INTRODUCTION
Photoaging is the result of ultraviolet (UV)-induced damage to exposed skin. Superimposed upon intrinsic aging, photoaging accounts for most age-related changes in the appearance of skin. As skin ages, it becomes thinner, drier, and less elastic due to slowing of regenerative processes.1
Youthful skin is characterized by its unblemished, evenly pigmented, smooth, pink appearance. This contrasts with intrinsically aged skin, which is thin, inelastic, and finely wrinkled with deepening of facial expression lines. These changes are evident histologically as a thinned epidermis and dermis with flattening of the rete pegs at the dermal epidermal junction. Extrinsically aged, sun-exposed skin appears clinically as blemished, thickened, yellowed, lax, rough, and leathery. These changes may begin as early as the second or third decade and accelerate beyond.
The best-studied ingredient category for anti-aging benefits is retinoids, investigated for their ability to reduce manifestations of photodamage such as wrinkles, hyperpigmentation, and skin laxity.2,3,4 Retinoids, especially retinoic acid, have been shown to decrease melanin, increase deposition of collagen in the papillary dermis and improve the morphology of elastic fibers.5,6,7 Retinoids include retinol (vitamin A) and its natural derivatives such as retinaldehyde, retinyl esters, and tretinoin (retinoic acid). The most extensively studied retinoid is retinoic acid.8,9,10 Tretinoin is a prescription retinoic acid commonly used as treatment for photoaged skin; however, it is associated with poor tolerability.11 It is well-documented that retinol produces less skin erythema and scaling than retinoic acid. Gold and colleagues wrote that burning, pruritus, dryness, and erythema were “minimal†with a topical formulation of 0.5% retinol.12,13
Although retinol appears to be a viable candidate for the treatment of photoaged skin, retinol is easily degraded to biologically inactive forms when exposed to light and air.14,15,16 For this reason, the efficacy of retinol in the treatment of photodamage depends greatly on its mode of delivery to the target area and formulation.
Youthful skin is characterized by its unblemished, evenly pigmented, smooth, pink appearance. This contrasts with intrinsically aged skin, which is thin, inelastic, and finely wrinkled with deepening of facial expression lines. These changes are evident histologically as a thinned epidermis and dermis with flattening of the rete pegs at the dermal epidermal junction. Extrinsically aged, sun-exposed skin appears clinically as blemished, thickened, yellowed, lax, rough, and leathery. These changes may begin as early as the second or third decade and accelerate beyond.
The best-studied ingredient category for anti-aging benefits is retinoids, investigated for their ability to reduce manifestations of photodamage such as wrinkles, hyperpigmentation, and skin laxity.2,3,4 Retinoids, especially retinoic acid, have been shown to decrease melanin, increase deposition of collagen in the papillary dermis and improve the morphology of elastic fibers.5,6,7 Retinoids include retinol (vitamin A) and its natural derivatives such as retinaldehyde, retinyl esters, and tretinoin (retinoic acid). The most extensively studied retinoid is retinoic acid.8,9,10 Tretinoin is a prescription retinoic acid commonly used as treatment for photoaged skin; however, it is associated with poor tolerability.11 It is well-documented that retinol produces less skin erythema and scaling than retinoic acid. Gold and colleagues wrote that burning, pruritus, dryness, and erythema were “minimal†with a topical formulation of 0.5% retinol.12,13
Although retinol appears to be a viable candidate for the treatment of photoaged skin, retinol is easily degraded to biologically inactive forms when exposed to light and air.14,15,16 For this reason, the efficacy of retinol in the treatment of photodamage depends greatly on its mode of delivery to the target area and formulation.
