Gingival inflammatory signaling pathways

Gingival inflammatory signaling pathways encompass the intricate network of molecular cascades, such as NF-κB, MAPK, JAK-STAT, and the NLRP3 inflammasome, that orchestrate the host immune response within periodontal tissues (Hajishengallis & Sahingur, 2014; Frontiers in Immunology, 2021). These pathways are primarily triggered by the activation of pattern recognition receptors (PRRs), including Toll-like receptors (TLRs), which recognize pathogen-associated molecular patterns (PAMPs) from oral biofilms (NIH, 2023). Upon activation, these signaling nodes promote the expression of pro-inflammatory cytokines, chemokines, and matrix metalloproteinases (MMPs) that drive the progression from gingivitis to destructive periodontitis (MDPI, 2024). Therapeutic targeting of these pathways aims to resolve chronic inflammation and prevent alveolar bone loss, with approaches including host modulatory therapies (e.g., sub-antimicrobial dose doxycycline) and experimental kinase inhibitors (Frontiers in Oral Health, 2023). However, the high degree of crosstalk between these pathways and their essential roles in systemic immunity present significant challenges for developing targeted, safe pharmacological interventions (Frontiers in Immunology, 2021).

Other names

Periodontal inflammatory signalingGingival cytokine signaling cascadesHost response pathways in periodontitis

Modulation of intracellular signaling cascades (e.g., NF-κB, MAPK, JAK-STAT) and inhibition of downstream inflammatory mediators such as cytokines (TNF-α, IL-1β) and matrix metalloproteinases (MMPs).