Periodontitis is a chronic inflammatory disease initiated by microbial biofilm and sustained by the hosts immune response, leading to progressive destruction of periodontal tissues. Type 2 diabetes mellitus significantly increases the risk of periodontitis, while periodontitis, in turn, negatively affects glycemic control, indicating a bidirectional relationshipT2DM influences periodontitis by promoting a hyperinflammatory state, impairing bone healing, and increasing advanced glycation end products Interleukin12 plays a central role in immune modulation by promoting Th1 cell differentiation, enhancing IFN gamma production, and linking innate and adaptive immunity. Elevated IL12 levels have been observed in periodontitis, with correlations to disease severity, though findings remain inconsistent across studies.Dipeptidyl peptidase 4  regulated by IL12, enhances Tcell responses, contributes to insulin resistance by degrading incretin hormones, and is involved in oxidative stress and osteoclastogenesis. Increased levels of DPP4 have been found in gingival crevicular fluid and saliva of periodontitis patients, though its role in T2D Massociated periodontitis remains unexplored.

Despite the known individual roles of IL 12 and DPP4 in T2DM and periodontitis, their combined contribution and interaction in T2DM associated periodontitis have not been studied. This study aims to evaluate salivary and serum levels of IL12 and DPP4 in periodontitis with and without T2DM. We hypothesize that in uncontrolled T2DMassociated periodontitis, both IL12 and DPP4 levels are elevated and positively correlated, contributing to enhanced immune dysregulation and tissue destruction.