Photoaging

Chronic absorption of UV radiation leads to photoaging, sunburn, immunosuppression, and carcinogenesis. Photoaging is the most common form of skin damage caused by UV exposure, affecting connective tissue, melanocytes, and the microvasculature. In photoaged skin, the thickness of the epidermis can either increase or decrease, corresponding to areas of keratinocyte atypia. Changes in the dermis of photoaged skin can vary based on the amount of acquired UV damage. Substantial progress has been made to ascertain the molecular mechanisms accountable for photoaging in human skin. DNA damage and defective DNA repair mechanisms have been implicated in carcinogenesis as well as the intrinsic aging process. One of the histologic hallmarks of photoaging is elastolysis and an accumulation of abnormal elastin in the superficial dermis known as solar elastosis. The pathophysiology of photoaging stems from the ability of UV irradiation to exploit established molecular mechanisms that have evolved to maintain the internal milieu of human skin connective tissue.