MODE OF ACTION OF GLYCOLIC ACID ON HUMAN STRATUM-CORNEUM - ULTRASTRUCTURAL AND FUNCTIONAL-EVALUATION OF THE EPIDERMAL BARRIER

Alpha-hydroxy acids (ARA) such as glycolic acid have recently been use d extensively in cosmetic and dermatological formulas, In low concentr ation (2-5%) glycolic acid is believed to facilitate progressive weake ning of cohesion of the intercellular material of the stratum corneum (SC), resulting in uniform exfoliation of its outermost layers (the st ratum disjunctum), Since thinning of the SC as well as changes of inte rcellular lipids could theoretically compromise the barrier functions of the skin, we investigated the mode of AHA action on the SC to deter mine whether enhanced desquamation compromises the barrier structures of the SC and changes transepidermal water loss (TEWL) values, Electro n microscopy of the epidermis biopsied from the volar forearm of human volunteers after 3 weeks of treatment with a 4% glycolic acid formula tion twice daily was employed to evaluate 1) epidermal morphology and thickness of the SC, (2) the lamellar body and SC lipid bilayer organi zation, and (3) desquamative events based on degradation of desmosomes , TEWL values and SC hydration were recorded prior to and at the end o f the study, Electron microscopy revealed no ultrastructural changes i n the nucleated layers of the epidermis, The lamellar body (LB) secret ory system in the stratum granulosum (SG), and intercellular lipid lam ellae in the SC in both vehicle-and glycolic acid-treated samples were comparable to normal human SC. Within the SC, enhanced desmosomal bre akdown, promoting loss of cohesion and desquamation, was restricted to the stratum disjunctum while desmosomes of the stratum compactum were unaffected, Treated areas displayed histologically, a more compact ap pearing SC, TEWL values remained unchanged in glycolic acid- and vehic le-treated skin, Our findings indicate that the barrier structures of the SC are not disrupted by glycolic acid formulations at the concentr ation used, One of the mechanism of action of AHA on the SC seemed to be a ''targeted'' desmosomal (corneosomal) action without compromising the barrier structures of the skin.