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India | Periodontology | Volume 14 Issue 7, July 2025 | Pages: 1179 - 1189
Role of Inflammasomes in Periodontitis
Abstract: Periodontitis is a chronic inflammatory disease characterized by the destruction of periodontal tissues, primarily driven by a dysregulated host immune response to subgingival biofilm. Recent advances in molecular immunology have highlighted the critical role of inflammasomes-intracellular multiprotein complexes-in orchestrating innate immune responses in periodontal disease. Among these, the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome has garnered significant attention due to its ability to activate caspase-1, leading to the maturation and secretion of interleukin (IL)-1? and IL-18, pivotal cytokines in periodontal inflammation and tissue breakdown. Dysregulated activation of inflammasomes contributes to excessive inflammatory cytokine release, increased osteoclastogenesis, and progressive alveolar bone loss. Additionally, microbial components such as lipopolysaccharides and danger-associated molecular patterns (DAMPs) act as potent triggers for inflammasome activation in gingival tissues. Understanding the role of inflammasomes provides novel insights into the immunopathogenesis of periodontitis and presents potential therapeutic targets for modulating host response. Targeted inhibition of inflammasome components or downstream cytokine pathways may offer promising adjunctive strategies in periodontal therapy. This review highlights current evidence on the involvement of inflammasomes in periodontitis and underscores their potential as biomarkers and therapeutic targets in the management of periodontal diseases.
Keywords: Periodontitis, Inflammasome, Innate Immunity, Interleukin-18, DAMPS
How to Cite?: G Sumanth, Lavanya R, "Role of Inflammasomes in Periodontitis", Volume 14 Issue 7, July 2025, International Journal of Science and Research (IJSR), Pages: 1179-1189, https://www.ijsr.net/getabstract.php?paperid=SR25717113517, DOI: https://dx.doi.org/10.21275/SR25717113517
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