Reactive arthritis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

It is thought that reactive arthritis is the result of previous gastrointestinal or genitourinary infections. The most commonly associated organisms include Chlamydia, Yersinia, Salmonella, Shigella, and Campylobacter infection.

• Reactive arthritis is associated with HLA-B27 (MHC class I molecule).
• It is estimated around 75% patients of reactive arthritis are positive for HLA-B27.
• HLA B27 association with reactive arthritis can also be attributed to the fact that patients with family history of reactive arthritis tend to have a more severe form of disease.
• The exact mechanism by which infecting organism cause reactive arthritis is not fully understood.
  • It is thought that microbial antigens are similar to certain body proteins (self proteins) and when the host immune system gets activated and releases antibodies, it leads to an autoimmune condition leading to destruction of self proteins and symptoms of reactive arthritis.
  • Microbial antigens leads to activation of T helper cells.
  • T helper cells differentiates into TH2 cells which leads to secretion of interleukins (IL-3, IL-4, IL-6),TGF-β and TH17 cells .
  • The Th17 cells release IL-17 which is a pro-inflammatory cytokine.
  • Furthermore, studies have shown the presence of T cells and intra-articular antibodies on synovial fluid analysis .

Reactive Arthritis in HIV patients

• Patients with HIV who later on develop reactive arthritis tend to have a more serious presentation.
• These patients present with severe generalised rash resembling psoriasis (pink color and scaly), severe arthritis and other AIDS related symptoms.

References

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