Potential Role of NLRP۳ Inflammasome Activation in the Pathogenesis of Periodontitis Patients with Type ۲ Diabetes Mellitus

Background: In response to microbial infection and cellular injury, the NLRP۳ inflammasome, an essential part of the innate immune system, causes caspase-۱ activation and the release of the proinflammatory cytokines IL-۱ β and IL-۱۸. However, various inflammatory diseases, including periodontal disease, have been linked to the abnormal activation of the NLRP۳ inflammasome.Aim of study: This study was conducted to investigate the crucial role of NLRP۳ inflammasome activation and IL-۱۸ in the pathogenesis of periodontitis patients with type ۲ diabetes mellitus.Materials and Methods: This case control study included eighty-five participants., their age range (۲۳-۵۵) years, they 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 analyzed using an ELISA kit designed to detect NLRP۳ inflammasome activity and interleukin-۱۸.Results: Conclusions: Elevated NLRP۳ and IL-۱۸ levels in PD +T۲DM patients, as well as their positive correlation with clinical parameters, suggest a critical role in the pathogenesis of PD with and without diabetes.. A significant positive correlation also noticed between NLRP۳ and each of (GI, PPD, CAL and BOP) in PD+T۲DM patients. Regarding the group of PD patients there was no significance correlation between NLRP۳ and clinical parameters. Additionally, IL-۱۸ was discovered to have a positive correlation with GI, PPD, CAL, and BOP in PD+T۲DM patients, w. Meanwhile, there is a significant correlation between NLRP۳ as well as interleukin-۱۸ in patients with and without type ۲ diabetic mellitus.Conclusions: Elevated NLRP۳ and IL-۱۸ levels in PD +T۲DM patients, as well as their positive correlation with clinical parameters, suggest a critical role in the pathogenesis of PD with and without diabetes.