Dry Skin: Environmental Aspects

Water is absolutely essential for the normal functioning of the skin and especially the stratum corneum (SC). However, as the SC is continuously exposed to varying humidities, maintenance of water within the tissue is crucial. Under most circumstances water present within the SC will be derived from bodily water, being lost by transepidermal water loss, and is normally bound by proteins together with naturally occurring hygroscopic compounds found largely within, but also external to, the corneocytes. Small amounts of water escape through this slightly leaky barrier to hydrate the dehydrated outer layers of the SC, and this is key to maintaining SC flexibility, SC maturation and SC desquamation. The retention of water in the SC is dependent on three major mechanisms: (a) the intercellular lamellar lipids whose physical conformation, predominantly an orthorhombic gel phase, provides a tight and effective barrier to the passage of water through the tissue, (b) the presence of corneodesmosome-bound and ceramide-hydrophobed corneocytes which influence the tortuosity of the SC and thereby the diffusion path length of water and (c) the presence of both intracellular and extracellular SC natural moisturizing factors (NMF). The structure, biochemistry and function of the SC and the epidermis can however be disturbed upon environmental challenge, particularly by disruption of the SC barrier resulting in the precipitation of dry flaky skin conditions. The maintenance of barrier function and thereby SC hydration is central to the production and optimal functioning of the SC. Fluctuating atmospheric conditions (high and low dew points) influence the formation of the epidermal barrier lipids, NMF, corneocyte envelope phenotypes and the desquamatory enzymes and are thus an initiator of dry skin. At low atmospheric dew points, the reduced SC water content precipitates the dry skin phenotype. On perturbation of barrier function, a cycle of events begins initially with the superficial dehydration of the SC (leaking of extracellular lipids, disruption of lipid lamellar architecture, loss of water-soluble NMF), the release of inflammatory mediators, induction of hyperproliferation of epidermal keratinocytes resulting in disturbed epidermal differentiation leading to an inferior SC (enhanced production of sphingosine-containing ceramides relative to phytosphingosine-containing ceramides and reduced transglutaminase activity leading to retention of fragile corneocyte envelopes in the superficial layers of the SC that have reduced levels of covalently bound ceramides), together with a flaky skin condition (reduced desquamatory enzyme activities and reduced corneodesmolysis). In extreme cases when inflammation is present, increased levels of proteases are observed in the SC and reduced interleukin 1 (IL-1) levels with increased IL-1 receptor antagonist protein levels. If left untreated, these events will continuously cycle to produce an even poorer skin condition, and ultimately mechanical cracking of corneodesmosomes between the corneocytes will result in mechanical trauma to the SC.