A chronic autoimmune illness that causes joint destruction and inflammation, rheumatoid arthritis (RA) often results in disability. Genetic, environmental, and immune system variables all have a role in the pathophysiology of RA. The complex community of bacteria that live in the gastrointestinal system, known as the gut microbiota, has been implicated in the onset and progression of RA in recent years, according to mounting data. An imbalance in the gut microbiota's composition, known as dysbiosis, has been noted in RA patients. This imbalance may impact inflammatory pathways and immunological responses, which in turn may contribute to the development and severity of the illness. Research has shown that some bacterial species, including Firmicutes, Bacteroidetes, and Proteobacteria, are either more abundant or less prevalent in RA patients than in healthy people. The gut-immune system axis may be modulated, immunological tolerance may be affected, and pro-inflammatory cytokine production may be enhanced by these microbial changes, all of which may lead to systemic inflammation linked to RA. Moreover, changes in intestinal permeability and a rise in microbial metabolite translocation may make autoimmune reactions worse. Probiotics, antibiotics, and dietary changes have also been investigated as possible treatment approaches to help RA patients regain the balance of their gut microbiota. Still up for debate, however, are the precise ways in which the gut microbiome affects RA. Comprehending the complex connection between gut microbiota and RA may give new perspectives on managing and preventing the condition, as well as future prospects for medicines that target the microbiome.