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 (PsA) involves prominent T-lymphocytic infiltrate, particularly CD4 cells, are the most common cells.The elevated levels of TNF leads to a high number of osteoclast precursor cells circulating in the blood.
Pathophysiology
The pathogenesis of psoriatic arthritis (PsA) involves the following events:[1]
- In joints there is a prominent lymphocytic infiltrate, limited to the dermal papillae in skin and to the underlying stroma.
- T lymphocytes, particularly CD4 cells, are the most common inflammatory cells in the skin and joints, with a CD4/CD8 ratio of 2:1.
- High levels of tumor necrosis factor alpha (TNF), IL-8, IL-6, IL-1, IL-10, and matrix metalloproteinases are present in the joint fluid of patients with early PsA.
- Collagenase mediated degradation of cartilage collagen begins in early phases of the disease and may be the result of the proteases produced as a result of above mentioned cytokines.
Osteoclast mediated joint destruction
- The elevated levels of TNF leads to a high number of osteoclast precursor cells circulating in the blood.
- Osteoclast precursors migrate to the joint where they encounter increased expression of receptor activator of nuclear factor kappa B ligand ( NF-κB), which favors the differentiation and activation of osteoclasts.
- Osteoclasts eventually lead to the joint destruction seen in psoriatic arthritis.
References
- ↑ 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.