Abstract
The pathogenesis of OLP is not completely known and is the subject of various hypotheses. Among the most widely accepted hypotheses, we find the unifying hypothesis of Sugerman and the modified hypothesis of Carrozzo. The first hypothesis is based on the theoretical interaction between CD4+ and CD8+ T lymphocytes, through a cell surface molecule called RCA (request cytotoxic activity) expressed by CD8+ T lymphocytes and an RCA receptor (RCAR) expressed by CD4+ T lymphocytes, which enable the initiation of cytotoxic activity by CD8+ T lymphocytes. In contrast, the second hypothesis involves APC cells, which may be stromal DCs or LCs, and basal keratinocytes that are “activated” by, for example, viral infection (such as HCV) and systemic contact sensitivity drugs (e.g., amalgam).
In any cases, pathology is thought to be triggered by the expression of a putative antigen on the surface of keratinocytes or by the recognition of body peptides or heat shock proteins as foreign antigens. There are many cells involved in the pathogenetic mechanism: keratinocytes, Langerhans cells, CD4+ and CD8+ T lymphocytes, macrophages, and mast cells. These produce and secrete cytokines and chemokines, which are involved in the initiation of pathology through the activation of various pathogenic pathways. The expression of these cells varies depending on the stage at which the lesions are found. In the early-stage T helper lymphocytes, CD4+ macrophages and dendritic cells are more represented than in advanced lesions, in which we find high levels of suppressor CD8+ T lymphocytes. Four main pathogenetic mechanisms have been described: cell-mediated immune response, non-specific immune response, chemokines, and autoimmune hypothesis.
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Isola, G., Santonocito, S., Leonardi, R., Polizzi, A. (2023). Pathogenesis. In: Oral Lichen Planus and Lichenoid Lesions. Springer, Cham. https://doi.org/10.1007/978-3-031-29765-6_4
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DOI: https://doi.org/10.1007/978-3-031-29765-6_4
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