Reactive Arthritis: From Clinical Features to Pathogenesis

Abstract

Reactive arthritis (ReA) is a sterile synovitis which occurs after a gastrointestinal or urogenital infection. ReA belongs to Spondyloarthritis (SpA), a group of diseases that share several clinical and radiological features including familiar clustering, absen ce of rheumatoid factor and association with HLA-B27. Clinically, ReA is characterized by an asym metric arthritis predominantly affecting the lower limbs, often associated with urethritis, conjunctivitis and other extra articular symptoms. The ReA prevalence depends on the incidence of causative pathogens. The ReA diagnosis is based on clinical features and serological tests to evidence previous infection. Different treatment including antibiotics, dis ease modifying antirheumatic drugs (DMARs) and biologic agents ha s been recommended. Even though knowing that infections trigger the joint inflammation, the ReA pathogenesis remains to be poorly understood. Several animal models and in vitro studies have been used to elucidate the mechanisms involved in ReA development. In this sense, HLA-B27 transgenic rat or mice have been used to explain the role of this molecule in SpA aetiopathogenesis. Moreover, the in fectious model of Yersinia -induced ReA in rodents ha s shed some lights on the relationship between host genetic susceptibility to infection and abnormal immune response in ReA development. Understanding the immune mediators triggering ReA will contribute to find a specific treatment for this arthritis. In this review, we focus o n clinical features, epidemiology, treatment, and the different attempts to understand the pathogenesis of ReA.