Polymorphisms of IL-17A and IL-17F in Periodontal Disease: A Case-Control Study

Abstract

Background: Increased interleukin-17 (IL-17) leads to the production of proinflammatory mediators and increases local inflammation. Interleukin-17 may also promote receptor activator of nuclear factor kappa-B ligand (RANKL) expression on gingival fibroblasts, T cells, and B cells, resulting in alveolar bone resorption. Interleukin-17A and IL-17F levels in saliva and gingival crevicular fluid (GCF), were found to be elevated in periodontitis patients. Thus, IL-17A and IL-17F polymorphisms were hypothesized to be associated with a risk of periodontitis. Methods: The present study was conducted on 60 subjects, including 20 stage II grade B periodontitis patients, 20 stage III grade C periodontitis patients, and 20 healthy controls. Blood samples were drawn from the subjects and analyzed for IL-17A G-197A and IL-17F 7488T/C genetic polymorphisms using the TaqMan assay. Results: There was a significant statistical difference between the distribution of the different genotypes and the different alleles in the three groups for IL-17A G-197A with the A allele presence indicating a risk of periodontitis. Conclusions: Interleukin-17A G-197A polymorphism is significantly associated with different clinical forms of periodontitis in the Egyptian population. The A allele could be considered a risk factor for periodontal diseases.