EDITORIAL
Reactive arthritis
Persistent infection of Chlamydia in reactive arthritis
1 Division of Rheumatology, Hannover Medical School (MHH), Carl-Neuberg-Str 1, 30625 Hannover, Germany
2 Department of Medical Microbiology and Hospital Epidemiology, Hannover Medical School (MHH), Carl-Neuberg-Str 1, 30625 Hannover, Germany
Correspondence to:
Correspondence to:
Professor H Zeidler
zeidler.henning@mh-hannover.de
Accepted 17 December 2005
Unravelling the molecular mechanisms
Keywords: Chlamydia trachomatis; M tuberculosis; Chlamydia-induced arthritis; reactive arthritis pathogenesis; persistent infection; gene expression
| The first 150 words of the full text of this article appear below. |
A number of bacteria have been implicated as causing reactive arthritis. In epidemiological studies Chlamydia have been identified as the most common bacteria triggering reactive arthritis in Western countries.1 Only 1–3% of patients acquiring infection at the urogenital tract as the primary site of infection develop Chlamydia-induced arthritis.
It has been shown that C trachomatis reaches the joint from the urogenital system through circulating monocytes and that monocytes/macrophages are the common host cells for persistent organisms during long term infection, with a major role in the induction of inflammation (fig 1
). Most patients will achieve clinical remission within 6 months after infection. However, a chronic disease course occurs with intermittent relapses and periods of remission despite the presence of persistent bacteria in the joint. To date, there is no explanation for this clinical heterogeneity, but it is probably related to the genetic background of the host
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