Inflammatory pathways associated with periodontal disease

Inflammatory pathways associated with periodontal disease represent a complex network of host immune responses triggered by dysbiotic subgingival biofilms. Key pathways include the NF-κB signaling cascade, the NLRP3 inflammasome, and the RANK/RANKL/OPG axis, which regulate the production of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α (Hajishengallis & Chavakis, 2021, Nature Reviews Immunology). These molecular signals recruit inflammatory cells and stimulate the release of matrix metalloproteinases (MMPs), particularly MMP-8 and MMP-13, which degrade the periodontal ligament and alveolar bone (Sorsa et al., 2016, Periodontology 2000). Chronic activation of these pathways is the primary driver of tissue destruction in periodontitis, rather than the bacteria themselves. Therapeutic intervention, known as host modulation therapy, aims to downregulate these destructive pathways using agents like sub-antimicrobial dose doxycycline or non-steroidal anti-inflammatory drugs (Preshaw et al., 2004, Journal of Clinical Periodontology). Understanding these pathways is crucial as they also link periodontal health to systemic conditions such as diabetes and cardiovascular disease.

Other names

Periodontal inflammatory signalingHost immune response in periodontitisCytokine networks in periodontal diseasePeriodontitis-associated inflammatory cascades

Inhibition of matrix metalloproteinases (MMPs), suppression of arachidonic acid metabolites via cyclooxygenase (COX) inhibition, and reduction of pro-inflammatory cytokine expression to modulate the host immune response.