EB 2017 Article: Changes in advanced glycation end products, beta-defensin-3, and interleukin-17 during diabetic periodontitis development in rhesus monkeys.

The bidirectional relationship between diabetes mellitus (DM) and periodontal disease has drawn great attention; however, the mechanisms underlying their association remain unclear. In this study, we aimed to develop a rhesus monkey model of diabetic periodontitis and explore the potential mechanisms by which DM affects the progression of periodontal disease. Three healthy rhesus monkeys were selected as the control group. Five streptozotocin-induced diabetic rhesus monkeys were chosen as the experimental group. Ligature placement was used to induce periodontitis. The changes in the levels of advanced glycation end products (AGEs), beta-defensin-3 (BD-3), and interleukin-17 (IL-17) were measured using enzyme-linked immunosorbent assays (ELISA) and real-time reverse transcription polymerase chain reaction (RT-PCR) at different stages during disease progression. Periodontitis was confirmed by clinical assessment, radiographic images, and histological examination. Significant changes in the levels of AGEs and BD-3 in serum were observed at the periodontitis stage in diabetic rhesus monkeys ( P < 0.05). The expression of BD-3 mRNA in the gingiva of diabetic group at baseline was significantly high ( P < 0.05). Diabetic monkeys exhibited significantly enhanced IL-17 mRNA expression at the periodontitis stage ( P < 0.05). Our findings indicated that the rhesus monkey can serve as an ideal model for exploring the pathogenesis of diabetic periodontitis, and the hyperglycemic environment may accelerate inflammatory response and weaken the defense system in periodontal tissues. Impact statement The mechanism underlying the association between diabetes mellitus (DM) and periodontal disease is not yet fully understood. Hence, there is a need to establish animal models to reveal the effect of DM on the pathogenesis of periodontitis. In this study, we explored the appropriate methods for inducing periodontitis and shortening the modeling time in rhesus monkeys, to investigate the pathogenesis of diabetic periodontitis and develop innovative therapies. Our results suggest that a hyperglycemic environment might lead to the destruction of periodontal tissues by accelerating inflammatory response and weakening the defense system in periodontal tissues. Therefore, this study has significant treatment implications regarding the regulation of the immune response against periodontal diseases in patients with DM.