Psoriasis is an inflammatory, noncontagious, genetically determined skin disorder that most commonly appears as inflamed, edematous skin lesions covered with a silvery white scale.
Up to 2% of the population develop Ps during their lifetime.
Stress, trauma and infections may induce Ps in susceptible individuals.
Ps can be present at any time from the first few weeks of life until 80 or more years of age
Most patients experience onset in the third decade of life
There is a definite familial tendency to inherit Ps: when one parent is affected, there is a one in four chance of Ps in each child; with two affected parents, the rate is one in two
Some genetic linkage between Ps and the HLA-Cw6 phenotype
An infiltrate comprising activated T cells is localized in the dermal papillae of skin and the sublining layer of the joint synovium. Other key cells include various forms of dendritic cells and macrophages; B cells are present but their role is as yet not well defined. These cells generate a number of proinflammatory cytokines, such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, and IL-6, which in turn contribute to activation of additional pathogenic cells. In the skin, through the influence of proinflammatory cytokines such as TNF-alpha, keratinocytes proliferate and have prolonged survival, leading to skin thickening and plaque. Proinflammatory cytokines such as TNF-alpha are instrumental in activating endothelial cells to express adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and E-selectin (upregulated more in the skin), which promote lymphocyte migration to sites of inflammation. Cutaneous lymphocyte-associated antigen (CLA) is expressed on lymphocytes homing to skin lesions, but not to areas of synovitis.
Vascular pathology is similar in both the skin and synovium, characterized by prominent angiogenesis with abnormal tortuous vessels. Upregulation of angiogenic growth factors, partly via the action of TNF-alpha, including vascular endothelial growth factor (VEGF), transforming growth factor beta (TGF-beta), platelet-derived growth factor (PDGF), and angiopoietins contribute to this phenomenon. Neovascularization is an important component of the inflammatory, erosive nature of the disease. TNF-alpha also contributes to the increased production of proteases such as matrix metalloproteinases (MMPs), which are involved in cartilage destruction.
Abnormal bone remodeling is a key feature of Ps arthritis. Joint-space narrowing and joint erosions occur, as well as osteolysis of both digital tufts and joint areas. However, juxta-articular periosteal new bone formation occurs, as well as ankylosis.