Rothman Orthopaedic Institute at Thomas Jefferson University, Philadelphia, Pennsylvania, United States of America.
Department of Medical Microbiology and Infection Prevention, University of Groningen, University Medical Center Groningen, RB, Groningen, Netherlands.
PLoS One. 2021 Dec 16;16(12):e0261353. doi: 10.1371/journal.pone.0261353. eCollection 2021.
Along with mechanical and genetic factors, emerging evidence suggests that the presence of low-grade inflammation has a role in the pathogenesis of osteoarthritis (OA) and seems to be related to the microbiome composition of the gut.
To provide evidence whether there is clinical or preclinical evidence of gut-joint axis in the pathogenesis and symptoms of OA.
An extensive review of the current literature was performed using three different databases. Human, as well as animal studies, were included. The risk of bias was identified using ROBINS and SYRCLE tools, while the quality of evidence was assessed using GRADE and CAMADARES criteria.
A total of nineteen articles were included. Multiple animal studies demonstrated that both obesity, and high-fat and high-sugar diets resulted in a gut dysbiosis status characterized by increased Firmicutes/Bacteroidetes (F/B) phyla ratio and increased permeability. These changes were associated with increased lipopolysaccharide serum levels, which consequently resulted in synovitis and OA severity. The administration of pre-and probiotics partially reversed this bacterial composition. In addition, in human studies, a decreased amount of gut Bacteroidetes, subsequent increased F/B ratio, have also been observed in OA patients.
Our review confirms preliminary yet sound evidence supporting a gut-joint axis in OA in primarily preclinical models, by showing an association between diet, gut dysbiosis and OA radiological severity and self-reported symptoms. Clinical studies are needed to confirm these findings, and to investigate whether interventions targeting the composition of the microbiome will have a beneficial clinical effect.
除了机械和遗传因素外，新出现的证据表明，低度炎症的存在在骨关节炎（OA）的发病机制中起作用，并且似乎与肠道微生物组的组成有关。
提供是否有肠道-关节轴在 OA 的发病机制和症状中存在临床或临床前证据。
使用三个不同的数据库进行了广泛的文献综述。包括人体和动物研究。使用 ROBINS 和 SYRCLE 工具确定偏倚风险，使用 GRADE 和 CAMADARES 标准评估证据质量。
共纳入十九篇文章。多项动物研究表明，肥胖、高脂肪和高糖饮食都会导致肠道菌群失调，表现为厚壁菌门/拟杆菌门（F/B）比例增加和通透性增加。这些变化与血清中脂多糖水平升高有关，进而导致滑膜炎和 OA 严重程度增加。益生菌和益生元的给药部分逆转了这种细菌组成。此外，在人类研究中，OA 患者也观察到肠道拟杆菌数量减少，随后 F/B 比值增加。
我们的综述证实了初步但合理的证据，支持 OA 中的肠道-关节轴主要在临床前模型中存在，表明饮食、肠道菌群失调与 OA 放射学严重程度和自我报告的症状之间存在关联。需要进行临床研究来证实这些发现，并研究针对微生物组组成的干预措施是否会产生有益的临床效果。
