Reactive arthritis is an incompletely understood inflammatory process of the joint. Classic reactive arthritis produces an oligoarthritis that normally involves the lower extremities; the disease also usually produces enthesitis and may include sacroiliitis.(1,2) The HLA B27 allele is seen in patients with reactive arthritis somewhat more frequently than in the general population, but it is not invariably present.(2) The disease shows inflammatory changes such as increased leukocyte counts in joint effusions, as well as inflammation of the synovium. In many cases, episodes of active arthritis last weeks or longer, but finally result in remission. Approximately half of all individuals with acute reactive arthritis become chronic or remitting, either with or without evidence of reinfection by the associated or by other organisms.
As indicated above, the spectrum of organisms involved in reactive arthritis is probably larger than that suggested by the strict ACR definition. Indeed, more than 75% of patients seen in an early arthritis clinic showed similar unexplained oligoarthritis (occasionally polyarthritis) with no documented history of antecedent infection;(1,2,10) this issue is developed in more detail below. Patients with classic reactive arthritis frequently display a variety of extraarticular features, including iritis, conjunctivitis, urethritis, cervicitis, and several types of dermatitis.(1,2) However, most rheumatologists indicate that such additional features are not required for diagnosis.
Reiter's syndrome is a subset of reactive arthritis, also defined by ACR criteria. The synovitis in patients with early Reiter's syndrome is characterized by superficial inflammation with large numbers of polymorphonuclear cells and vascular congestion;(11) this is distinctly different from findings in the early rheumatoid arthritis synovium.(12,13) In chronic Reiter's syndrome, synovial changes tend to be similar to those seen in patients with rheumatoid arthritis, with higher levels of lymphocyte and plasma cell infiltration. Fibrin deposition may be seen in both acute and chronic disease. Electron microscopic studies show microvascular occlusion by platelet-fibrin thrombi, electron-dense proteinlike deposits in vessel walls, and strands of infiltrating fibrin. While C. trachomatis has long been associated with development of Reiter's syndrome in some patients, no information is available at present concerning a possible role for C. pneumoniae in the genesis of this clinical entity. Thus the discussion following will focus primarily on classic reactive arthritis.
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