Pathophysiology and prevention of photoaging : the role of melanin, reactive oxygen species and infiltrating neutrophils

Photoaging of human skin involves epidermal and dermal changes. The hallmark of photoaged skin is an accumulation of elastotic material in the mid and upper dermis, so-called solar elastosis. This elastotic material is mostly derived from degraded elastic fibers and consists mainly of insoluble elastin. In areas of severe solar elastosis collagen fibers are reduced and fragmented. Photoaged skin is inelastic and severe wrinkling occurs at sites of mechanical stress as the skin is continuously stretched and bent (e.g., neck and face). Neutrophil-derived mediators and proteolytic enzymes, particularly neutrophil elastase, play a key role in the development of solar elastosis. Neutrophil-derived matrix metalloproteinase(MMP)-9 contributes to collagen degradation. The role of keratinocyte-derived MMP-1 is insignificant and the role of MMP-1 derived from dermal cells is limited. Together with directly ultraviolet radiation(UV)-induced DNA damage, UV-induced reactive oxygen species (ROS) play a major role in the cascade of events that precede UV-induced inflammation and neutrophil influx. UV-induced ROS and neutrophil-derived ROS can also contribute directly to the extracellular matrix damage observed in photoaged skin. Prevention of sunburn which is accompanied by skin-infiltrating neutrophils is key in the prevention of photoaging. Black skin is much less prone to photoaging because it is much less likely to develop a sunburn with accompanying neutrophil-influx, and because ROS are less likely to be generated in the dermis. Sun avoidance, wearing of protective clothing and application of sunscreens remain the foremost methods to prevent sunburn and photoaging