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

Table 1 Tripartite mechanisms linking salivary uric acid dysfunction to periodontitis

Mechanism	Brief description	Key interactions
Antioxidant depletion	Chronic inflammation oxidizes UA, depleting reserves and impairing antioxidant capacity	ROS from inflammation oxidize UA. UA depletion reduces antioxidant defense. Oxidative stress fuels inflammation
Microbial metabolic hijacking	Pathogens use UA as a carbon source, disrupting redox balance and promoting inflammation	UA depletion correlates with elevated microbial metabolites. Short-chain fatty acids activate NF-κB, exacerbating inflammation
Epithelial barrier dysfunction	UA deficiency weakens epithelial integrity, facilitating microbial translocation and tissue damage	UA deficiency reduces tight junction proteins. Increased microbial translocation triggers immune responses and tissue destruction
Synergistic cycle	Pathways interact, forming a vicious cycle of inflammation, oxidation, and infection	Microbial metabolism consumes UA and produces ROS. Barrier disruption enhances pathogen invasion

UA: Uric acid; ROS: Reactive oxygen species; NF-κB: Nuclear factor-kappaB.