A physiological process characterized by the progressive thinning and structural degradation of the skin’s layers, specifically the epidermis and dermis, occurring as a function of chronological aging. This atrophy is clinically manifested by reduced skin thickness, diminished elasticity, and increased fragility, contributing to the visual hallmarks of skin aging. The condition reflects a net loss of key dermal components, including collagen and elastin fibers, due to altered cellular metabolism.
Origin
The term is derived from the biological concepts of age-related decline and dermal atrophy, where ‘atrophy’ (from Greek atrophia, meaning “lack of nourishment”) describes the wasting away of tissue. In dermatology and endocrinology, this term describes the observable consequences of intrinsic aging and hormonal shifts on the integumentary system. Reduced synthesis of structural proteins and diminished fibroblast activity are central to its development.
Mechanism
The mechanism is multifactorial, heavily influenced by declining estrogen and androgen levels post-menopause or with andropause, which typically reduce fibroblast proliferation and collagen synthesis. Decreased production of hyaluronic acid and other glycosaminoglycans impairs the dermis’s ability to retain water, further contributing to volume loss. Concurrently, cumulative oxidative stress and chronic low-grade inflammation accelerate the breakdown of existing extracellular matrix proteins, weakening the skin’s supportive architecture.
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