Occupational screening studies (n = 48,380) showed that approximately every third employee (29.4%) between the ages of 16 and 70 years is affected by xerosis.14 The prevalence of xerosis increases in mature skin at 55.6% at a mean age of 75.1 years.14 Xerosis is characterized by decreased quantity and quality of lipids and/or moisturizing factors and is generally diagnosed on clinical presentation.9,10,13,14-16 It is essential to distinguish between constitutional xerosis and xerosis due to dermatoses such as atopic dermatitis (AD), psoriasis, or ichthyosis and xerosis triggered by exogenous factors.9,10,13,14 Xerosis may be due to systemic diseases such as diabetes, renal and biliary diseases, infections, and hormonal changes, or triggered by medication (Table 1).13,14
Statement 2: Xerosis in older adults is multifactorial and may include: intrinsic age-related changes, use of diuretics and similar medications, systemic conditions, hypothyroidism, and overuse of heaters or air conditioners.
Xerosis is a common skin condition in matured skin characterized by xerosis, and pruritic, excoriated, and exfoliated skin.17-24 The exact etiology of mature skin xerosis is not understood and likely depends on several genetic and environmental mechanisms.17-19
Intrinsic aging is a fundamentally unsustainable process that affects the entire body, including sun-protected sites.16 Intrinsic skin aging is primarily characterized by atrophy, as the number of cells that make up the skin and the amount and quality of the extracellular matrix decrease.16 Further, the amount and the conduction of blood vessels and nerves that supply the skin deteriorate or decrease.16 Xerosis in older adults is multifactorial: intrinsic changes in keratinization and lipid content, use of diuretics and similar medications, systemic conditions, hypothyroidism, medications, and overuse of heaters or air conditioners can all contribute to the disease.19-24 Skin is a target of reactive oxygen species (ROS) and oxidative stress from both extrinsic (solar radiation) and intrinsic sources (oxidative metabolism).17 Chronic exposure to extrinsic factors, such as ultraviolet radiation, air pollution, smoking, alcohol consumption, or malnutrition, induces an age-associated skin microenvironment, including inflammation and reduced collagen production.17,18
Changes in the keratinization process and lipid content in the SC probably represent the main factors in mature skin xerosis.19-24 From about 50 years of age, epidermal dysfunction may occur, such as compromised permeability homeostasis, SC hydration reduction, and skin surface pH elevation.19-23 The reduction of epidermal growth factors, keratinocyte proliferation, and increased keratinocyte apoptosis has been shown to lead to a thinner epidermis and SC.7 Further aging-related skin changes included a decline in the levels of structural proteins for the epidermal permeability barrier, including filaggrin, loricrin, and other late cornified envelope proteins.8 In mature skin, the barrier function weakens, leading to increased transepidermal water loss (TEWL) and decreased protective functions (Figure 1).20-23
The speed of the aging process depends mainly on individual genetic factors.16 Women develop these signs earlier due to a decrease in the protective effects of estrogen hormones during menopause.14-16
