Fig. 4
A hypothetical illustration of the differences in uric acid levels between blood, saliva and GCF in periodontitis populations. Saliva and GCF purine levels are found to be elevated in hosts with periodontitis. However, uric acid levels of decrease rather than increase, which may be due to an enhanced uric acid consumption by oral/periodontal bacteria and ROS. Purines in saliva and GCF may also be consumed by XOR-like purine-degrading enzymes that are produced by bacteria. By inhibiting XOR activity, increased levels of nitrate and nitrite produced by salivary glands to combat oral microbiota would reduce the production of uric acid in saliva. In periodontal tissues, circulation and systemic organs (e.g., liver and gut), elevated levels of uric acid have been detected in periodontitis patients or animals, which may be the result of accelerated purine degradation and enhanced XOR activity. The XOR activity in circulation may be increased by periodontitis-related systemic inflammation, but inhibited by anticoagulants such as EDTA. Uric acid may be exchanged between periodontal tissues and systemic organs through circulation. EDTA, ethylenediamine tetraacetic acid; GCF, gingival crevicular fluid; NOX, NO3− and NO2−; PDE, purine-degrading enzymes; ROS, reactive oxygen species; XOR, xanthine oxidoreductase.