Assessment of Genetic Factors in Oral Mucosal Lichen Planus

Annotation. Oral lichen planus (OLP) is a chronic autoimmune disease characterized by a recurrent and prolonged course, affecting up to 1.5% of the global population—predominantly middle-aged and elderly women. A hallmark of the disease is an inflammatory response to an unidentified antigen in the basal epithelial layer or basement membrane zone. The condition typically involves the buccal mucosa, tongue, and gingiva (presenting as desquamative gingivitis). Most patients experience ulcers, erosions, papules, and mucosal detachment in the oral cavity, while others report symptoms such as roughness, numbness, and pain. The aim of our study was to evaluate the association between polymorphisms in the TLR, VEGF, IL17A, VDR, and DEFB1 genes and the development of oral lichen planus, as well as to assess their role in disease pathogenesis and potential impact on immune response and inflammation. The study included 12 women aged 42–65 years diagnosed with oral mucosal lichen planus. DNA was extracted from buccal epithelial cells using a modified Chelex-based protocol. Genotyping was performed for the following polymorphisms: TLR2 (Arg753Gln), VEGF (C-634G), IL17A (G-197A), VDR (BsmI, IV S7G>A), and DEFB1 (G-52A). The obtained results were processed using statistical analysis, including a Hardy-Weinberg equilibrium (HWE) deviation test, as well as an assessment of the association between genotypes and alleles (gene variants) and the risk of developing periodontitis using Pearson’s χ² method. This analysis was performed with the DeFinetti genetic statistics software available on the website of the Institute of Human Genetics (Munich, Germany). Associations were characterized by odds ratios (OR) with 95% confidence intervals and evaluated using Pearson’s χ² test for goodness of fit. A p-value <0.05 was considered statistically significant. It was demonstrated that gene polymorphisms may play an important role in the susceptibility to oral lichen planus and in the pathogenesis of this condition.