There are two main processes of skin aging, intrinsic and extrinsic.1 Intrinsic aging is controlled by genes. The genes that contribute to skin aging have not yet been elucidated although some are thought to play a role in aging. Extrinsic aging is caused by external factors such as smoking, excessive use of alcohol, poor nutrition, and sun exposure, which in many cases can be reduced with effort. It is believed that as much as 80 percent of facial aging can be ascribed to sun exposure (extrinsic aging).2 It is also speculated that some factors implicated in extrinsic cutaneous aging may impact the intrinsic aging process.3
Extrinsic aging accounts for most facial aging. Extrinsically aged skin appears predominantly in exposed areas such as the face, chest, and extensor surfaces of the arms. It is a result of the cumulative effects of a lifetime of exposure to ultraviolet radiation (UVR) and other insults such as pollution. Clinical findings of photoaged skin include fragility, thinning, wrinkles, dryness, rough texture, poor light reflection, sallowness, pigmented lesions such as lentigines (dark patches), sagging, diminished elasticity, and decreased hysteresis (ability to resume shape after deformation).
The clinical signs of aged skin are primarily thought to be caused by a loss of or dysfunction in collagen, elastin, and/or the glycosaminoglycans hyaluronic acid (HA). The goal of antiaging skin care products is to prevent the loss of collagen, elastin, and HA as well as increase the production of collagen and HA. At this time, no procedures or products have been developed to increase the production of functional elastin. Matrix metalloproteinases (MMPs), glycation, dysfunction of organelles such as mitochondria and lysosomes, telomere shortening, sirtuin expression, stem cell function, accumulation of senescent cells, and DNA damage also play a role in skin aging.
The mechanism of action of UVR induction of collagen damage has been well characterized in the last decade. It is now known that UVR exposure dramatically upregulates the production of enzymes known as MMPs. This occurs by the following mechanism: UV exposure causes an increase in the amount of the transcription factor c-Jun; c-Fos is abundant without UV exposure. When UV exposure occurs, these two transcription factors, c-Jun and c-Fos, combine to produce activator protein (AP)-1, which activates the MMP genes resulting in production of MMPs including collagenase, gelatinase, and stromelysin. It has been demonstrated in humans that MMPs, specifically collagenase and gelatinase, are induced within hours of UVB exposure.4 Fisher et al. showed that multiple exposures to UVB yield a sustained induction of MMPs.5 Because collagenase degrades collagen, long-term increases in collagenase and other MMPs likely result in the disorganized and clumped collagen seen in photoaged skin.
Collagen gives skin its strength and support – it is the scaffolding ...