photoaging

Photoaging refers to premature aging of the skin caused by cumulative ultraviolet radiation exposure, primarily UVA and UVB, with contributions from visible light and other environmental factors. It is distinguished from intrinsic aging by its strong association with sun exposure and characteristic skin changes.

The main pathogenic mechanism involves UV-induced reactive oxygen species, DNA damage, and upregulation of matrix metalloproteinases in the dermis, which degrade collagen and elastin. This leads to thinning, laxity, and the development of fine and coarse wrinkles, textural changes, and lentigines.

Clinical features commonly appear on sun-exposed areas such as the face, neck, and hands and include coarse wrinkling, dyspigmentation (solar lentigines and mottled hyper- or hypopigmentation), rough skin, telangiectasia, and a thickened, inelastic dermis known as actinic elastosis.

Risk factors include fair-skinned individuals (phototypes I–III), a history of sunburns, chronic outdoor exposure, tanning bed use, smoking, and aging. Genetics and geographic location affect risk and onset.

Prevention emphasizes sun protection: broad-spectrum sunscreen (SPF 30 or higher), protective clothing, hats, shade, and avoidance of tanning beds. Adjunct approaches include topical antioxidants and retinoids. Treatments for established photoaging include laser therapy, chemical peels, dermabrasion, and other procedures, in addition to ongoing sun protection.

Photoaging is often discussed alongside intrinsic aging; distinguishing features include prominent dyspigmentation and elastosis. It increases the risk of actinic keratoses and skin cancer in some individuals. The condition is common in populations with high UV exposure and tends to progress with continued sun exposure.