Potential Role of NLRP3 Inflammasome Activation in the Pathogenesis of Periodontitis Patients with Type 2 Diabetes Mellitus

In response to microbial infection and cellular injury, the NLRP3 inflammasome, an essential part of the innate immune system, causes caspase-1 activation and the release of the proinflammatory cytokines IL-1 β and IL-18. However, various inflammatory diseases, including periodontal disease have been linked to the abnormal activation of the NLRP3 inflammasome. This study was conducted to investigate the crucial role of NLRP3 inflammasome activation and IL-18 in the pathogenesis of periodontitis patients with type 2 diabetes mellitus. This case control study included eighty-five participants and their age range was (23-55) years old. They were divided into three groups: two groups had periodontitis one of them with type two diabetic mellitus and the other one systemically healthy, the third group was the control group with clinically healthy periodontium and systemically healthy. Serum samples from both patients and controls were analysed by using an ELISA kit designed to detect NLRP3 inflammasome activity and interleukin-18. The elevated NLRP3 and IL-18 levels in PD +T2DM patients and their positive correlation with clinical parameters suggested a critical role in the PD pathogenesis with and without diabetes. A significant positive correlation was also noticeable between NLRP3 and each of (GI, PPD, CAL, and BOP) in PD+T2DM patients. Regarding the group of PD patients, there was no significance correlation between NLRP3 and clinical parameters. In addition, IL-18 was discovered to have a positive correlation with GI, PPD, CAL, and BOP in PD+T2DM patients. Meanwhile, there was a significant correlation between NLRP3 and interleukin-18 in patients with and without type 2 diabetic mellitus. Elevated NLRP3 and IL-18 levels in PD +T2DM patients and their positive correlation with clinical parameters suggested a critical role in the PD pathogenesis with and without diabetes.