Psoriatic arthritis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]

Overview

The pathogenesis of psoriatic arthritis involves prominent T-lymphocytic infiltrate, particularly CD4 cells in the skin and joints. High levels of tumor necrosis factor alpha (TNF), IL-8, IL-6, IL-1, IL-10, and matrix metalloproteinases are present in the synovial fluid of patients with early psoriatic arthritis.The elevated levels of TNF and various interleukins lead to a high number of osteoclast precursor cells circulating in the blood which ultimately leads to joint destruction.

Pathophysiology

The pathogenesis of psoriatic arthritis (PsA) involves the following events:[1]

Osteoclast mediated joint destruction

References

  1. Ritchlin CT, Haas-Smith SA, Li P, Hicks DG, Schwarz EM (2003). "Mechanisms of TNF-alpha- and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis". J. Clin. Invest. 111 (6): 821–31. doi:10.1172/JCI16069. PMC 153764. PMID 12639988.

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