23 Sun-exposed aged skin is characterized by the solar elastosis. 21 A marked loss of fibrillin-positive structures 22 as well as a reduced content of collagen type VII (Col-7), may contribute to wrinkles by weakening the bond between dermis and epidermis of extrinsically age skin.

20 On the other side, many of these features are targets to product application or procedures to accelerate the cell cycle, in the belief that a faster turnover rate will yield improvement in skin appearance and will speed wound healing. This fact is important when esthetic procedures are scheduled. 19 Slowing of the epidermal turnover rate and cell cycle lengthening coincides with a slower wound healing and less effective desquamation in older adults. 13 - 18 Gradual loss of skin elasticity leads to the phenomenon of sagging. 2 - 12 In contrast to thin and atrophic, finely wrinkled and dry intrinsically aged skin, premature photoaged skin typically shows a thickened epidermis, mottled discoloration, deep wrinkles, laxity, dullness and roughness.

1 These factors lead together to cumulative structural and physiological alterations and progressive changes in each skin layer as well as changes in skin appearance, especially, on the sun-exposed skin areas. Skin aging is a complex biological process influenced by combination of endogenous or intrinsic (genetics, cellular metabolism, hormone and metabolic processes) and exogenous or extrinsic (chronic light exposure, pollution, ionizing radiation, chemicals, toxins) factors. While the aging signs of internal organs are masked from the ambient “eyes,” the skin provides first obvious marks of the passing time. Skin aging is a part of a natural human “aging mosaic” which becomes evident and follows different trajectories in different organs, tissues and cells with time.

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