Atopic xerosis: employment of noninvasive biophysical instrumentation for the functional analyses of the mildly abnormal stratum corneum and for the efficacy assessment of skin care products

Abstract

The subtle dryness of the skin surrounding the lesions of atopic dermatitis (AD) is called atopic dry skin or atopic xerosis (AX). AX is more susceptible to the development of AD skin lesions under various environmental stimuli than the clinically normal skin of the people who have or have had or will have AD, which might be called normal atopic skin (NAS) that shows no functional differences as compared to the skin of normal individuals. Routine histopathologic studies of AX that involve the invasive procedures of biopsy are not so helpful in clarifying the underlying pathogenesis. Modern, noninvasive biophysical instrumentation provides rich and quantitative information about various functional aspects of skin. The stratum corneum (SC) of AX reveals not only decreased hydration but also mildly impaired barrier function demonstrable as an increase in transepidermal water loss, elevated pH values, and an increased turnover rate of the SC consisting of thick layers of smaller-sized corneocytes. These data suggest that AX is related to mildly increased epidermal proliferation as a result of the presence of subclinical cutaneous inflammation. Although AX skin does not display any impairment in the recovery of barrier function after physical skin irritation by tape-stripping, it produces a much more severe, long-lasting inflammatory response together with a delay in barrier repair after chemical irritation such as that induced by sodium lauryl sulphate. The SC of AX is biochemically characterized by reduction in the amounts of ceramides, especially ceramide I, sebum lipids, and water-soluble amino acids. None of these changes in SC functions are seen in NAS, which includes not only the normal-looking skin of AD patients long after regression of all active lesions but also of latent atopic skin such as neonates who later develop AD. This suggests that all of the observed functional as well as biochemical abnormalities of AX are a reflection of subclinical inflammation. The presence of the underlying inflammation in AX also differentiates it from senile xerosis. The mildly impaired SC functions of AX can be improved by daily repeated applications of effective moisturizers, i.e., corneotherapy, which is effective in preventing the exacerbating progression of AX to AD resulting from inadvertent scratching of the skin that facilitates the penetration of environmental allergens into the skin. The biophysical confirmation of such efficacy of moisturizers, including cosmetic bases on the mildly impaired barrier function and decreased water-holding capacity of the SC of AX, definitely substantiates the importance of skin care for the cosmetic skin problems that affect every individual in the cold and dry season ranging from late autumn to early spring.

Essential Fatty Acids and Atopic Dermatitis

“…Redoules et al (1999) observed reduced activity of SC trypsin-like kallikreins in dry noneczematous AD skin (i.e., AX lesions). As this class of enzyme is essential for the degradation of desmoglein 1, its reduced activity may explain the increased number of SC cell layers reported by Tagami et al (2006) Equally, Tarroux et al (2002) demonstrated that its activity increases as the lesions are resolved. Conversely, Komatsu et al (2007) found increased mass levels of SC kallikreins together with plasmin and furin in mild lichenified AD lesions, which may be attributed to the decreased number of cell layers in AD lesions reported by White et al (1987) Equally, Hansson et al (2002) reported increased SCCE (KLK7) immunostaining in skin biopsies taken from AD subjects with chronic eczematous lesions on the flexural sides of the lower arms.…”

“…AX is more susceptible to the development of AD lesions than clinically normal skin. Tagami et al (2006) reported that the number of SC cell layers in AX is significantly greater than in normal skin, whereas White et al (1987) reported that the number of SC cell layers is significantly lower in patients with chronic eczematous AD conditions. These differences can only come from changes in the balance between desquamation and epidermal proliferation.…”

“…Elevated TEWL and reduced skin hydration are signs of impaired SC function and are associated with AD (Tagami et al 2006). Barrier function is related to the total architecture of the SC.…”

Update on Atopic Eczema with Special Focus on Dryness and the Impact of Moisturizers

“…Xerosis has been reported in both lesional and nonlesional skin in AD, and the degree of xerosis often corresponds to the overall severity of the disease [ 73 ] . The etiology of xerosis in AD is multifactorial, but reduced NMF levels play a major role.…”

The Effect of Natural Moisturizing Factors on the Interaction Between Water Molecules and Keratin

“…Amino acids are degraded from fi laggrin in the SC during cornification [ 5,6 ] and play the role of an NMF. For example, the amino acid content of the SC was lower in diseases displaying symptoms of dry skin, such as atopic dermatitis and atopic respiratory disease [ 7,8 ] . Recently, it was reported that fi laggrin mutation was a predisposing factor for atopic dermatitis and ichthyosis [ 9 ] and that the amino acid content of the SC was lower in carriers of fi laggrin mutation than in healthy subjects [ 10 ] .…”