The current belief that the clinical manifestations of psoriasis (excessive scaling) are due to a twelve-fold speeding up or shortening of the cell division cycle time of the germinative cells in psoriatic epidermis (from 457 to 37-5 h) is shown to be incorrect. A new concept is introduced--that the germinative layer in human epidermis is composed of not one, but three separate and distinct populations of epidermal cells. First, there are cycling cells which are actively moving through the cell cycle. Then there are two categories of non-cycling cells (blocked in the G1 or the G2 periods of the cell cycle) which are capable of moving into the proliferative pool upon specific stimulation. Thus, increased epidermal cell proliferation in active lesions of psoriasis would be brought about mainly by a recruitment or a relase of the two categories of non-cycling cells. The idea that germinative epidermal cells are primarily non-cycling, leads to the suggestion of focusing attention on non-cycling cells (rather than on cycling cells) for the control and treatment of psoriasis. It might be worthwhile considering treating psoriatic patients during periods of clinical remission--with factors to keep the germinative cells in the non-cycling state--rather than during psoriatic flare up--with cancer chemotherapy drugs.

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This article deals with and compares cell cycle information obtained in mouse and in human epidermis in vivo. In order to compare data in mouse and in man, DNA labeling and mitotic index experiments were performed to obtain cell cycle information in normal human epidermis in vivo. Experiments were also performed on genetically inbred and outbred strains of mice--to provide a clue to the differences observed between mouse and man. The article makes the following points: 1. In contrast to mouse epidermis, there are no consistent diurnal fluctuations in and there is no cell kinetic relationship between mitotic and DNA-labeling indices in normal human epidermis in vivo. The variability from individual to individual in human subjects and the lack of cell cycle-related circadian fluctuations, preclude the use of statistical analysis and the use of conventional cell kinetic principles in understanding epidermal cell proliferation in man and may preclude the use of circadian rhythmicity for therapy scheduling. 2. The consistent and intelligible cell cycle information obtained in laboratory mice (as compared to man) is not due to the genetically inbred condition of mice. 3. This report introduces the use of ambient temperature as a potential nontoxic cell cycle tool for manipulating epidermal cell proliferation in the therapy of human proliferative skin diseases.