Hypothesis
How can a causal role for small bacteria in chronic inflammatory arthritides be established or refuted?
D Taylor-Robinsona, A Keatba Department of
Genitourinary Medicine, Imperial College School of Medicine, St Mary's
Campus, London W2 1NY, UK, b Department of Rheumatology, Northwick Park and
St Mark's Hospitals, Harrow, Middlesex HA1 3UJ, UK
Correspondence to: Dr Keat
Accepted for publication 29 August 2000
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Introduction |
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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
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