Newborn and elderly skin: two fragile skins at higher risk of pressure injury.

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Skin is a key organ maintaining internal homeostasis by performing many functions such as water loss prevention, body temperature regulation and protection from noxious substance absorption, microorganism intrusion and physical trauma. Skin ageing has been well studied and it is well known that physiological changes in the elderly result in higher skin fragility favouring the onset of skin diseases. For example, prolonged and/or high-intensity pressure may suppress local blood flow more easily, disturbing cell metabolism and inducing pressure injury (PI) formation. Pressure injuries (PIs) represent a significant problem worldwide and their prevalence remains too high. A higher PI prevalence is correlated with an elderly population. Newborn skin evolution has been less studied, but some data also report a higher PI prevalence in this population compared to older children, and several authors also consider this skin as physiologically fragile. In this review, we compare the characteristics of newborn and elderly skin in order to determine common features that may explain their fragility, especially regarding PI risk. We show that, despite differences in appearance, they share many common features leading to higher fragility to shear and pressure forces, not only at the structural level but also at the cellular and molecular level and in terms of physiology. Both newborn and elderly skin have: (i) a thinner epidermis; (ii) a thinner dermis containing a less-resistant collagen network, a higher collagen III:collagen I ratio and less elastin; (iii) a flatter dermal-epidermal junction (DEJ) with lower anchoring systems; and (iv) a thinner hypodermis, resulting in lower mechanical resistance to skin damage when pressure or shear forces are applied. At the molecular level, reduced expression of transforming growth factor β (TGFβ) and its receptor TGFβ receptor II (TβRII) is involved in the decreased production and/or increased degradation of various dermal extracellular matrix (ECM) components. Epidermal fragility also involves a higher skin pH which decreases the activity of key enzymes inducing ceramide deficiency and reduced barrier protection. This seems to be correlated with higher PI prevalence in some situations. Some data also suggest that stratum corneum (SC) dryness, which may disturb cell metabolism, also increases the risk of PI formation. Besides this structural fragility, several skin functions are also less efficient. Low applied pressures induce skin vessel vasodilation via a mechanism called pressure-induced vasodilation (PIV). Individuals lacking a normal PIV response show an early decrease in cutaneous blood flow in response to the application of very low pressures, reflecting vascular fragility of the skin that increases the risk of ulceration. Due to changes in endothelial function, skin PIV ability decreases during skin ageing, putting it at higher risk of PI formation. In newborns, some data lead us to hypothesize that the nitric oxide (NO) pathway is not fully functional at birth, which may partly explain the higher risk of PI formation in newborns. In the elderly, a lower PIV ability results from impaired functionality of skin innervation, in particular that of C-fibres which are involved in both touch and pain sensation and the PIV mechanism. In newborns, skin sensitivity differs from adults due to nerve system immaturity, but the role of this in PIV remains to be determined.