Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent synovial inflammation and progressive bone destruction. In recent years, the gut–bone axis has emerged as an important conceptual framework linking gut microbiota to immune regulation and bone metabolism. This review aims to summarize current evidence on how gut microbiota dysbiosis, intestinal barrier dysfunction, and microbiota-derived metabolites contribute to RA pathogenesis, and to discuss potential microbiota-targeted therapeutic approaches.

Relevant studies on the interaction between gut microbiota and RA were reviewed and analyzed. Particular attention was given to alterations in microbial composition, disruption of intestinal barrier integrity, and the regulatory effects of microbial metabolites, including short-chain fatty acids, bile acids, and tryptophan-derived compounds. In addition, recent research on microbiota-based interventions, such as probiotics, prebiotics, dietary modifications, fecal microbiota transplantation, and traditional Chinese medicine, was examined.

Accumulating evidence suggests that gut microbiota dysbiosis is closely associated with the initiation and progression of RA. Altered microbial communities can impair intestinal barrier function by disrupting tight junction proteins and increasing intestinal permeability, which facilitates microbial translocation and promotes systemic inflammation. Microbiota-derived metabolites play an important role in immune regulation. For instance, short-chain fatty acids contribute to the maintenance of immune homeostasis by promoting regulatory T cell differentiation and limiting pro-inflammatory responses. Bile acids and tryptophan metabolites further modulate immune signaling pathways and influence the balance of immune cell populations. Together, these mechanisms are involved in shaping inflammatory responses and bone metabolism in RA. Moreover, interventions targeting the gut microbiota have shown potential in alleviating inflammation and improving disease outcomes in experimental and clinical settings.

The gut–bone axis represents an important mechanism in RA pathogenesis, highlighting the role of gut microbiota and their metabolites in linking intestinal homeostasis with immune and skeletal systems. Although microbiota-targeted therapies offer promising prospects, further studies are needed to clarify their long-term efficacy and safety, as well as to support their application in personalized treatment strategies.