Psoriasis: highly reactive early cellular inflammation.

Abstract

Psoriasis is the result of highly reactive early cellular inflammation. Psoriasis simultaneously has a rapidly proliferating epidermis, a vigorous acute inflammatory reaction, an accelerated rate of dermal breakdown and repair, and vascular and fibroblast proliferation. Understanding the primary role of early cellular inflammation allows explanation of other factors. All clinical, experimental and therapeutic facts can be explained on this basis. There are extensive biologic changes. Early cellular inflammation is influenced by genetic and environmental factors. It is proposed that the defect is quantitative rather than qualitative. Psoriasis commonly localizes at sites of injury. Several authors have noted that the first histologic change in psoriasis is the spurting of granulocytes from the dermal papillae. This is a cyclical event. Connective tissue-active peptides released from granulocytes produce a ninefold increase in the size of the dermal papille. This results in a ninefold increase in the size of the germinative cell base of the epidermis. The vast literature on rapid epithelial proliferation in psoriasis measures a secondary phenomenon. The concept presented does not provide an answer to the biochemistry of early cellular inflammation except to point out the initial importance of dilution of tissue fluids. The author considers early cellular inflammation to result from multiple, simultaneous, overlapping, amplifying and inhibitory systems. There are multiple ways to arrive at the final biologic effect which is too essential to depend on a single series of events. There is a large amount of empiric knowledge on psoriasis which can aid in understanding early cellular inflammation.