Related Experiment Videos
Reiter's syndrome and reactive arthritis: a current view
1Department of Rheumatology, St Peter's Hospital Trust, Chertsey, United Kingdom.
Seminars in Arthritis and Rheumatism
|December 1, 1994
Summary
Reactive arthritis, an inflammatory joint disease, is linked to prior infections. Bacterial components are found in joints, and the role of HLA-B27 in pathogenesis is under investigation.
Area of Science:
- Rheumatology
- Immunology
- Microbiology
Background:
- Reactive arthritis is an inflammatory aseptic joint disease.
- It is often preceded by infections from various microorganisms.
- The presence of bacterial antigens in joints of affected patients is established.
Purpose of the Study:
- To review advances in understanding reactive arthritis pathogenesis.
- To discuss the role of microbial components and HLA-B27.
- To explore immunopathogenesis and future research directions.
Main Methods:
- Review of recent literature on reactive arthritis.
- Detection of bacterial antigens (DNA, RNA, lipopolysaccharide) in joints.
- Immunological techniques and polymerase chain reaction (PCR) for pathogen identification.
- Analysis of humoral and cellular immune responses.
- Discussion of HLA-B27's role and molecular mimicry.
Main Results:
- Bacterial components, including DNA and lipopolysaccharide, are confirmed in affected joints.
- Specific pathogens like Chlamydia trachomatis, Salmonella enteritidis, and Shigella flexneri have been detected.
- While viable bacteria are unlikely, chlamydial DNA is found in sexually acquired reactive arthritis.
- HLA-B27 may influence disease susceptibility through mechanisms beyond antigen presentation.
- Evidence for molecular mimicry remains inconclusive.
Conclusions:
- Advances in understanding reactive arthritis pathogenesis have been made.
- Bacterial antigens play a significant role, though viable organisms are rare.
- The interplay between genetic factors like HLA-B27 and microbial triggers is crucial.
- Further research into antimicrobial therapy and immunopathogenesis is warranted.