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Annals of the Rheumatic Diseases logoLink to Annals of the Rheumatic Diseases
. 1999 Dec;58(12):737–741. doi: 10.1136/ard.58.12.737

Two forms of reactive arthritis?

P Toivanen 1, A Toivanen 1
PMCID: PMC1752815  PMID: 10577958

Abstract

Inflammatory arthritides developing after a distant infection have so far been called reactive or postinfectious, quite often depending on the microbial trigger and/or HLA-B27 status of the patient. For clarity, it is proposed that they all should be called reactive arthritis, which, according to the trigger, occurs as an HLA-B27 associated or non-associated form. In addition to the causative agents and HLA-B27, these two categories are also distinguished by other characteristics. Most important, HLA-B27 associated arthritis may occur identical to the Reiter's syndrome with accompanying uretheritis and/or conjunctivitis, whereas in the B27 non-associated form this has not been clearly described. Likewise, only the B27 associated form belongs to the group of spondyloarthropathies.



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Figure 1  .

Figure 1  

Pathogenesis of reactive arthritis, compared with that of experimental antigen induced arthritis. In the reactive arthritis, bacterial antigens end up in the joint tissue as a result of the infection. In the experimentally induced arthritis, the antigen (for example, BSA or non-viable bacterial antigen) is first given parenterally and two weeks later intra-articularly. In addition to the pathogenetic mechanism depicted here, an HLA-B27 dependent, so far unknown mechanism operates in the B27 associated form of reactive arthritis.

Selected References

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