibitors (TGF-␤1, TNF-␣, IFN-␥, IL-12) and promoters (MIF,. We present our recent data implicating antigen-specific and non-specific mechanisms in the pathogenesis of OLP and propose a unifying hypothesis suggesting that both may be involved in lesion development. The initial event in OLP lesion formation and the factors that determine OLP susceptibility are unknown.

Possible link between Hashimoto's thyroiditis and oral lichen planus: a novel association found

“…Thus, in a predisposed subject, an imbalance in CTLA-4 function can lead to T cell proliferation and cytokine production. Since it has been recognized that the immune system is controlled by Th1/Th2 balance, both HT and OLP are considered to be a Th1-type diseases [12,13].…”

“…Indeed, Sugerman proposed that, at the lesion site, keratinocytes express a lichen planus antigen and that known (e.g. systemic drugs, dental restorative materials, mechanical trauma or bacterial or viral infection) or unidentified agents could induce keratinocyte antigen expression [13]. Subsequently, CD8+ cytotoxic T cells recognize the lichen planus antigen associated with MHC class I on lesional keratinocytes and trigger keratinocyte apoptosis [13].…”

“…systemic drugs, dental restorative materials, mechanical trauma or bacterial or viral infection) or unidentified agents could induce keratinocyte antigen expression [13]. Subsequently, CD8+ cytotoxic T cells recognize the lichen planus antigen associated with MHC class I on lesional keratinocytes and trigger keratinocyte apoptosis [13]. All the same, thyroid antibodies linked on the keratinocyte surface may be directly recognized as target antigens by cytotoxic T cells.…”

Analysis of a possible association between oral lichen planus and drug intake. A controlled study

“…Lichen planus (LP) is an inflammatory mucocutaneous disease of unknown etiology, and thought to arise as a result of an immune response -mainly by CD8+ lymphocytes-to antigens on lesional keratinocytes (1,2). Oral lichen planus (OLP) affects from 0.1 to about 4% of individuals, occurring mostly in middle-aged adults, with a female predominance at a ratio of approximately 2:1 (3,4).…”

Diagnosis and management of common non-viral oral ulcerations

“…LP presents with three distinct clinical patterns: reticular, erosive and plaques. 9 It is common for patients to have a mixture of these three patterns. Reticular LP is the most common form and consists of bilateral, raised, delicate thin white lines that produce a lace-like pattern set on an erythematous background.…”