Review explores ACh and IL-17 impact on inflammation in periodontitis, suggesting new treatment avenues.
Periodontitis is a chronic inflammatory disease affecting the supporting structures of the teeth, often leading to tooth loss. Saliva and gingival crevicular fluid (GCF) serve as important diagnostic fluids, offering noninvasive access to biomarkers that reflect disease activity. This review focuses on the roles of acetylcholine (ACh) and interleukin-17 (IL-17) in the pathogenesis of periodontitis. ACh, traditionally known for its neuronal functions, also plays a regulatory role in immune responses through the cholinergic anti-inflammatory pathway (CAP). Altered levels of ACh in saliva and GCF have been observed in periodontal disease, suggesting its involvement in modulating inflammation. IL-17, a cytokine primarily secreted by Th17 cells, promotes the production of inflammatory mediators and neutrophil recruitment, contributing to tissue damage and bone resorption. Emerging evidence indicates that activation of CAP may suppress IL-17 activity, highlighting a potential regulatory interaction between neural and immune responses in periodontitis. The detection of ACh and IL-17 in GCF and saliva underscores their potential as biomarkers for diagnosis and disease monitoring. Understanding the interplay between ACh and IL-17 may lead to novel therapeutic strategies targeting neuroimmune pathways to control periodontal inflammation and improve clinical outcomes.
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Shajahan et al. (2026) studied this question.
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