Aging and photoaging

They say that the legendary Coco Chanel introduced the tanning trend to Parisian women when, returning from a Mediterranean cruise, she amazed the pale Parisian beauties with her bronze tan. Soon, the capricious fashion made a 180° turn, and ladies who had previously never left home without wide-brimmed hats, long gloves and veils, went to the beaches, where at first timidly, and then more and more boldly, they bared their bodies, exposing them to the hot rays of the sun.

According to another theory, the fashion for tanning appeared when pale skin became associated with hard work in closed factories and plants, and tanning became a privilege of those who could afford to spend a lot of time in the fresh air, relaxing and playing sports. Be that as it may, in almost all European countries and in America, tanning turned into a symbol of health and an active lifestyle, and therefore many people, especially at a young age, lay under the scorching rays of the sun until they got burnt and dizzy, trying to get it.

In America, the generation that became so actively friends with the sun was the generation of people born during the post-war baby boom in the 40s and 50s, or the baby boomers. As the years went by, doctors began to notice that the aging of the baby boomers' facial skin had its own characteristics - sharp wrinkles, unevenness, bumpiness of the skin, pigment spots, the presence of areas of thickened flaky skin and branches of dilated vessels on the cheeks. Such changes were found only in areas exposed to increased sun radiation, while in places usually protected from the sun (for example, the lower abdomen, inner thighs, etc.), the skin, as a rule, looked much better. It took careful research before doctors came to a unanimous conclusion - not age, but solar radiation was responsible for the appearance of these signs. As it turns out, UV radiation, although not as destructive as ionizing radiation, still has enough energy to cause damage to DNA and other skin molecules.

Currently, the following signs of sun damage to the skin, or photostosis, are distinguished:

• wrinkles that appear in areas of damaged collagen;
• unevenness of the skin that occurs in areas where atypical elastin accumulates (solar elastosis);
• dry skin;
• dilation of superficial vessels (telangiectasia);
• pigment spots (solar lentigo);
• actinic, or solar, keratosis (patches of reddish, thickened, flaky skin).

Photoaging is most often observed in fair-skinned people over 50 years of age, while it is less common in people with dark skin. The concept of photoaging has revolutionized cosmetology. Before that, scientists believed that it was impossible to prevent aging or rejuvenate aged skin, and that all attempts to create products that smooth out wrinkles or restore the skin's youthful glow were doomed to failure. It turned out that sun-damaged skin retains a reserve of vitality that can be awakened. A number of products and methods have now been developed that can partially eliminate the signs of photoaging. Although they are all advertised as "anti-wrinkle" or "anti-aging" products, it is important to understand that in this case we are not talking about true rejuvenation, but about "treatment" (or rather, restoration) of sun-damaged skin.

By now, extensive information has been accumulated about the negative impact of ultraviolet radiation on the skin. The spectrum of ultraviolet radiation is represented by three groups of rays.

• Ultraviolet rays C (UVC, short UV, far UV) - rays with the shortest wavelength (100-280 nm). They have the most damaging effect on the human body. However, their impact is minimal, since they are adsorbed by the ozone layer and practically do not reach the earth's surface
• Ultraviolet rays B (UVB, mid UV) are rays with a medium range of wavelengths (280-320 nm). They damage the skin to the maximum, but their effect is significantly weakened by cloudiness, and penetration is delayed by clothing and ordinary window glass. Adsorption and dispersion of UVB in the atmosphere is observed when the sun is low on the horizon (early morning and late evening), at high latitudes, and in winter.

The lowest absorption and scattering of these rays is observed at midday, at low latitudes and in the summer.

• Ultraviolet rays A (UVA, long UV, near UV, black light) - rays with the longest wavelengths (320-400 nm) The damaging effect of UVA is 1000 times weaker than UVB. However, they reach the earth's surface much better, and their penetration does not depend on the time of day, latitude and season. It is known that these rays are not retained by the ozone layer, penetrate through clouds, clothes, and untinted window glass. That is why many modern buildings use tinted glass, which is not only a certain architectural and aesthetic solution, but also a factor of protection from UVA.

The source of ultraviolet radiation is not only the sun, but also solarium lamps. It is believed that gas-discharge lamps can produce a small share of ultraviolet radiation. As for daylight lamps andhalogen lamps, TV screens and computer screens, they are not sources of ultraviolet radiation. It is important to remember that white sand, snow and water reflect up to 85% of solar radiation. Therefore, when on the beach or in the mountains, a person receives almost twice as much energy due to the reflection and scattering of rays.

Ultraviolet rays A and B differ in the depth of penetration into the skin - it is directly proportional to the wavelength. It is known that 90% of UVB are blocked by the stratum corneum, while UVA are able to penetrate into the deeper layers of the epidermis and more than 50% of them can get into the papillary and reticular layers of the dermis. This is why, when exposed to B rays, changes occur in the epidermis, and when exposed to A rays - structural changes in the main substance of the dermis, its fibrous structures, microcirculatory bed and cellular elements.

The mechanisms of action of ultraviolet rays on the skin and their consequences are well studied. It is known that UVC has a pronounced mutagenic effect. UVB causes sunburn, partly, suntan. The main negative effect of UVB is proven carcinogenesis, which is induced due to cell mutations. Ultraviolet rays A cause skin pigmentation, i.e. suntan. These rays are the least erythemogenic, which is why this spectrum of ultraviolet radiation is presented in solarium lamps. UVA, as well as UVB, cause carcinogenesis, while the potentiating effect of A rays on B rays is known. Some researchers believe that A rays play a greater role in the development of melanoma than B rays. In this regard, it is necessary to emphasize the importance of using sunscreens from the action of A and B rays simultaneously.

The combined effect of ultraviolet rays on the skin includes a number of morphological changes. Thus, the effect on the proliferation and differentiation of keratinocytes, fibroblasts, melanocytes (stimulation of alteration of cellular elements, disruption of DNA reparation) is known. It has been proven that the combined effect of rays A and B leads to a number of serious violations of local immunological surveillance. In particular, the production of a number of immunosuppressive cytokines in the skin (for example, IL-10), a decrease in the number of killer lymphocytes involved in the elimination of tumor cells, the appearance of CD8 lymphocytes stimulating the apoptosis of Langerhans cells, the induction of trans-cis isomerization of urocanic acid in the epidermis (an endogenous component that is credited with an immunosuppressive effect) have been recorded. In addition, UVA is the main cause of the development of photosensitivity. Most dermatoses associated with increased congenital or acquired sensitivity to ultraviolet radiation arise or worsen when exposed to the long-wave spectrum. Such dermatoses include photoallergic reactions, porphyria, solar urticaria, lupus erythematosus, pigment xeroderma, and other diseases.

It should be especially emphasized that ultraviolet A rays are associated with a type of skin aging - photoaging. It is characterized by certain morphological manifestations that differ from biological aging. Under the influence of UVA, uneven thickening of the stratum corneum and the epidermis itself as a whole occurs in the epidermis due to uneven acceleration of basal keratinocyte proliferation and disruption of keratinization processes. Dysplasia of keratinocytes develops. Chronic inflammation is formed in the dermis, fibrous structures are destroyed, primarily elastic fibers (homogenization, thickening, twisting and fragmentation of elastic fibers, a decrease in their diameter and number - "solar elastosis"), serious changes in small-caliber vessels occur. The latter subsequently leads to restructuring of the microcirculatory bed and the formation of telangiectasias.

It is known that prolonged exposure to UVA, such as excessive use of solariums, causes structural changes in the skin similar to prolonged sun exposure. It is appropriate to emphasize the importance of dosed use of solariums.

There are acute and chronic ultraviolet exposures, which cause different clinical manifestations.

Clinical signs of acute ultraviolet exposure include sunburn and skin pigmentation. Sunburn is a simple dermatitis and manifests itself as erythema and edema (1st degree) or erythema and blistering (2nd degree). A 3rd degree burn is extremely rare, mainly in infants, and is accompanied by heat shock. It is believed that a 1st degree sunburn can occur if a person has received 4 minimum erythemal doses within 24 hours, and a 2nd degree sunburn - 8. Pigmentation, or sun tan, can be immediate or delayed. Instant darkening of the skin occurs a few minutes after insolation and is associated with photooxidation of already synthesized melanin and its rapid redistribution into the dendrites of melanocytes and, subsequently, into epidermal cells. Delayed pigmentation occurs after 48-72 hours and is associated with active melanin synthesis in melanosomes, an increase in the number of melanocytes, and activation of synthetic processes in previously inactive melanocytes. These changes reflect the protective properties of the skin in response to ultraviolet radiation. Delayed pigmentation can also be explained by the formation of secondary post-inflammatory pigmentation as a result of simple dermatitis or a burn.

Clinical signs of chronic exposure to ultraviolet radiation are as follows: vascular changes, pigmentation disorders, skin neoplasms, changes in turgor, elasticity, and skin pattern. Vascular changes resulting from chronic exposure to UVR are represented by persistent diffuse erythema, formation of telangiectasias, ecchymosis in areas most susceptible to radiation (face, hands, parietal and occipital regions, back of the neck, etc.). Pigmentation disorders manifest themselves as freckles, solar lentigo, dyschromia, chronic guttate idiopathic hypomelanosis, and poikiloderma. This complex of clinical manifestations, along with signs of photoaging, is called "sun-damaged skin" in the English-language literature. Excessive UVR is most often associated with the development of such skin neoplasms as actinic keratosis, basalioma, squamous cell carcinoma, and melanoma.

Changes in skin turgor, elasticity and pattern are the basis for photoaging. Clinically, photoaging is manifested by dry skin, its rough, emphasized skin pattern, decreased turgor and elasticity of the skin. The consequence of these changes are small superficial and deep wrinkles. In addition, with photoaging, a yellowish tint of the skin, dyschromia, lentigo, telangiectasia, seborrheic keratoses, comedo senilis are noted. It is noteworthy that the complex of changes in the skin associated with chronic exposure to UFO was well described in dermatology at the beginning of the last century (for example, "sailors' skin", "peasants' skin", "rhomboid atrophy of the neck", Favre-Racouchot disease, etc.).

When assessing the nature of age-related skin changes, it is important to consider the type of aging. Morphological and clinical signs of photoaging have their own characteristic picture, which differs from that of other types of aging.

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