This article discusses photoaging or premature skin aging from chronic ultraviolet exposure. This is an important cosmetic concern for many dermatologic patients. Clinical signs include rhytids, lentigines, mottled hyperpigmentation, loss of translucency, and decreased elasticity. These changes are more severe in individuals with fair skin and are further influenced by individual ethnicity and genetics. Photoaging may be prevented and treated with a variety of modalities, including topical retinoids, cosmeceuticals, chemical peels, injectable neuromodulators, soft tissue fillers, and light sources.
Key points
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Photoaging is caused by chronic ultraviolet exposure leading to a complex process of skin changes that occur predominately on the sun-exposed cutaneous surfaces.
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Photoaging is more pronounced in fair-skin individuals and is characterized by subtle differences across ethnicities.
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Clinical manifestations of photoaging include rhytids, lentigines, telangiectasias, mottled pigmentation, coarse texture, laxity, and loss of translucency.
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Patients are concerned about their appearance related to photoaging and are influenced by society, culture, and personal values.
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A variety of modalities exist to prevent and treat photodamage, including sun protection, topical retinoids, cosmeceuticals, chemical peels, neuromodulators, soft tissue fillers, and light sources such as lasers.
Introduction
Photoaging is characterized by a complex process of skin changes induced over time by ultraviolet light exposure. It results in premature aging of the skin and is superimposed on the changes caused by chronologic aging. Not all photoaging is equal. The process is influenced by skin type and ethnicity. The degree of photoaging also depends on geographic location (ie, latitude and altitude), extent of sun exposure in relation to occupation and lifestyle, and photoprotective practices, including using sunscreens and photoprotective clothing, and seeking shade. Many patients use antiaging products or have corrective procedures.
Generally, patients are concerned about appearance and are influenced by society, culture, and personal values. Aesthetic ideals of beauty vary, yet the appearance of youthfulness remains a constant benchmark. Photoaging plays an important role in the degree to which youthfulness is retained despite advancing age.
This article discusses the clinical features, epidemiology, histopathology, pathogenesis, and management of photoaging.
Introduction
Photoaging is characterized by a complex process of skin changes induced over time by ultraviolet light exposure. It results in premature aging of the skin and is superimposed on the changes caused by chronologic aging. Not all photoaging is equal. The process is influenced by skin type and ethnicity. The degree of photoaging also depends on geographic location (ie, latitude and altitude), extent of sun exposure in relation to occupation and lifestyle, and photoprotective practices, including using sunscreens and photoprotective clothing, and seeking shade. Many patients use antiaging products or have corrective procedures.
Generally, patients are concerned about appearance and are influenced by society, culture, and personal values. Aesthetic ideals of beauty vary, yet the appearance of youthfulness remains a constant benchmark. Photoaging plays an important role in the degree to which youthfulness is retained despite advancing age.
This article discusses the clinical features, epidemiology, histopathology, pathogenesis, and management of photoaging.
History
The term photoaging was first coined in 1986 and has been used interchangeably with the term dermatoheliosis. However, the latter is a faulty neologism that implies a pathologic condition (osis) of the sun (helio). Thus, photoaging is more accurate and is used exclusively throughout this article.
Epidemiology
Photoaging is more prevalent among populations with fair skin. Fitzpatrick skin types I, II, and III are more prone to photoaging than skin types IV, V, and VI. Ethnic origin, in particular Northern European descent, also plays an important role. In an Australian study of participants younger than the age of 30, moderate to severe photoaging was observed in 72% of men and 47% of women. In populations with darker skin, wrinkling is not readily apparent until the age of 50 and the severity is not as marked as in fairer skinned populations of similar age. One study found that the onset of wrinkles in Chinese women occurred on average 10 years later than in French women.
Photoaging is directly associated with cumulative sun exposure and, by extension, increasing age. Other factors include geographic location, such as high altitude and proximity to the equator where the harmful effects of ultraviolet light from the sun are most severe. Lifestyle practices, including outdoor occupations and outdoor recreational activities, increase cumulative sun exposure. For example, farmers, sailors, construction workers, and truck drivers frequently show severe effects of sun exposure over a lifetime. Indoor tanning is a practice that is also responsible for accelerated photoaging.
Factors that diminish the features of photoaging include rigorous sun-protection practices. In Asian culture, in particular, women fastidiously avoid exposing their face to the sun. They may wear large brimmed hats, carry parasols, and avoid the beach or other outdoor activities. These practices are highly influenced by societal ideals of beauty and attractiveness.
Pathogenesis
Both UV-A (320–400 nm) and UV-B (290–320 nm) seem to be implicated in the photoaging process, although UV-A is emerging as the major contributor because it penetrates deeper into the dermis and reaches the earth at least 10-fold more abundantly than UV-B. UV-B radiation is mainly absorbed in the epidermis by cellular DNA, inducing damage with formation of cyclobutane pyrimidine dimers. UV-B is responsible for sunburn, photocarcinogenesis, and immunosuppression.
Cumulative UV-A radiation causes damage to the dermal extracellular matrix and blood vessels. UV-A also indirectly damages DNA, as well as lipids and proteins, through the generation of reactive oxygen species (ROS). ROS cause oxidative damage to cellular components such as cell membranes, mitochondria, and DNA. Mitochondria are the main endogenous source of ROS and are produced during the conversion of ADP to ATP. Endogenous ROS, including superoxide anion, hydrogen peroxide, and singlet oxygen, activate cytokine and growth factor receptors, which in turn induce transcription factor activator protein 1 (AP-1) and NF-κB.
Fig. 1 demonstrates the pathogenesis of photoaging. UV radiation activates growth factor and cytokine receptors, which induce transcription factor AP-1. The induction of AP-1 promotes collagen breakdown by upregulating matrix metalloproteinases (MMP), including interstitial collagenase (MMP-1), stromelysin-1 (MMP-3), and 92 kDa gelatinase (MMP-9). The combined actions of MMP-1, MMP-3, and MMP-9 degrade most of type I and III dermal collagen. Furthermore, AP-1 inhibits collagen production by decreasing gene expression of types I and III procollagen in the dermis. AP-1 binds to the transcriptional complex responsible for procollagen transcription or blocks the activity of transforming growth factor beta (TGF-β), a cytokine that promotes procollagen formation. With repeated sun exposure, degraded collagen accumulates over time and attenuation of collagen production results in the clinical and histologic features of photoaging.
The activation of NF-κB by ROS regulates the expression of proinflammatory cytokines, such as interleukin (IL)-1β, TNF-α, IL-6, IL-8, and various adhesion molecules. These cytokines, in turn, can amplify AP-1 and NF-κB pathways, further enhancing the response to UV radiation.
Clinical manifestations
Photoaging can manifest as rhytids, lentigines, telangiectasias, mottled pigmentation, coarse texture, loss of translucency, sallow color, laxity, and decreased elasticity and turgor. More severe photoaging may result in accentuated ridging, deep furrows, leathery appearance, severe atrophy, open comedones, milia, cobblestone effect from elastosis, actinic purpura, and epidermal and dermal thickening. Chronologic aging is dominated by fine lines and increased skin laxity. The latter is primarily due to soft tissue volume loss from fat atrophy, gravity-induced soft tissue redistribution, and reduction of facial skeletal support related to bone resorption.
Photoaging is significantly affected by an individual’s skin type and ethnicity. Darker skin is more photoprotected than fair skin because of the increased melanin content. A cadaveric study comparing black and white skin found the photoprotective effect of melanin against UV radiation has an average sun protective factor (SPF) of 13.4. Thus, individuals with higher Fitzpatrick skin types are inherently more protected because they generally experience the effects of photoaging 10 to 20 years later and with less severity.
Ethnicity plays a strong factor in determining the specific clinical features of photoaging. Wrinkle patterns and pigmentary changes differ between white and Asian skin. A population study evaluating the effects of ethnicity and genetics on photoaging was conducted in the Pokhara valley of Nepal, which is cohabited by two distinct ethnic groups of Aryan-origin and Mongolian-origin. It was found that Aryan-origin participants showed deeper wrinkles, particularly around the eye area and forehead, even though they had darker skin on average. Thus, ethnic origin and genetics are independent factors in determining the effects of photoaging. Another epidemiologic study investigating the role of genetics compared Japanese women from Japan and white women from Germany. The Japanese women had less facial wrinkling and more pigment spots than their German counterparts. Plausible explanations for the underlying differences include higher antioxidant levels in fasting blood (for less wrinkling) and greater frequency of the SLC45A2 gene allele involved in melanin synthesis (for more pigmented lesions) in Japanese women. These metabolic and genetic differences may further illuminate the role of ethnicity and genetics in the complex process of photoaging.
Histology
Microscopic changes in photodamaged skin affect the epidermis and dermis. Fig. 2 compares the histology of normal, sun-protected skin and damaged, photoaged skin. In photoaging, epidermal changes include either atrophy with thinning of the spinous layer and flattening of the dermoepidermal junction (loss of rete ridges), or epidermal thickening and acanthosis. In the dermis, there is decreased extracellular matrix and breakdown of collagen fibers, which clinically manifest as rhytids. The most pronounced histologic feature of photoaging is disintegration of elastic fibers, also called solar elastosis, which results in deposition of amorphous masses of abnormally thickened, curled, and fragmented elastic fibers. Increased numbers of atypical melanocytes and keratinocytes may be seen. By contrast, histologic changes of chronologically aged skin are less complex and characterized by epidermal atrophy with decreased amounts of fibroblasts and collagen content.
Photobiologic evaluation
Photoaging can be characterized on a scale from minimal to severe involvement. Multiple photoaging scales have been developed by experts in the field. In one of the earliest efforts, Griffiths and colleagues used five photographic standards with assigned grades of 0, 2, 4, 6, and 8 ( Fig. 3 ) to develop a photonumeric nine-point scale illustrating the severity of photodamage (0 = no photodamage, 8 = severe). Helfrich and colleagues studied photoprotected skin of the upper inner arm and developed a similar photonumeric nine-point scale to assess chronologic aging. Chung and colleagues designed two photonumeric scales, one for wrinkling and the other for dyspigmentation, to grade the severity of photoaging in Asian skin. The Glogau classification divides the degree of photoaging into four groups: mild, moderate, advanced, and severe. It predominately measures the severity of rhytids. The Wrinkle Severity Rating Scale and Global Aesthetic Improvement Scale is a five-point photonumeric scale designed to quantify facial folds (1 = absent, 5 = severe). It has been used in clinical research studies to provide objective quantification of improvement after skin rejuvenation interventions such as soft tissue fillers. Carruthers and Carruthers also developed a set of validated grading scales (0 = none, 4 = severe) to rate brow positioning, forehead lines, melomental folds, and crow’s feet for clinical and research purposes.
