Periodontal disease is defined as a plaque–induced inflammation of the periodontal tissues that results in a loss of support around the teeth. It is the leading cause of tooth loss among adults. This process is characterized by destruction of the periodontal attachment apparatus, loss of alveolar bone, apical migration of the epithelial attachment, and formation of periodontal pockets. Although the presence of periodontal pathogens is a prerequisite, the progression of periodontal disease is dependent on the host response to pathogenic bacteria that colonize the tooth surface. Processing of IL–1β and IL–18 is regulated by intracellular innate immune response system, known as NLRP3 (NALP3 or cryopyrin) inflammasome complex. NLRP3 belong to NOD– like receptor family, is a type of pattern recognition receptor (PRR) which is activated by a number of microbial and host components such as proteoglycans, lipopolysaccharide, extracellular ATP, monosodium urate crystals. Aberrant activation of the innate immune system in type–2 diabetes has been recognized to be an important mechanism of disease pathogenesis which involves formation of NLRP3 inflammasome that secretes pro–inflammatory cytokines such as IL–1β and IL–18 leading to periodontal tissue destruction. Hence the present study is conducted to estimate NLRP3 inflammasome level in GCF and serum of diabetic and non diabetic patients with chronic periodontitis and correlation with the clinical periodontal parameters