DIABETES WORSENS PERIODONTITIS; SEVERE PERIODONTITIS CAN WORSEN GLYCEMIC CONTROL.

Chronic periodontitis is a multifactorial inflammatory disease characterized by progressive destruction of periodontal tissues and alveolar bone. Although microbial biofilm is the primary etiological factor, tissue damage largely depends on the host immune-inflammatory response. Pro-inflammatory cytokines play a central role in mediating periodontal inflammation, connective tissue degradation, and bone resorption. The aim of this study was to analyze the role of key pro-inflammatory cytokines in the pathogenesis of chronic periodontitis based on clinical, microbiological, and molecular-genetic evidence, with particular emphasis on TNF-α and IL-1β. The review integrates data from clinical observations, microbiological findings, and genetic association studies evaluating cytokine activity and gene polymorphisms related to periodontal disease. Special attention is given to single nucleotide polymorphisms of TNF-α and IL-1β genes and their association with disease susceptibility and severity. Accumulating evidence indicates that elevated expression of pro-inflammatory cytokines contributes to periodontal tissue destruction by enhancing leukocyte recruitment, matrix metalloproteinase activation, and osteoclastogenesis. Genetic polymorphisms affecting cytokine regulation may amplify inflammatory responses and predispose individuals to more aggressive forms of chronic periodontitis. Understanding cytokine-mediated mechanisms provides a biological basis for personalized periodontal diagnostics and targeted therapeutic strategies. Integration of clinical and genetic markers may improve risk assessment, early diagnosis, and treatment outcomes in periodontal practice.

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