Introduction. Reactive Arthritis(ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body.Reactive arthritis is known to be triggered by a bacterial infection, particularly of the genitourinary (Chl. trachomatis, Neisseria gonorrhea, Mycoplasma hominis, and Ureaplasma urealyticum) or GI tract (Salmonella enteritidis, Shigella flexneri, and disenteriae, Yersinia enterocolitica, Campylobacter jejuni, Cl.difficile). The incidence is about 2% to 4% after a urogenital infection mainly with chlamydia trachomatis and varies from 0% to 15% after gastrointestinal infections with Salmonella, Shigella, Campylobacter, or Yersinia. Aim of the study. To identify the most common infections that lead to the reactive arthritis and to highlight the pathogenetic mechanisms of action, which would help to improve the treatment tactic. Materials and methods. The relevant articles on the topic were taken from the databases NCBI, PubMed, Medline,and ScienceDirect . Results. Reactive arthritis is an immune-mediated syndrome triggered by a recent infection. It is hypothesized that when the invasive bacteria reach the systemic circulation, T lymphocytes are induced by bacterial fragments such as lipopolysaccharide and nucleic acids. These activated cytotoxic-T cells then attack the synovium and other self-antigens through molecular mimicry. This is supported by the evidence of Chlamydia trachomatis and C pneumoniae ribosomal RNA transcripts, enteric bacterial DNA and bacterial degradation products in the synovial tissue and fluid. It is believed that anti-bacterial cytokine response is also impaired in reactive arthritis, resulting in the decreased elimination of the bacteria. Conclusions. Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intraarticular persistence of viable, nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. The mechanisms that lead to the development of ReA are complex and basically involve an interaction between an arthritogenic agent and a predisposed host. The way in which a host accommodates to invasive facultative intracellular bacteria is the key to the development of ReA. The details of the molecular pathways that explain the articular and extra-articular manifestations of the disease are still under investigation.