Unraveling the enigma of salivary uric acid in periodontitis: Independent association, mechanistic insights, and future trajectories.

Abstract

This article explores the association between salivary uric acid (UA) and periodontitis, systematically analyzing its dual roles and research progress. Studies indicate that UA acts as a primary antioxidant in saliva under physiological conditions (accounting for 70%), protecting periodontal tissues by scavenging reactive oxygen species. However, when gum disease becomes severe, UA can switch roles and fuel inflammation, worsening tissue damage. Lorente et al's research found an independent inverse correlation between salivary UA levels and periodontitis severity (odds ratio = 6.14, P = 0.001), establishing 111 nmol/mL as a diagnostic threshold (area under the curve = 66%). Nevertheless, limitations include sample heterogeneity and failure to distinguish between gingivitis and periodontitis. Mechanistically, three hypotheses are proposed: The Antioxidant Depletion Hypothesis (UA oxidation consumption leading to feedback loops), the Microbial Metabolic Hijacking Hypothesis (pathogens utilizing UA as a carbon source to disrupt redox balance), and the Epithelial Barrier Dysfunction Hypothesis (UA deficiency causing downregulation of tight junction proteins). Future research should prioritize longitudinal cohorts to validate predictive value, integrate multi-omics to explore dysregulated signatures, and develop UA supplementation or targeted antioxidant therapies. This study provides novel insights into periodontitis diagnosis and mechanisms, advancing the application of salivary biomarkers in precision periodontics.