The association of IL-17A, IL-17F gene polymorphism and serum levels with oral lichen planus
Project no. 21195 · Status: Kapanmış (Yayın bekleniyor) · 2020
Summary
AIM: Oral lichen planus is a non-infectious, chronic inflammatory disease affecting the squamous epithelium of the oral mucosa and the underlying lamina propria, accompanied by skin lesions. Although the exact etiology is still unknown, it is thought that genetic factors, some drugs, dental materials, systemic diseases such as diabetes mellitus, high blood pressure, infections, stress and trauma have a potential role in the pathogenesis of the disease. Although it is known that it is an autoimmune disorder mainly mediated by T lymphocytes, there are currently unclear points regarding pathogenesis. While the roles of many cytokines in the pathogenesis of the disease have been clarified, studies on interleukin-17A and interleukin-17F have been limited. In this study, it was aimed to investigate the roles of these two cytokines in the pathogenesis of oral lichen planus and to obtain the necessary data to be used as potential biomarkers in the diagnosis and treatment of the disease. REASON AND METHOD: 50 OLP patients and 50 healthy volunteers included in this study. OLP diagnosis was confirmed clinically and histopathologically in our outpatient clinics from December 2019 to July 2020. Participants were evaluated in detail in terms of age, gender, smoking/alcohol use history, clinical classification (erosive, non-erosive), duration of disease, presence of periodontal disease, presence of accompanying systemic disease (viral hepatitis, diabetes mellitus, hypertension, etc.). Serum IL-17A and IL-17-F levels of patients blood samples and healthy volunteers were determined by ELISA method, IL17A rs8193037, IL17A rs2275913, IL17F rs763780 and IL17F rs2397084 polymorphisms were determined using Sanger Sequence Analysis method. In the analysis of categorical variables, Pearson's chi-square test was used and the levels of the variables were examined with cross tables. The Shapiro-Wilk normality test was used to examine whether the continuous variables were normally distributed. Since the normal distribution assumption was not provided, the Mann-Whitney U test was used to compare two independent groups; The Kruskal-Wallis test was used to compare more than two groups. Correlations between continuous variables were analyzed using Spearman correlation coefficient. The significance level was taken as 0.05 in all group comparisons. RESULTS: Serum IL-17A and IL-17F levels of patients with OLP were found to be higher than the control group, but this difference was not considered statistically significant. IL-17A and IL17F serum levels of female patients were found to be higher than male patients, but the difference was not statistically significant. There was no correlation between serum IL-17A and IL-17F levels with the patients' age, disease duration, smoking and alcohol use habits. Serum IL-17A and IL-17F levels of patients with erosive OLP are higher than non-erosive patients, but the difference is not statistically significant. There was no statistically significant correlation between OLP sensitivity and IL17A rs2275913, IL17A rs8193037, IL17F rs763780 and IL17F rs2397084 polymorphisms. CONCLUSION: A potential role of IL-17 in the pathogenesis of OLP disease can be mentioned in the local inflammatory environment of OLP lesions, independent of the patients' systemic inflammation status. Therefore, serum IL-17A and IL-17F levels of the patients cannot be used as a biochemical marker in the diagnosis and follow-up of the disease. There was no evidence that IL17A rs2275913, IL17A rs8193037, IL17F rs763780 and IL17F rs2397084 gene polymorphisms contribute to the pathogenesis of the disease. There was no evidence that different genotypes of these genes affect serum IL-A and IL-17F levels. However, studies with large sample sizes are required for genetic polymorphism examination to yield more reliable results.