Report on the fourth International workshop on reactive arthritis

Abstract

There are large differences in the antigenicity and biology of the ReA-associated bacteria. For induction of arthritis, the relevance seems to be only that antigenic material reaches the joint, alive or dead. If there is a common antigen, it has to be a highly conserved one. Bacterial hsp60 seems to be an immunodominant T cell antigen in ReA, but there must be other relevant antigens shared by these different bacteria. An ineffective immune response (for example, low production of TNFalpha) seems to contribute to the manifestations and course of ReA. Although arthritis can also occur in its absence, HLA-B27 plays an important role in the pathogenesis of ReA and the other SpA. Current data suggest that B27 probably acts as an antigen-presenting molecule for a still-unknown arthritogenic molecule. Comparison of ReA with IBD-associated arthritis suggests that there might indeed be a common antigen shared by ReA-associated bacteria and bacteria of the gut flora. CD8+ T cells seem to be important in ReA and other SpA. In some parts of the world, such as in Mexico, ReA could be a major predisposing cause of the development of AS. Antibiotic treatment is not effective, probably because the triggering bacteria are already dead or in a partly latent state at the time arthritis occurs. Based on this knowledge and on new technologies, it should be possible in future years to derive answers to the questions about ReA and the other SpA and, as a consequence, to find a cure.

Influence of stimulatory and suppressive DNA motifs on host susceptibility to inflammatory arthritis

“…A similar time course was observed for the induction of immunoprotection by CpG ODNs in mice (18)(19)(20)28,29): protection generally developed several days after administration and persisted for 1-2 weeks (depending upon the pathogen). A longer delay is typical for the development of reactive arthritis in humans following bacterial infection (2,3). The delayed kinetics may reflect differences in the exposure to DNA.…”

“…Reactive arthritis presents as an asymmetric oligoarticular inflammatory condition that typically appears 1-3 weeks after microbial infection of the gastrointestinal or genitourinary tract (1,2). Bacterial DNA, but not viable microorganisms, can be found in the affected joints, suggesting that DNA may trigger or contribute to this inflammatory process (1,3,4).…”

Diagnosing reactive arthritis: Role of clinical setting in the value of serologic and microbiologic assays

“…Therefore, only these pathogens will be discussed, but similar conclusions can be drawn for other bacteria if the respective data are available. The prevalence of infections with these bacteria certainly differs between countries and even between areas in the same country and might also change over time (20). Therefore, the examples given below have to be adjusted to the local conditions.…”

“…However, DNA of these bacteria is only rarely detected inside the joint, and it has been suggested that, instead, mucosa and lymph nodes might serve as a reservoir for Yersinia and Salmonella (for discussion, see ref. 20). Therefore, a Salmonella-or Yersinia-specific PCR for joint material does not currently play a role in the diagnosis of ReA.…”

“…A major drawback for the diagnostic evaluation of a patient with suspected ReA is the fact that at the moment, no gold standard for the diagnosis of ReA is available (20,45). We are aware that the numbers for the pretest probability applied in this study are mainly based on experts' opinion derived from the interpretation of clinical symptoms and tests in the various studies.…”