虽然自身免疫有助于类风湿性关节炎(RA),一些证据挑战了它主要是一种自身免疫性疾病的教条。由于RA相关的人类白细胞抗原形成微生物群并增加粘膜生态失调的风险,RA可能是由长寿命滑膜呈递细胞的表观遗传变化引起的,由于过度易位到细菌的关节中而受到压力,肺,或口腔微生物群(以同样的方式,更多的病原菌可以导致“反应性关节炎”)。这篇叙述性评论(I)列出了支持这一情景的证据,包括鉴定RA滑膜中(但也包括健康滑膜)的口腔和肠道微生物群的DNA,以及通过血液易位的可能性,从粘膜到关节,微生物群,直接从口腔或肠道,随着口腔细菌如牙龈卟啉单胞菌在肠道内的迁移,肠道通透性增加后恶化;(ii)除了RA患者与对照组患者的牙周微生物群的横断面研究之外,还提出了其他未来工作的方法,即,口腔纵向研究,gut,gut血,和滑膜微生物群结合免疫细胞转录组学分析在有RA风险的个体患者中,在公开的RA中,之前,during,跟随RA的耀斑。
Although autoimmunity contributes to rheumatoid arthritis (RA), several lines of evidence challenge the dogma that it is mainly an autoimmune disorder. As RA-associated human leukocyte antigens shape microbiomes and increase the risk of dysbiosis in mucosae, RA might rather be induced by epigenetic changes in long-lived synovial presenting cells, stressed by excessive translocations into joints of bacteria from the poorly cultivable gut, lung, or oral microbiota (in the same way as more pathogenic bacteria can lead to \"reactive arthritis\"). This narrative
review (i) lists evidence supporting this scenario, including the identification of DNA from oral and gut microbiota in the RA
synovium (but in also healthy synovia), and the possibility of translocation through blood, from mucosae to joints, of microbiota, either directly from the oral cavity or from the gut, following an increase of gut permeability worsened by migration within the gut of oral bacteria such as Porphyromonas gingivalis; (ii) suggests other methodologies for future works other than cross-sectional studies of periodontal microbiota in cohorts of patients with RA versus controls, namely, longitudinal studies of oral, gut, blood, and synovial microbiota combined with transcriptomic analyses of immune cells in individual patients at risk of RA, and in overt RA, before, during, and following flares of RA.