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Porphyromonas gingivalis and rheumatoid arthritis

机译:Porphyromonas Gingivalis和类风湿性关节炎

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Purpose of review To explore the pathogenic association between periodontal disease and rheumatoid arthritis focusing on the role of Porphyromonas gingivalis. Recent findings In the last decades our knowledge about the pathogenesis of rheumatoid arthritis substantially changed. Several evidences demonstrated that the initial production of autoantibodies is not localized in the joint, rather in other immunological-active sites. A central role seems to be played by periodontal disease, in particular because of the ability of P. gingivalis to induce citrullination, the posttranslational modification leading to the production of anticitrullinated protein/peptide antibodies, the most sensitive and specific rheumatoid arthritis biomarker. The pathogenic role of P. gingivalis has been demonstrated in mouse models in which arthritis was either triggered or worsened in infected animals. P. gingivalis showed its detrimental role not only by inducing citrullination but also by means of other key mechanisms including induction of NETosis, osteoclastogenesis, and Th17 proinflammatory response leading to bone damage and systemic inflammation.
机译:审查目的以探讨牙周病与类风湿性关节炎的致病关联,重点是卟啉核糖瘤的作用。最近发现在过去几十年中,我们了解类风湿性关节炎的发病机制的知识显着变化。几个证据表明,自身抗体的初始生产不是在接头中局部化,而是在其他免疫活性部位。牙周病似乎扮演核心疾病,特别是由于P. Gingivalis诱导瓜氨酸的能力,导致抗鞘化蛋白/肽抗体的产生,最敏感和特异性类风湿性关节炎生物标志物。在小鼠模型中证明了P.Gingivalis的致病作用,其中关节炎被触发或在感染的动物中恶化。 P. Gingivalis不仅通过诱导瓜骨而且借助于其他关键机制表达了其有害作用,包括诱导未降低的骨质细胞发生和导致骨损伤和全身炎症的植物炎症反应。

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