IL-1 gene polymorphisms in Korean periodontitis patients

Abstract

The primary cause for developing periodontitis is bacteria, but host factors such as diabetes, smoking, and genetics could contribute to the clinical appearance as well as the extent and severity of periodontal destruction. The host inflammatory response to the bacterial challenge is one of the factors contributing to the destruction of periodontal tissue1,2). The role of proinflammatory cytokines has been studied extensively in periodontal diseases. Involvement of interleukin-1 (IL-1) in the pathogenesis of periodontal disease has been suspected because of association between the known biological effects of the cytokine and the manifestations of the disease. IL-1 level has been reported to be elevated in inflamed periodontal tissues and gingival crevicular fluid associated with periodontitis3,4). Masada et al.3) reported that IL-1 might serve as a marker of periodontal tissue destruction because IL1 was produced and released locally in periodontal disease at concentrations sufficient to mediate tissue inflammation and bone resorption. IL-1 enables ingress of inflammatory cells into sites of infection; stimulates eicosanoid release by monocytes and fibroblasts; stimulates matrix metralloproteinases; and contributes to the inflammatory cascade of the microbial immune response5,6). Proinflammatory cytokine IL-1 exists in 2 forms, IL1α, and IL-1β. There are 3 genes that regulate the production of IL-1 variants: IL-1A, IL-1B, and IL-1 receptor antagonist (IL-1 RN)7). These genes are located close to each other on chromosome 2q13. Genes IL-1A and IL-1B control the production of proinflammatory proteins, IL-1αand IL-1β, respectively. IL-1 RN controls the synthesis of an antagonist protein (IL-ra) that impedes IL-1αand IL-1β8,9). The specific forms alleles of each IL-1A and IL-1B gene present in an individual vary. The term “genetic polymorphism”refers to a change in the sequence