Effects of IL-17 Inhibition with Secukinumab in Experimental Periodontitis

Abstract

Abstract Objective IL-17 plays a key role in the pathogenesis of periodontitis and systemic inflammatory diseases. This study investigates the effect of secukinumab, an IL-17 inhibitor, on the development of periodontal disease in a rat model of experimental periodontitis. Materials and Methods Experimental periodontitis was induced in rats by suturing silk around the mandibular first molar tooth (n = 32). After inducing periodontitis with ligature, the animals were divided into two groups: experimental and control. In the experimental group secukinumab was given intraperitoneally. The experiment was terminated 14 days after the induction of experimental periodontitis. Alveolar bone loss (ABL) was measured from microscope images, and the level of inflammatory cell infiltration (ICI) was analyzed by hematoxylin-eosin staining. IL-17, nuclear factor kappa B ligand receptor activator (RANKL), osteoprotegrin (OPG) levels and RANKL/OPG ratio were evaluated by immunohistochemistry. Results In the development process of experimental periodontitis, it was observed that the IL-17 inhibitor secukinumab decreased IL-17 levels, ABL, ICI and RANKL/OPG ratio (p < 0.05); and increased OPG levels (p < 0.05). No statistically significant effect of secukinumab application was observed on RANKL levels (p > 0.05). Conclusion The results obtained from this study suggested that inhibition of IL-17 with secukinumab slows down the development of periodontitis and IL-17 plays a key role as a pro-inflammatory cytokine in periodontitis pathogenesis. Clinical Relevance: This study is the first to examine the effect of secukinumab on periodontal tissues, despite of its limitations. It sheds light on the role of IL-17 in periodontal inflammation in experimental periodontitis.