Contact dermatitis is a common clinical problem . Even though irritant contact dermatitis is considered far more common than the allergic form [15, 28], most research has been focused on the contact allergic reaction during the past decades. Irritant contact dermatitis is the result of a nonspecific cellular damage to the skin caused either by physical factors, such as mechanical friction or cold, or more commonly chemicals [4, 62]. In clinical practice, the disease can display a broad spectrum of signs and symptoms and it has been described under several different clinical names. Irritant contact dermatitis can be divided into four main clinical types, namely acute irritant contact dermatitis (following a single exposure to a noxious factor), chronic irritant contact dermatitis (following repeated exposures to noxious factors over a period of time), chemical burns, and sensory irritancy (stinging) (c.f. [28, 95]). The most frequent clinical sign of the dermatitis and other inflammatory diseases is dry skin. However, the term "dry skin" is not well defined . In most instances, it reflects the clinical appearance of a rough and/or scaly skin surface and no functional parameter. However, dry skin usually exhibits an impaired barrier function , which is believed to make skin more susceptible to chemicals in the environment (Fig. 1). Furthermore, increased transepidermal water loss (TEWL) has been suggested to enhance the risk of a more persistent dermatitis . Chemically different irritants cause different responses in the skin both at the cellular and subcellar level, for example in the production of inflammatory mediators, the expression of adhesion molecules, and the composition of cell infiltrate (reviewed in [4, 46, 97]). The dynamics of chronic irritant reactions are less well known, both regarding mechanisms and possible changes in the skin. External factors may disturb the stratum corneum and thus impair the diffusion barrier. There can also be an indirect effect on the production and maintenance of the permeability barrier in the stratum corneum, as irritants can affect the keratinocytes and their maturation and migration and also induce a release of inflammatory mediators causing the appearance of an inflammatory cell infiltrate [4, 19, 46, 68, 97]. There are three key points in the strategy for treatment of irritant contact dermatitis: 1. Identification and reduction of external noxious factors 2. Treatment of the inflammation (e.g., with local corticosteroids, UVA-UVB phototherapy, PUVA treatment, or other immunomodulating agents such as cyclosporine) 3. Application of moisturizers to improve the structure and function of the diffusion barrier in the stratum corneum (Fig. 2). The beneficial effect of moisturizers in clinical practice is compatible with the recently proposed hypothesis that a normalization of a defect barrier function is prerequisite to preventing persistent dermatitis (Fig. 2) . Combined with the increasing knowledge on the structure and function of stratum corneum, this opens up new possibilities to design and adapt treatments for different skin conditions with a perturbed barrier function. This paper will focus on stratum corneum, its lipids, and the possibility of using moisturizers to repair or improve a disrupted barrier function in irritant contact dermatitis.