These changes are due to both internal aging, which is inevitable, and external aging, which can be slowed with a tailored homecare regimen and sun safe practices. Externally-aged, mature skin can be attributed to a reduction in muscle mass and skin thickness, cross-linking of collagen and elastin in the dermis, dehydration of the stratum corneum, and cumulative ultraviolet exposure.

Many of the changes that are seen in mature skin occur in the dermis, which loses 20 to 80 percent of its thickness during aging. This loss of thickness is due to changes of the fibroblasts, the cells that are responsible for the biosynthesis of elastin, glycosaminoglycans, and collagen. As a result, collagen and elastin production slows, impacting the skin’s ability to repair itself.
Furthermore, collagen and elastin breakdown is controlled by matrix metalloproteinase enzymes (collagenase and elastase). These enzymes are activated by ultraviolet radiation within hours of exposure. Long-term exposure to ultraviolet radiation causes an excessive breakdown of collagen and elastin, resulting in damaged, aged skin.
Between the ages of 30 and 80, the epidermal cell turnover rate slows by 30 to 50 percent, meaning that cells are only shed every 30 days or more. Young adults, in comparison, have a cell turnover time of 20 days. This slowdown in the cell cycle accounts for the dull and rough skin that is often seen in clients with mature skin.
By the 40s, the amount of hyaluronic acid found in the dermis begins to diminish. This loss contributes to skin dehydration and the loss of skin tone. Furthermore, a reduction in the moisture content of the stratum corneum results in the skin’s inability to bind and retain water. This lack of moisture contributes to the formation of fine lines and wrinkles.

References
Shuster, S., Black, M., and McVite, E. (2006). The influence of age and sex on skin thickness, skin collagen, and density. British Journal of Dermatology, 93(6), 639-43.