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HLA-B27-associated reactive arthritis: pathogenetic and clinical considerations Colmegna I; Cuchacovich R; Espinoza LRClin Microbiol Rev 2004[Apr]; 17 (2): 348-69Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable, non-culturable 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. Several studies have been done to gain a better understanding of the pathogenesis of ReA; these constitute the basis for a more rational therapeutic approach to this disease.|*Arthritis, Reactive/diagnosis/epidemiology/microbiology/physiopathology/therapy[MESH]|*HLA-B27 Antigen/genetics/metabolism[MESH]|Animals[MESH]|Chlamydia/isolation & purification[MESH]|Enterobacteriaceae/isolation & purification[MESH]|Gram-Negative Bacterial Infections/complications[MESH]|Humans[MESH]|Mice[MESH]|Prohibitins[MESH]|Rats[MESH] |
