Reactive arthritis

Reactive arthritis (ReA) has been recognized as a clinical disease entity for nearly 100 years. The prevalence is estimated to be 30–40/100,000 adults. The HLA-B27-associated form is part of the spondyloarthritis concept. According to the current hypothesis the arthritis follows a primary extra-articular infection and is characterized by the presence of bacterial antigen and/or of viable but non-culturable bacteria persisting within the joint. Pathogenesis involves the modification of host cells by pathogen-associated molecular patterns (PAMPs, e.g. lipopolysaccharide), bacterial effector proteins, the adaptive immune system, and the genetic background. Up to 30% of patients develop chronic symptoms, and therapeutic options for these patients are still limited. Data for recommendations to apply conventional disease-modifying anti-rheumatic drugs (DMARDs) are rare; however, sulfasalazine seems to be effective, and first reports on agents that block tumour necrosis factor (TNF) are promising. Combination therapy of several antibiotics might open the window to curing the disease; however, controlled clinical studies are needed.