FOTOENVEJECIMIENTO FACIAL PDF

Nejin No toda la piel es igual y hay zonas que necesitan un cuidado especial. Hence, in addition to the epidermal faclal, the dermal layer will also be damaged. Tretinoin is also efficacious for the treatment of acne. The major methods of sun protection are sunscreen products, sun protective clothingand reducing exposure to the sun, especially during peak sun hours 10 AM-4PM in the spring and summer seasons. With vitamin E that contributes to the antioxidant and regenerative action of the fotoenvejecikiento. Treatments for skin imperfections.

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Effects of UV light[ edit ] Molecular and genetic changes[ edit ] UVB rays are a primary mutagen that can only penetrate through the epidermal outermost layer of the skin, resulting in DNA mutations. These 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. Upon exposure to UVB rays, melanocytes will produce melanin , a pigment that gives the skin its color tone.

However, UVB will cause the formation of freckle s 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. Hence, in addition to the epidermal layer, the dermal layer will also be damaged. 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.

However, with constant UVA exposure, the size of the dermis layer will 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.

Pigmentation[ edit ] UV exposure can also lead to inflammation and vasodilation which is clinically manifested as sunburn. This then attract neutrophils which lead to an increase in oxidative damage through the generation of free radicals. Additionally, UV radiation would cause 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 neoplasm s. Immunosuppression[ edit ] It has been reported that UV radiation leads to local and systemic immunosuppression, due to DNA damage and altered cytokine expression.

This has implications in cutaneous tumor surveillance. The Langerhans cells may undergo changes in quantity, morphology, and function due to UV exposure and may eventually become depleted. One proposed explanation for this immunosuppression is that the body is attempting to suppress an autoimmune response to inflammatory products resulting from UV damage. MMP-1 is a major metalloproteinases for collagen degradation. This entire process is aided by the presence of reactive oxygen species that inhibits protein-tyrosine phosphatases via oxidation, thereby resulting in the up-regulation of the above-mentioned receptors.

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. In addition, the presence of damaged collagen would also down-regulate the synthesis of new collagen. The impaired spreading and attachment of fibroblasts onto degraded collagen could be one of the contributing factors to the inhibition of collagen synthesis. Retinoic acids and photodamage[ edit ] UV radiation decreases the expression of both retinoic acid receptors and retinoid X receptors in human skin, thereby resulting in a complete loss of the induction of RA-responsive genes.

It also leads to an increase in activity of the AP-1 pathway, increasing MMP activity and thus resulting in a functional deficiency of vitamin A in the skin. Signs, symptoms and histopathology[ edit ] Early symptoms of photoaging: Dyspigmentation, the formation of wrinkle s and other symptoms appear around regions of skin commonly exposed to sun, mostly the eyes, mouth and forehead.

Telangiectasias spider veins most commonly seen around the nose, cheeks and chin. Skin becomes leathery and laxity occurs. Solar lentigines age spots appear on the face and hands. Possibly pre-cancerous red and scaly spots actinic keratoses appear. Cutaneous malignancies In addition to the above symptoms, 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.

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