Journal of clinical periodontology · 2025
Hyperuricemia Exacerbates Experimental Periodontitis via Uric Acid-Induced Periodontal Inflammation and Oxidative Stress.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wu Zhicong, Zhao Li, Guo Yi, Lin Chuyin, Lu Peipei, He Qian, Zhou Yinghong, Wang Xinhong, Yu Ting
Аннотация
AIM: To investigate the effects of hyperuricemia on periodontitis and the underlying mechanisms by establishing combined animal and cell models.
METHODS: A hyperuricemia mouse model was established by potassium oxonate injection, with sodium carboxymethylcellulose treatment serving as controls. Both models were treated with or without periodontitis induction (n = 10/group). RAW264.7 macrophages and THP-1-derived macrophages were stimulated with Porphyromonas gingivalis -lipopolysaccharide in the presence of normal or excessive concentrations of uric acid. Allopurinol intervention was applied to both animal and cell models. Periodontal destruction was measured by micro-computed tomography and histology. The immune response and oxidative stress in the periodontium and macrophages were assessed using various methods including immunohistochemistry, quantitative PCR, western blotting, flow cytometry and multiplex cytokine assays.
RESULTS: Potassium oxonate successfully induced hyperuricemia without affecting serum glucose/lipid levels or xanthine oxidoreductase activity. In mice with periodontitis, hyperuricemia exacerbated alveolar bone loss and the presence of osteoclasts and M1 macrophages. Mechanistically, hyperuricemia promoted NLRP3 inflammasome activation, disrupted the inflammatory cytokine response and exacerbated oxidative stress both in the periodontium and in vitro. Allopurinol treatment reversed all relevant changes in both mice and macrophages.
CONCLUSION: Hyperuricemia exacerbates periodontitis possibly via uric acid-induced periodontal inflammation and oxidative stress.
METHODS: A hyperuricemia mouse model was established by potassium oxonate injection, with sodium carboxymethylcellulose treatment serving as controls. Both models were treated with or without periodontitis induction (n = 10/group). RAW264.7 macrophages and THP-1-derived macrophages were stimulated with Porphyromonas gingivalis -lipopolysaccharide in the presence of normal or excessive concentrations of uric acid. Allopurinol intervention was applied to both animal and cell models. Periodontal destruction was measured by micro-computed tomography and histology. The immune response and oxidative stress in the periodontium and macrophages were assessed using various methods including immunohistochemistry, quantitative PCR, western blotting, flow cytometry and multiplex cytokine assays.
RESULTS: Potassium oxonate successfully induced hyperuricemia without affecting serum glucose/lipid levels or xanthine oxidoreductase activity. In mice with periodontitis, hyperuricemia exacerbated alveolar bone loss and the presence of osteoclasts and M1 macrophages. Mechanistically, hyperuricemia promoted NLRP3 inflammasome activation, disrupted the inflammatory cytokine response and exacerbated oxidative stress both in the periodontium and in vitro. Allopurinol treatment reversed all relevant changes in both mice and macrophages.
CONCLUSION: Hyperuricemia exacerbates periodontitis possibly via uric acid-induced periodontal inflammation and oxidative stress.