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Ultraviolet radiation in sunlight causes a number of changes in the external and internal aspects of cell metabolism. Ultraviolet B (UVB) rays are a known mutagen which can cause DNA changes in the cells forming the superficial epidermal layers.
These mutations are mediated by biochemical changes, which leads to the formation of abnormal dimers of pyrimidines and other light-induced pyrimidine alterations. It is thought that these mutations underlie the signs of photoaging, such as collagen breakdown, increased elastin content, and wrinkled skin. Further constant exposure can result in precancerous lesions and even skin malignancies.
The cells most affected are melanocytes and basal cells because the superficial epidermis is devoid of blood vessels and nerve endings. UVB rays induce increased melanin production by the melanocytes, leading to the formation of freckles and dark spots. They are also implicated in the pathogenesis of skin cancer.
However, ultraviolet A (UVA) rays are of greater penetrative power than UVB rays, enabling them to be absorbed deeper in the epidermis and even the dermal cells. This leads to both direct mutations and indirect damage via reactive oxygen species such as oxygen radicals, causing breaks in the nucleic acid, as well as damage to the collagen, elastin, and extracellular matrix of the dermal layer, which supports the skin and keeps it smooth and young. Constant exposure to UVA rays thin out the dermis and cause loss of skin support, causing epidermal drooping to occur. In addition, the dermal blood vessels dilate or break, most often on the nose and the cheeks. This leads to the appearance of telangiectasia in these regions.
Thus UV damage extends to lipids and proteins in the skin in addition to the DNA within the skin cells.
In the early stages, continued exposure of the skin to UV light causes symptoms such as:
With long-term exposure, the wrinkles become permanent, more telangiectasia occur over the skin surrounding the cheeks, the nose and the chin, and malignant or premalignant lesions may appear.
The epidermal thickness increases in order to prevent or minimize the penetration of UV light. The increase in melanin production is also a defense mechanism to prevent sunlight-induced keratinocyte activation, reduce matrix metalloprotein production and so protect the skin from drooping and wrinkling, and lower the risk of carcinoma occurrence. Melanin absorbs and scatters UV rays so that they are not available for deeper penetration and this results in lower photodamage.
Ultraviolet rays cause damage to the walls of the superficial blood vessels in the skin, causing them to thin out. This leads to the appearance of bruising and bleeding. The dilated and broken blood vessels become visible through the overlying epidermis. This appearance is most common near the nose, over the cheeks and the chin. It is caused mostly by UVA rays due to their greater depth of penetration. However, UVB rays also contribute by causing superficial epidermal damage which stimulates the skin to dilate the cutaneous veins and capillaries. This in turn leads to fluid leakage and inflammation from the dilated blood vessels under the skin which is what is commonly known as sunburn.
Actinic purpura, solar purpura, senile purpura, or Bateman’s purpura is due to structural damage to the blood vessel by UV effects over several decades of sun exposure. The UV rays act primarily on the supporting collagen of the vessels walls in this case, especially in the elderly. This makes the veins more likely to rupture with only a minor trauma. Actinic purpura occurs over the back of the hands and the arms, as areas of bruising which are initially reddish, become purplish and darken steadily over several days before fading.
They are never painful or even tender and take a few weeks to fade in typical cases. The surrounding skin offers a clue, being thin and heavily wrinkled, and easily injured. They are more common in patients who are on oral, topical or inhaled corticosteroid medication, which thins the skin; on anticoagulant or antiplatelet drugs such as aspirin or coumadin, which make bleeding more likely; or who drink alcohol.
It is important to prevent photodamage on a consistent basis as this is linked with cutaneous tumor formation as a result of DNA damage and failure of apoptosis. Two types of prevention are possible, namely, primary and secondary.
Primary prevention refers to the reduction of sun exposure. It is important to minimize or avoid being in the sun between 10 am and 4 pm especially if one is fair-skinned. In addition, if sun exposure during this period is inevitable, measures such as wearing appropriate clothing and using sunscreens are highly recommended.
This includes long-sleeved high-necked shirts and pants made of tightly-woven cloth, which will cover most of the body skin, in addition to wide-brimmed hats and good-quality sunglasses. Sunscreens used should be broad-spectrum and have an SPF of at least 30, though the American Dermatological Association recommends those with an SPF of 40 and above.
Secondary protection refers to having frequent checkups of the skin to detect any premalignant changes, as well as using retinoids to thicken the epidermal layer, antioxidants such as topical and oral vitamin C preparations or coenzyme Q 10, or estrogens.
Tertiary prevention is the term used to treat an existing skin condition caused by photodamage by various techniques such as microdermabrasion, laser resurfacing, dermal fillers to augment the skin and chemical peels. Broken veins are treated by: