The etiology and pathogenesis of rheumatoid arthritis remain unclear. Existing studies suggest that genetics, sex hormones, pathogenic microbial infections, smoking, and the environment are associated with the development of the disease. Currently, it is believed that people with SLE susceptibility genes or family history are more likely to develop rheumatoid arthritis. These people, especially women, are under the influence of sex hormones, or infected with certain pathogenic microorganisms, or living in a cold and humid environment for a long time, resulting in the disruption of the body’s immune balance and the proliferation of a large number of lymphocytes in the synovial membrane, which secrete a variety of inflammation-promoting factors, leading to an inflammatory response in the synovium. Persistent synovial inflammation can gradually destroy the joint surface, cartilage and a series of other components, eventually leading to joint deformities. Since rheumatoid arthritis patients can also produce auto-antibodies, these auto-antibodies do not recognize the body’s own tissue components, treating them as foreign “foreign bodies” and activating antigenic antibody reactions to induce immune inflammation, which can cause multi-system organ damage in addition to synovitis. For patients with a clear diagnosis of rheumatoid arthritis, factors such as cold, flu, exertion, and overuse of the joints can trigger activity or aggravate the disease. Therefore, the pathogenesis of rheumatoid arthritis is complex, involving multiple factors such as genetics, sex hormones, and the environment.