Abstract

This chapter focuses on the most popular pathogenic concepts relevant for UV-induced skin aging, because photoaging is by far the best studied and probably also most relevant example of extrinsic skin aging. Solar ultraviolet (UV) radiation is most important for premature skin aging, a process accordingly also termed photoaging. Other factors include exposure to near-infrared radiation from sunlight or artificial near-infrared radiation (IRA) radiation devices, tobacco smoke, and particulate matter from airborne traffic pollution. UV-induced alterations at the level of the dermis are best studied and appear to be largely responsible for the phenotype of photoaged skin. UVB acts preferentially on the epidermis, where it not only damages DNA in keratinocytes and melanocytes but also causes the production of soluble factors including proteolytic enzymes, which then in a second step affect the dermis. There is increasing evidence that cutaneous blood vessels may play a role in the pathogenesis of photoaging. Photoaged skin shows vascular damage that is absent from intrinsically aged skin. In mildly photodamaged skin, there is venular wall thickening, whereas in severely damaged skin the vessel walls are thinned and supporting perivascular veil cells are reduced in number.

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