Synonyms
Reiter syndrome = reactive arthritis
Definition
Reactive arthritis belongs to the rheumatological clinical pictures (rheumatism) and falls under the category of spondylarthropathies. Specifically, reactive arthritis is an inflammatory disease of the joints with sterile synovial fluid, which occurs after a bacterial gastrointestinal or urogenital infection. Gastrointestinal infections affect the stomach or intestine, urogenital kidneys or urinary tract. Sterile or aseptic synovial fluid means that no pathogens are found in the joint. However, in reactive arthritis, certain parts of the pathogen, usually nucleic acids (DNA or RNA), can be detected.
Frequency
Two to three percent of patients develop reactive arthritis after certain gastro- or urogenital infections caused by bacteria. The incidence of reactive arthritis is 30 to 40 per 100 000 population. There is no gender clustering, men and women are equally affected by reactive arthritis, but there is a higher incidence rate among younger people.
Causes
The cause of reactive arthritis is a genetic predisposition; the genes therefore define an increased susceptibility to this disease. This can be seen in the detection of certain factors in the blood of the patients. These factors are HLA-B27, the human leukocyte antigen of type B 27.
These antigens are MHC class I proteins, which are found on the surface of almost all cells and play an important role in the body’s immune system. In addition, in the development of reactive arthritis, there is a triggering infection that manifests itself either in the urinary tract or the gastrointestinal tract. With regard to the urinary tract, this includes gonorrhea and non-gonorrheic urethritis.
Gonorrhea develops after infection with gonococci, while non-gonorrheic urethritis is caused by chlamydia and mycoplasma (Ureaplasma urealyticum). Gastrointestinal infections after which reactive arthritis may occur include infections with Yersinia, Salmonella, Shigella or Campylobacter jejuni. Some of these bacterial infections persist in the body and cause reactive arthritis if genetically predisposed.
The exact relationship between infection and reactive arthritis is not clear, but there are two suspicions. The first hypothesis is that there is cross-reactivity between bacterial components and similar human cell structures in the development of reactive arthritis. This means that the immune system was sensitized to the pathogen components after the bacterial infection and subsequently confuses human cell components – which are structurally similar to these – with the bacterial ones. As a result, an immune reaction directed against these human structures is triggered, which in turn manifests itself as reactive arthritis. A second hypothesis on the pathogenesis of reactive arthritis includes the theoretical consideration that pathogen components remain in synovial cells and thus also trigger an immune reaction of the body, which manifests itself as reactive arthritis.