Why reactive arthritis?

A role for bacterial infection in the aetiology of inflammatory arthritis has been suspected for many years. Yet over that relatively long period of time only a few acute or chronic arthritides have been unequivocally linked to an infectious agent; these include septic arthritis, rheumatic fever, and, more recently, Lyme arthritis. The term reactive arthritis was first introduced to describe the association between Yersinia enterocoliticainfection and arthritis, and it was intended to differentiate this form of acute, non-suppurative arthritis, which is characterised by negative joint culture, from infectious, purulent arthritis; the differentiation was meant to suggest an underlying sterile immune mediated pathomechanism.1 A few years later, immediately after discovery of the association between HLA-B27 and ankylosing spondylitis and Reiter’s syndrome, the term reactive arthritis was also related to this genetic marker; at this time the term was more strictly applied to the HLA-B27 associated reactive arthritides, following infections with enterobacteria and chlamydia.2 This concept has been widely recognised and accepted. However, non-HLA-B27 associated arthritides, such as Lyme disease induced byBorrelia burgdorferi, Neisseria gonorrhoeae induced reactive arthritis, post-streptococcal reactive arthritis, and rheumatic fever are viewed presently as reactive arthritides (see table1 for the spectrum of bacterial species triggering reactive arthritis). This inclusion is based on the observation that these arthritides also develop after a primary extra-articular infection, and that despite negative culture results, the organisms can be detected in the joint (for example,Borrelia,7 Neisseria 9).

This brief historical outline demonstrates not only the changing definition of “reactive arthritis” over time, but also illuminates the lack of general consensus concerning the precise clinical and scientific conditions to which this term should be …