years of age) and adults (aged 20–35 years) evaluating maturation and organization of the SC showed a relative immaturity of the epidermal barrier from birth to one to two years of age.8
A randomized controlled study on biophysical, biological, and functional properties of neonatal SC from birth to four weeks of age revealed that impaired skin barrier function correlated with elevated protease activity and reduced amounts of NMF at birth.9
The hydration of the stratum corneum is lower over the first two weeks of life and increases from two weeks onwards.5,10 Compared to adults SC, the level of hydration is lower in children up to the age of five.5,10 Although the content of the SC NMF content in neonatal skin compared to adult SC is higher during the first two weeks of life due to the presence of vernix caseosa; there is a higher water vapor loss.5,10 Two weeks after birth, NMF content of the SC is lower compared to adults, and during maturation, over six months, NMF content of the SC reaches adult levels.5,10 Variations in SC lipids throughout infancy may be associated with a disease, such as lower levels of ceramides in atopic dermatitis. 13,16
Neonatal and infant stratum corneum is about 30% thinner (mean of μm 7.3 [SD ± 1.1]) than adult stratum corneum (mean of μm 10.5 [SD ± 2.1]) and reaches a similar thickness of the SC of adults by three to five years of age.17,18
Statement 3: The permeability skin barrier of the skin is controlled by the intercellular lipid-enriched matrix, which is composed of ceramides, free fatty acids, and cholesterol.
The stratum corneum is essential for the protective barrier functions of the skin.19 Corneocytes are the building blocks of the epidermal barrier. A water-resistant layer of lipid lamellae encases the corneocytes (cornified lipid envelope), preventing water loss and controlling barrier permeability.19,20 The cornified lipid envelope and the extracellular mortar-like multilayered lipid lamellae are crucial elements of the epidermal barrier.19,20 The lipids contained in the lamellar bodies can be derived from both epidermal lipid synthesis and extracutaneous sources. The integrity of the lipid lamellae is dependent on a cocktail of proteases and protease inhibitors. The balance between expression and activity of proteases and protease inhibitors determines the rate of desquamation and, thereby, the thickness of the skin barrier.19,20 The SC extracellular lipids are mainly composed of ceramides, cholesterol, and free fatty acids and contain NMF, derived from pro-filaggrin, a mix of hygroscopic compounds, which help maintain skin hydration.19,20
Ceramides have an essential role in maintaining the water permeability barrier function of the skin (Table 5).19-23 After birth, the lipids that constitute the extracellular matrix now have a different and unique composition compared to the intrauterine period.1,3,5 The ratio of free fatty acids/cholesterol/ ceramides is not static in neonatal skin.1,3,5 The ceramide proportion changes from 20% in the vernix to 50% in postnatal skin.1,3,5 Without the proper ratio of ceramides, the stratum corneum can become incompetent.21-25 Impaired synthesis of cholesterol, ceramides, and fatty acid adversely affects lamellar layer formation, thereby impairing barrier homeostasis, leading to dryness, irritation, erythema, and itching.19,21-25 Essential fatty acid deficiency results in abnormalities in SC structure and function. 19,21-25
Statement 4: Ceramides are important lipids found within the stratum corneum, contributing to the intercellular lipid bilayer, essential in the regulation of trans-epidermal water loss (TEWL) and healthy barrier function. Ceramide depletion is associated with dermatologic problems, eg, atopic dermatitis.
Most skin barrier disorders, including atopic dermatitis (AD), are associated with decreased ceramide content impairing skin barrier function.22-36 The lifelong condition AD commonly occurs in early childhood and may present without signs of sensitization. 27-30 The initial phase of AD in a genetically predisposed child presents with non-pathological xerosis only, in the absence of positive specific serum immunoglobulin E (IgE) serology.16,27-36 In a cohort study including over 1900 infants evaluated at six and twelve months of age, the impaired skin barrier function correlated with elevated protease activity and reduced natural moisturizing factors at birth shown at two months of age and preceding clinical AD.16 Abnormalities in skin barrier function and ceramide content as well as highly expressed ceramide synthase four was shown in AD affected skin.30-36 The atopic child with extrinsic AD typically presents with a defective skin barrier and sensitivity to allergens in the presence of an IgE response to environmental allergens.29-36
Statement 5: Skincare of neonates and infants has to be safe and effective and has to exclude agents that can negatively influence the skin barrier or induce systemic toxicity. Baby skincare with ceramides mimics physiological lipids and supports natural homeostasis.
Newborns and infants have an increased vulnerability to poisoning from transcutaneous exposures due to their high surface-to-weight ratio, immature epidermis, and compromised