HLA-B27-associated reactive arthritis: pathogenetic and clinical considerations

Abstract

Current 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.

FIG.1.

Events in the natural history of the arthritogenic infection. Data are from reference .

FIG. 2.

(A) Diagnostic approach to Chlamydia-induced ReA. (B) Diagnostic approach to Yersinia- or Salmonella-induced ReA. Reprinted from reference with permission.