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.