Abstract

Epidermal lipids constitute an ultimate frontier between the organism and its environment. Their essential role consists of providing a barrier limiting both transepidermal water loss and penetration of external factors, such as irritants. Efficacy of the barrier depends on the physicochemical properties of the substance applied to the skin surface and the increase in transepidermal water loss, which may be quantified, is proportional to the provoked perturbation in the barrier function. In atopic dermatitis epidermis, a significant decrease in the ceramide content and abnormally low levels of omega-6 fatty acids correlate with an increased rate of water loss at the skin surface--a sign of an impaired barrier. However, similar signs are observed in the atrophic epidermis provoked by long term local corticotherapy. Epidermal lipid profiles are also seriously modified in various ichthyoses, and are partially responsible for the hyperkeratosis observed clinically, e.g.: the recessive X-linked form is provoked by a mutation of the steroid sulphatase gene and the resulting accumulation of unconverted precursor of cholesterol. Modification of the lipid composition in acne contributes to comedo formation, whereas UV improves barrier function (and may provoke hyperkeratosis) through an increase in the stratum corneum lipid content. Another source of lipids at the epidermal surface is sebaceous glands. Waxes present in the sebum increase friction coefficient of the skin surface. Sebum also influences (decreases) the rate of penetration of lipophilic substances applied on the skin. Its role in the skin biology appears to be less vital than that of the lipids constituting the permeability barrier of the stratum corneum.