Psoriatic arthritis pathophysiology

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.

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.

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.