Abstract
The term psoriatic disease encompasses the array of disorders (arthritis, inflammatory bowel disease, uveitis, obesity, metabolic syndrome, type II diabetes, and cardiovascular disease) that are associated with psoriasis. Psoriatic arthritis (PsA) is present in about 25% of patients with psoriasis; in most cases, the psoriasis precedes joint disease by about 10 years. Previous studies revealed that osteoclast precursors (OCP) are elevated in PsA and that the frequency of these circulating cells correlates with bone destruction. More recently OCP were found to be increased also in early rheumatoid arthritis and in 25% of psoriasis patients without arthritis. Bone marrow edema, observed on magnetic resonance imaging, in PsA represents infiltration of underlying marrow with inflammatory cells based on studies in transgenic tumor necrosis factor (TNF) arthritis murine models. Studies in the TNF transgenic mouse model also revealed that changes in lymph node volume precede joint flare. These translational studies point to potential biomarkers of arthritis in psoriasis patients and generate alternative hypotheses to explain the events that lead to arthritic flare.