Photoaging refers to skin damage caused by prolonged sun exposure, specifically UVA and UVB rays, and can lead to skin cancers.

Photoaging is also known as dermatoheliosis.

The deterioration of biological functions and ability to manage metabolic stress is one of the major consequences of the aging process. 

Photoaging is a complex, progressive process that leads to functional and aesthetic changes in the skin. 

Photoaging process can result from both intrinsic, genetic, as well as extrinsic processes by environmental factors.

Photoaging is attributed to continuous, long-term exposure to ultraviolet (UV) radiation of approximately 300–400 nm, either natural or synthetic to the skin.

UVB rays are a primary mutagen that can only penetrate through the epidermal (outermost) layer of the skin, resulting in DNA mutations. 

DNA mutations arise due to chemical changes, the formation of cyclobutane pyrimidine dimers and photoproducts formed between adjacent pyrimidine bases. 

These mutations may be clinically related to specific signs of photoaging such as wrinkling, increasing in elastin and collagen damage.

The epidermal layer does not contain any blood vessels or nerve endings but melanocytes and basal cells are embedded in this layer. 

UVB exposure causes melanocytes to produce melanin, a pigment that gives the skin its color tone. 

UVB causes the formation of freckles and dark spots, both of which are symptoms of photoaging. 

With constant exposure to UVB rays, signs of photoaging might appear and precancerous lesions or skin cancer may develop.

UVA rays are able to penetrate deeper into the skin as compared to UVB rays, 

in addition to the epidermal layer, the dermal layer will also be damaged. 

Most of the skin changes that occur with age are accelerated by sun exposure.


((Skin)) is composed of three layers: the ((epidermis)), the ((dermis)), and subcutaneous tissue. 


The dermis contains proteins, including collagen, elastin, and other important fibers, that affect the skin’s strength and elasticity and are responsible for skin’s smooth, youthful appearance. 

The dermis is the second major layer of the skin and it comprises collagen, elastin, and extrafibrillar matrix which provides structural support to the skin. 

Constant UVA exposure causes them size of the dermis layer to be reduced, thereby causing the epidermis to start drooping off the body. 

Due to the presence of blood vessels in the dermis, UVA rays can lead to dilated or broken blood vessels which are most commonly visible on the nose and cheeks. 

UVA can also damage DNA indirectly through the generation of reactive oxygen species (ROS), which include superoxide anion, peroxide and singlet oxygen.

ROS damage cellular DNA as well as lipids and proteins.

UV exposure can also lead to inflammation and vasodilation which is clinically manifested as sunburn. 

UV radiation activates the transcription factor, NF-κB, which is the first step in inflammation. 

NF-κB activation results in the increase of proinflammatory cytokines, for example: interleukin 1 (IL-1), IL-6 vascular endothelial growth factor, and tumor necrosis factor (TNF-α). 

Skin aging is caused in part by TGF-β, which reduces the subcutaneous fat that gives skin a pleasant appearance and texture. 

This then attracts neutrophils which lead to an increase in oxidative damage through the generation of free radicals. 

UV radiation causes the down-regulation of an angiogenesis inhibitor, thrombospondin-1, and the up-regulation of an angiogenesis activator which is platelet-derived endothelial cell growth factor, in keratinocytes. 

These enhance angiogenesis and aid in the growth of UV-induced neoplasms.

UV radiation may lead to local and systemic immunosuppression, due to DNA damage and altered cytokine expression. 

The Langerhans cells may undergo changes in quantity, morphology, and function due to UV exposure and may eventually become depleted. 

Langerhans cells changes occurs with immunosuppression asbthe body is attemptisbto suppress an autoimmune response to inflammatory products resulting from UV damage.

UV exposure leads to the activation of receptors for epidermal growth factor, IL-1, and TNF-α in keratinocytes and fibroblasts, which then activates signaling kinases throughout the skin.

The nuclear transcription factor activator protein, AP-1, which controls the transcription of matrix metalloproteinases (MMP), is expressed and activated. 

MMP-1 is a major metalloproteinases for collagen degradation. 

Another transcription factor NF-κB, which is also activated by UV light, also increases the expression of MMP-9.

The up-regulation of MMP can occur even after minimal exposure to UV, hence, exposure to UV radiation which is inadequate to cause sunburn can thus facilitate the degradation of skin collagen and lead to presumably, eventual photoaging. 

Thus, collagen production is reduced in photoaged skin due to the process of constant degradation of collagen mediated by MMPs.

The presence of damaged collagen also down-regulates the synthesis of new collagen, and the  impaired spreading and attachment of fibroblasts onto degraded collagen could be one of the contributing factors to the inhibition of collagen synthesis.

UV radiation decreases the expression of both retinoic acid receptors and retinoid X receptors in human skin, resulting in a complete loss of the induction of RA-responsive genes. 

It also leads to a functional deficiency of vitamin A in the skin.

Dyspigmentation, the formation of wrinkles and other symptoms appear around regions of skin commonly exposed to sun, mostly the eyes, mouth and forehead.

Photoaging can also result in an orderly maturation of keratinocytes and an increase in the cell population of the dermis where abundant; hyperplastic, elongated and collapsed fibroblasts and inflammatory infiltrates are found.

Photodamage can also be characterized as a disorganization of the collagen fibrils that constitute most of the connective tissue, and the accumulation of abnormal, amorphous, elastin-containing material, a condition known as actinic elastosis.

UV exposure which would lead to an increase in epidermal thickness could help protect from further UV damage.

Fairer individuals who have lesser melanin pigment show more dermal DNA photodamage, infiltrating neutrophils, keratinocyte activation, IL-10 expression and increased matrix metalloproteinases after UV exposure. 

The distribution of melanin provides protection from sunburn, photoaging, and carcinogenesis by absorbing and scattering UV rays, covering the skin lower layers and protecting them from the radiation.

The damage of DNA due to exposure of UV rays leads to expression of p53, thereby leading to eventual arrest of the cell cycle, allowing DNA repair mediated by endogenous mechanisms like the nucleotide excision repair system. 

Apoptosis occurs if the damage is too severe. 

As apoptotic mechanisms decline with age, and if neither DNA repair mechanism nor apoptosis occurs, cutaneous tumorigenesis may result.

Tissue inhibitors of major metalloproteinases regulate the activity of MMP. 

Many studies have shown that UV rays would induce major metalloproteinases-1.

The skin contains several antioxidants, including vitamin E, coenzyme Q10, ascorbate, carotenoids, superoxide dismutase, catalase, and glutathione peroxidase, which provide protection from reactive oxygen species produced during normal cellular metabolism. 

However, overexposure to UV rays can lead to a significant reduction in the antioxidant supply, thus increasing oxidative stress.

These antioxidants are essential in the skin’s defense mechanism against UV radiation and photocarcinogenesis.

Treatment and intervention for photoaging:

Primary prevention aims to reduce the risk factors before a disease or condition occurs.

Sun protection is the most effective form of primary prevention of photoaging: sunscreen products, sun protective clothing, and reducing exposure to the sun, especially during peak sun hours.

Broad-spectrum sunscreen products provide optimal protection against UV damage:  protecting against both types of UVA rays (UVA1 and UVA2) along with UVB rays. 

Secondary protection refers to prevent, delay, or attenuate the symptomatic clinical condition: retinoids, antioxidants such as topical vitamin C, CoQ10, Lipoic acid, and estrogens, growth factors and cytokines.

Topical retinoids. 

Tretinoin, considered to be the most efficacious treatment for photoaging.

Retinoids are vitamin A derivatives that bind to retinoic acid receptors (RARs) and retinoid X receptors (RXRs). 

Binding to these receptors induces cellular processes that lead to increased collagen production and epidermal thickening, reducing the appearance of skin sagging and wrinkling. 

Tretinoin is also efficacious for the treatment of acne. 

Adapalene and tazarotene are also third-generation synthetic retinoids that are used for the treatment for acne. 

Retinoid derivatives, retinol and retinal, are often used in over the counter cosmeceutical products for anti-aging purposes. 

Tertiary prevention is the treatment of an existing symptomatic disease process to ameliorate its effects or delay its progress. 

Such tertiary prevention includes:  chemical peels, resurfacing techniques of micro-dermabrasion, ablative or non-ablative laser resurfacing, radio-frequency technology, soft tissue augmentation with fillers, and botulinum toxins. 

Wrinkles deepen and forehead frown lines can be seen even when not frowning.

Telangiectasias most commonly seen around the nose, cheeks and chin.

Skin becomes leathery and laxity occurs.

Solar lentigines, or age spots, appear on the face and hands.

Possibly pre-cancerous red and scaly spots, actinic keratoses, appear.

UV radiation damages these important proteins, leading to photoaging.

Risk factors include fair skin, difficulty in getting a tan, ease of sun-burns and severe sun-burns before the age of 20 years and old age.

Photoaging-exposure to sun causes wrinkling, skin roughness, drying, pigmentation, telangiectasia and brown spots (lentigines).

Signs of photoaging can include:




Drooping skin 


Dark spots 




A yellowish tint to the skin


Leathery texture to the skin


Mottled pigmentation


Easy bruising


((Favre-Racouchot syndrome)) 


UV radiation is made up of UVA and UVB rays. 


In general, UVB rays burn, while UVA rays age the skin, but there is considerable overlap in the damage these rays cause.


UVA rays have longer wavelengths and can deeply penetrate the dermis. 

Even minimal exposure to UV radiation can facilitate the degradation of skin collagen and lead to photoaging.

The rays damage existing collagen, which causes increased elastin production. 


Abnormal amounts of elastin lead to the production metalloproteinases enzymes that repair damaged collagen. 


But, these enzymes cause more harm to the collagen than good by incorrectly restoring the skin.


Daily exposure to UVA rays keeps repeating, resulting in wrinkles and leathery skin.


UVA exposure,causes fine lines and wrinkles around the eyes, mouth, and forehead, as well as age spots, sometimes called liver spots. 


An age spot is a spot of pigmentation caused by sun exposure. 

Photoaging reduces the amount of subcutaneous tissue, making blood vessels more fragile and more likely to rupture from minor trauma.

Age spots can appear on the face but also on the rest of the body, including the hands, arms, chest, and back.


Preventing photoaging:


Avoid sun exposure when the sun is strongest, usually between 10 am and 2 pm.


Sitting under shade when possible.


Wearing  a wide-brim hat to protect the face.


Wearing protective clothing.


Applying sunscreen with an SPF of at least 30 every day to areas that are exposed to the sun, such as the face, neck, chest, hands, arms, and legs. 


Daily application of sunscreen can also reduce the risk of developing skin cancer.


Getting sun exposure in order to boost levels of vitamin D s not recommended: getting this vitamin from a healthy diet that includes foods naturally rich in vitamin D, foods and beverages fortified with vitamin D, and/or vitamin D supplements is recommended.


Treatment of  mild to moderate photoaging is with the use of vitamin A products such as retinol and Retin A. 


Retin A and Differin are more concentrated than over-the-counter formulations, and likely to be more effective. 


These medications have been found to reduce wrinkling, especially fine lines and facial wrinkles. 


Retinoids work by increasing cell turnover and can take a few months before a change. 


Light-based technologies used to treat photoaging, including:


Photodynamic therapy

Laser therapy:  Different wavelengths are used for minimizing blood vessels, treating age spots, reducing wrinkles, and removing hair.


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