Pathogenesis of Reiter's syndrome and reactive arthritis

Genetically determined HLA-B27 associated reactivity pattern to certain infections plays a key role in the pathogenesis of Reiter's syndrome and related arthritides. So far the enteric pathogens Shigella, Salmonella, Yersinia and Campylobacter as well as sexually acquired Chlamydia have seriously been incriminated as triggering agents. Yet infections by these microbes do not explain all cases, implying that other, hitherto unknown aetiological factors are involved. The above enteric pathogens share the feature of mucosal involvement, whereas invasion of the lymph nodes and bacteremia do not take place in shigella infection. Thus the latter features are hardly crucial determinants in the pathogenesis of arthritis. Microbes belonging to the indigenous microbial flora of man, such as the common urinary tract pathogens, have not been associated with reactive arthritis. Studies have been carried out on humoral and cellular immune responses in yersinia and chlamydial infections accompanied and not accompanied with arthritis, but they have not revealed any unifying feature that could explain the pathogenesis of arthritis. It is possible that HLA-B27 -positive subjects are unduly sensitive to some mediators of inflammation.