The concept of septic arthritis in which bacteria replicate in joint tissue and cause inflammation, joint destruction, and sometimes death is well established. Equally, the idea that some forms of aseptic inflammatory arthritis, such as rheumatoid arthritis, may well be provoked or sustained by the direct or indirect effects of microbial infection is familiar and attractive, though the notion is underpinned more by logic than by data. Between these extremes, reactive arthritis appears to offer a new understanding of microbial pathogenesis as joints, conventionally aseptic, have been found to contain small numbers of bacteria. These bacteria, principally chlamydiae and mycoplasmas, may well provoke and maintain the arthritis. Much evidence has accumulated that they have proinflammatory components, induce immune responses, and could interact with HLA-B27 in a manner consistent with current theories of disease pathogenesis.

The issue of searching for bacteria in joint tissue, however, has become complex. When conventional cultures are positive, the effect of eradication of the micro-organism can readily be gauged, so that the significance of finding the bacterium in the joint can be established. But, when a small number of intra-articular bacteria can only be detected by using ultrasensitive molecular techniques, mainly those based on the polymerase chain reaction (PCR), and there is no discernible benefit from antimicrobial treatment, at least so far as current data show, how can we tell whether these bacteria are part of the normal milieu, have spread from elsewhere into an already inflamed joint as innocent passengers, have spread from elsewhere and contribute to disease persistence or, in fact, are the cause of the disease? By comparison, identifying Mycobacterium tuberculosis in diseased lung by culture provides satisfactory evidence of specific infection and using a PCR or other nucleic acid amplification technique may reduce the time for diagnosis in acute cases by 40-fold. …