Skin aging is a culmination of genetic and environmental factors and is largely influenced by the cumulative damage from exposure to ultraviolet (UV) radiation.
The structural integrity of the skin is formed primarily by collagen. UV radiation exposure can induce tremendous insult to the skin through various mechanisms. One understood mechanism involves the generation of reactive oxygen species (ROS). Excessive ROS are harmful to the skin because they can cause oxidative damage to cells thus contributing to collagen breakdown.
With chronological aging, exacerbated by photoaging, collagen synthesis is reduced. Increased collagen breakdown coupled with decreased neo-collagenesis results in the integrity of the dermis being compromised and the reparative response becoming defective.
The joint result of these combined mechanisms is visible skin damage evident as wrinkles. Advancing age results in natural cellular attrition and senescence that must also be acknowledged as contributors to the clinical manifestations of skin aging.
The specific histological changes in the skin caused by photoaging are distinct from those that occur due to chronological aging.
In chronologically-aged skin, collagen fiber bundles are loose, short, and thin and disorganized when compared to sun protected young skin. The epidermis is thinner, and the number of rete pegs is reduced.
In contrast, photo-damaged skin is marked by elevated elastosis and collagen fragmentation beneath the dermal-epidermal junction. The epidermal thickness can be irregular, as can the morphology of epidermal cells.
The exact nature of UV skin damage depends on skin type; type III and IV skin display leathery skin, lentigines and an overall “bronzed” appearance.
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