Photoaging is the premature aging of the skin due to chronic exposure of skin to ultraviolet (UV) light, predominantly from the sun or sun beds. Photoaging ranges from wrinkled, discoloured skin through to precancerous lesions, actinic keratoses.
While human skin will naturally age, photoaging, and thus UV, is considered an accelerant to the process.
The symptoms of photoaging vary, but are generally recognised as premature degradation of skin on areas where the skin has been exposed long-term to UV light, predominantly on the face and hands, but also on the torso, arms and legs. Symptoms include:
- Deep, course wrinkles
- Discolouration - either lightening or darkening of the skin, predominantly in patches, or sallowness
- Solar lentigo - ‘age’ spots or ‘liver’ spots
- Telangiectasia - dilated or broken blood vessels close to the surface of the skin
- Leathery or ‘weathered’ appearance
- Elastosis - sagging skin
- Actinic purpura
Premalignant lesions, such as actinic keratoses, are also considered part of the photoaging process.
Collagen, found in the dermis, is predominantly responsible for the strength of skin, providing firmness. As skin ages, collagen in the dermis breaks down and the ability to produce new collagen is reduced, causing skin to appear wrinkled and damaged.
When UV radiation penetrates skin, it acts on two separate levels to reduce the amount of collagen present in the skin. UV penetration causes skin to generate reactive oxygen species (ROS). These molecules damage the skin cells around them, including collagen cells, causing the skin to loose some of its firmness. UV radiation also decreases the skin’s ability to express transforming growth factor ((TGF)-β), which promotes the development of collagen. This suppression of TGF-β reduces the production of collagen.
Each time skin is damaged by UV it has been likened to leaving a “solar scar”, where skin cells have not been replaced or repaired. Accumulative “solar scars”, caused by repeated UV exposure, lead to visible damage and wrinkling of the skin. In short, UV both destroys collagen in skin and inhibits its production. This lack of collagen causes skin to lose its firmness, resulting in visible damage.
UVA (radiation between 320-400nm in wavelength) has been identified as the primary cause of photoaging, as the longer wavelengths are able to penetrate deeper into the skin to cause damage.
It has been proposed that there is a genetic predisposition to photoaging, with individuals with skin types I-III (fair skinned individuals) more likely to suffer skin damage from UV than those with darker complexions.
In an attempt to clinically classify photoaged skin, Glogau (1996) proposed four types:
- Type I: “no wrinkles” (seen mostly in patients in their late 20’s);
- Type II: “wrinkles in motion” - some wrinkles and discolouration with onset of precancerous lesions (seen mostly in patients aged 35-50);
- Type III: “wrinkles at rest” - many wrinkles and significant discolouration and lesions (seen mostly in patients aged 50-60);
- Type IV: “only wrinkles - severely wrinkled, discoloured and damaged skin with lesions and possible skin cancers (seen in patients over 65).
By preventing or reducing exposure to UV radiation, photoaging can be largely avoided. Sun and sun bed avoidance, and skin photoprotection, are key to preventing photoaging. As photoaging is believed to be the result of UVA damage, daily use of broad spectrum sunscreens which block out UVA radiation are important for reducing potential damage to skin. Covering exposed skin with long sleeved clothing and broad brimmed hats, and avoiding sun light - particularly between the hours of 10am and 4pm - will reduce exposure to UV radiation and thus reduce photoaging.
Smoking, being overweight and poor diet have all been linked to increased ‘aging’ of the skin. While these factors may compound photoaging, their mechanisms are independent.
The majority of photoaging treatments aim to increase the firmness and elasticity of photoaged skin, or to camouflage wrinkles.
Regular application of topical retinoids (vitamin A) has been shown in clinical studies to reduce wrinkling in photoaged skin, even in individuals with sensitive skin. Topical fluorouracil has also been shown to improve the appearance of photoaged skin.
Topical alpha-hydroxy acids (AHAs) may also reduce the appearance of wrinkles. Topical creams containing antioxidants, such as vitamin C, aim to reduce the formation of ROS and may be able to reduce the effects of photoaging.
Cosmetic procedures such as botulinum toxin or collagen injections are also used to reduce the appearance of wrinkles. A range of cosmetic surgical procedures exist, each designed to reduce or reverse the visible appearance of skin wrinkling, sagging or discolouration, including:
- Intense pulsed light (IPL), a laser treatment for reducing wrinkles;
- 5-aminolevulinic acid (5-ALA) and pulsed-dye laser, a form of photodynamic therapy;
- Chemical peels for discolouration and smoothing damaged skin
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- Glogau RG, (1996). “Aesthetic and anatomic analysis of the aging skin.” Semin Cutan Med Surg, 15(3): 134-8.
- Helfrich YR, Sachs DL and Voorhes JJ, (2008). “Overview of skin aging and photoaging.” Dermatology Nursing, 20(3): 177-83.
- Kang S, Fisher GJ and Voorhees JJ, (2001). “Photoaging: pathogenesis, prevention, and treatment.” Clin Geriatr Med, 17(4): 643-59, v-vi.
- Kikuchi K, et al (2009). “Improvement of photoaged facial skin in middle-aged Japanese females by topical retinol (vitamin A alcohol): a vehicle-controlled, double-blind study.” Journal of Dermatological Treatment, 20(5): 276-81.
- Kligman AM, (1992). “Current status of topical tretinoin in the treatment of photoaged skin.” Drugs and Aging, 2(1): 7-13.
- Kligman D and Zhen Y, (2004). “Intense pulsed light treatment of photoaged facial skin.” Dermatological Surgery, 30(8): 1085-90.
- Kligman D and Kligman AM, (1998). “Salicylic acid peels for the treatment of photoaging.” Dermatological Surgery, 24(3): 325-8.
Online resources for photoaging