ABSTRACT
The molecular basis of the keratolytic activity of retinoids has for long been a matter of debate. Historically, the detergent-like characteristics of many retinoids were believed to exert a membrane-loosening effect that would aHow somal enzymes to appear between keratinocytes (65). However, this mechanism may be in vitamin A toxicity, no significant release of lysosomal enzymes observed ordinary retinoid treatment More specific mechanisms are involved since retinoid-induced dyshesion correlates both with loss of desmosomes (67), reduction in the of tonofilaments (31), and formation of intercellular amorphous material in the upper epidermis (23). The amorphous material has been tentatively identified as hyaluronate, consistent with the fact that RA induces synthesis of hyaluronic acid
by kcratinocytes (68,69)0 It is also possible that retinoids act specifically by increasing the number of lamellar bodies in stratum granulosum, thus reducing comeocyte cohesiveness through altered discharge of intercellular lipids and enzymes (70).
