One to three per cent of most populations have psoriasis, which is most prevalent in European and North American white people, uncommon in American black people and almost non-existent in American Indians. It is a chronic non-infectious inflammatory skin disorder, characterized by well-defined erythematous plaques bearing large adherent silvery scales. It can start at any age but is rare under 10 years, and appears most often between 15 and 40 years. Its course is unpredictable but is usually chronic with exacerbations and remissions. Cause and pathogenesis The precise cause of psoriasis is still unknown.
However, there is often a genetic predisposition, and sometimes an obvious environmental trigger. There are two key abnormalities in a psoriatic plaque: hyperproliferation of keratinocytes; and an inflammatory cell infiltrate in which neutrophils and TH-1 type T lymphocytes predominate. Each of these abnormalities can induce the other, leading to a vicious cycle of keratinocyte proliferation and inflammatory reaction; but it is still not clear which is the primary defect. Perhaps the genetic abnormality leads first to keratinocyte hyperproliferation that, in turn, produces a defective skin barrier
allowing the penetration by, or unmasking of, hidden antigens to which an immune response is mounted. Alternatively, the psoriatic plaque might reflect a genetically determined reaction to different types of trauma (e.g. physical wounds, environmental irritants and drugs) in which the healing response is exaggerated and uncontrolled. To prove the primary role of an immune reaction, putative antigens (e.g. bacteria, viruses or autoantigens) that initiate the immune response will have to be identified. This theory postulates that the increase in keratinocyte proliferation is caused by inflammatory cell mediators or signalling. Theories about the pathogenesis of psoriasis tend to tag along behind fashions in cell biology, and this idea is currently in vogue.