Psoriatic arthritis is a seronegative spondyloarthropa-thy consisting of inflammatory arthritis associated with psoriasis. The understanding of the immunologic mechanisms that contribute to psoriatic arthritis is evolving, but the importance of TNF-a has been demonstrated. As in rheumatoid arthritis, blood mononu-clear cells from patients with psoriatic arthritis secrete significantly larger amounts of biologically active TNF-a than cells from healthy controls (Ritchlin et al. 2003). TNF-a is also found at elevated levels in synovial fluid in patients with psoriatic arthritis and is expressed by psoriatic synovial explants and lining cells, especially in patients with the erosive form of arthritis (Partsch et al. 1997; Ritchlin et al. 1998).
Osteoclast precursors are markedly elevated in pso-riatic arthritis and are thought to be important factors in the unique bone erosions observed in this condition (Mease 2004). These precursors arise from TNF-a-activated peripheral mononuclear cells and migrate to inflamed synovium and subchondral bone, where they become mature osteoclasts causing bone erosion. Twelve weeks' treatment with etanercept (25 mg twice weekly) significantly reduced osteoclast precursors by 79-96%, and these decreases were accompanied by a clinical response as measured by the number of tender and swollen joints (Ritchlin et al. 2003). In addition to its effects on the arthritis components of psoriatic arthritis, TNF-a antagonism produces improvements in the psoriatic manifestations of the disease, discussed in the following section.
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