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Therapy

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<hr />Lesya Andriutsa , cosmetologist, dermatovenerologist, Medicum clinic, trainer at the JES cosmetology training center<hr /> Modern sunscreens are presented on the market in such quantities that even an experienced specialist sometimes finds it difficult to assess the effectiveness and safety profile of the prescribed drugs. And since this year the insolation season will last for a certain part of our patients who are not easily able to tolerate quarantine and will go on vacation after some hot countries open their borders, I propose to figure out which products are more relevant for sun protection. And how we, dermatocosmetologists, can help a client with existing signs of skin photoaging. Types of UV filters The effectiveness of sunscreens depends on their composition: chemical and (or) physical UV filters. Chemical UV filters provide skin protection by absorbing UV radiation, and physical ones by reflecting, scattering and absorbing it (depending on the size of the filter particles). Physical UV filters are mineral pigments that, at wavelengths above 400 nm, have reflective and scattering effects, and at wavelengths less than 400 nm, in addition to those described above, the effect of energy absorption is also predominant. The following macropigments are most often used in their production: titanium dioxide, zinc oxide, iron oxide, calcium carbonate, talc, koalin, mica [1]. The protective ability of these pigment particles in a cosmetic product depends on the number and size of the molecule, the ratio of the refractive indices of light at the interface of the pigment and the environment, as well as the wavelength of the emitted light and the amount of light absorption. Macropigments, when present in large quantities in a sunscreen, give a whitish effect on the skin, which makes it difficult to use them in daily cosmetic practice. Modern technologies make it possible to grind titanium dioxide or zinc oxide to the nanometer range (1-100 nm), which leads to a decrease in their reflective and scattering ability in the visible range and a shift to the UV range [2]. The use of micropigments in emulsions and other forms of sunscreens eliminates unwanted whiteness. However, not all micropigments can be used in the production of external cosmetics due to the ability to penetrate the transepidermal barrier and accumulate in the body, and the possible photoreactivity of these molecules can lead to damage to keratinocytes [3]. Titanium dioxide using Nano-TIO 2 technology has been approved as an acceptable safe composition of sunscreens. Unlike the nanomolecule, titanium dioxide produced in the form of Aeroxide-P25, “Nano-TIO 2” has a particle size of at least 25 nm, a rutile form, and to reduce photoreactivity, the surface of the molecule is coated with silicone or aluminum [4]. It is also necessary to take into account the amount of silicone in a sunscreen product, since it can have an occlusive effect, which is undesirable for use by persons with increased oily skin and inflammatory dermatoses [5]. International studies indicate a minimal percentage of nanoparticles entering the biological tissues of the body when applied topically to the skin. The risk of this accumulation increases with the use of aerosol and powder forms of sunscreens in alveolar tissue, therefore, for greater safety, the use of these products is not recommended by the Scientific Committee on Consumer Safety (SCCS) [6]. The concentration of titanium dioxide in sunscreens that is safe for the body is limited to a concentration of 25% [7]. SPF Range The range of sun protection factors in cosmetics is quite wide - from 10 to 100. However, the SPF value only indicates the degree of protection against sunburn, but does not prevent immunosuppression, induction of skin cancer and photoaging. This fact prompted the US Food and Drug Administration (FDA) to introduce changes in the concept of the definition of “sun protection factor” in 2007, limiting the maximum protection to 50 and prohibiting the use of sunblocker or sunbloc labels on the product [8]. This is because using SPF 70 or higher may lull the consumer into a false sense of security, although modern manufacturing methods can produce sunscreens with SPF 100 or higher. Drugs with maximum sun protection belong to a group of medications that are sold without a prescription and are used in dermatology for the treatment of photodependent dermatoses (erythematous lupus, etc.) [4]. For example, the well-known Echte sunblocker paste (which contains 20% zinc oxide or 20% titanium oxide with the addition of 1% iron oxide), having a high degree of protection, cannot be used in cosmetology due to its rich color and thick consistency, which makes it difficult to distribute it over a large area of the skin [9]. <img alt="" src="https://pro.bhub.com.ua/cosmetology/upload/files/m2.jpg" style="width: 1200px; height: 800px;" /> Correct Application The application of sunscreen should be constant and long-term, since cell damage from ultraviolet radiation has a cumulative effect. The composition of these products must be effective, safe and protect the skin from exposure to rays of different lengths. Therefore, the priority for the consumer will be those products that are labeled with UVB/UVA protection [5]. The details of sunscreen application are very important to its effectiveness. Until now, many conflicting arguments on this matter can be found in the instructions for use and various advisory publications. Chemicals must be absorbed into the skin. Therefore, it is recommended to first apply SPF, then a moisturizing care component. But there are also supporters of the theory, which indicates the need to first moisturize the skin, allow the product to be completely absorbed, and only then apply sunscreen. There are much more like-minded people in this step-by-step application of skincare products, because it has been proven that a moisturizing component applied to SPF reduces the concentration of sunscreen, thereby affecting its effectiveness [1,6]. Experts have a clear opinion regarding the use of sunscreens with mineral components, because their main purpose is to reflect solar radiation, so they should be applied as the last step in care. A good solution that depreciates all disputes and contradictions is a multifunctional product that contains care and sun protection components. Although the most important rule for using sunscreen is to apply it 20 minutes before the expected sun exposure and add it to the skin every 2 hours [7]. Photodamage to the skin But if the rules of ultraviolet protection are not followed, photodamage occurs with changes in the epidermis, dermis and blood vessels of the skin. The process of photoaging is characterized by clinical, biochemical and histological signs that have clear differences from the chronological aging of those areas of the skin that are protected from exposure to ultraviolet rays. Thickening of the stratum corneum is observed when photodamage processes begin and its thinning with prolonged exposure [6]. A tendency towards reduction of epidermal outgrowths and degradation of the basement membrane, a decrease in the number of Langerhans cells, atrophy of the extracellular matrix, increased angiogenesis and a decrease in the number of collagen fibers are also observed. An integral part of photodamage to the skin is an increase in melanin synthesis with an uneven distribution of melanocytes, and less commonly, the presence of atypical melanocytes [10]. These processes during photodamage to the skin are determined by the presence of hereditary and environmental factors. The first mainly includes the skin phototype, or rather its natural protection from UV radiation, and the environmental ones include ultraviolet radiation itself (UVA and UVB ranges.) Clinically, photodamage manifests itself in the form of xerosis, actinic elastosis, dermal creases and the development of various skin neoplasms (seborrheic or actinic keratosis, etc.), hyperplasia of the sebaceous glands, as well as vascular pathologies, including telangiectasia, purpura and venous lakes [7]. However, dyschromia is the most common consequence after active insolation and manifests itself in the form of hyperpigmentation (solar lentigo, melasma, chloasma), rarely - hypopigmentation. Often, at an appointment, a dermatocosmetologist has to differentiate UV-induced hyperpigmentation from genetically determined pathologies that are associated with an increase in the number of melanocytes (Peutz-Egers syndrome, lentiginosis, Leopard syndrome) and conditions that are characterized by an increased content of melanin in the skin (neurofibromatosis, ephelides, etc. ). Some endocrine and metabolic diseases can also lead to increased melanin synthesis in the skin: Addison&#39;s disease, ACTH and MSH-producing tumors, ACTH or estrogen therapy, Pellagra, pregnancy, intestinal malabsorption. Hyperpigmentation is also a side effect of ionizing radiation against the background of oncopathology, a manifestation of toxic melanosis (Habermann-Hoffmann melasma, Siwatt poikiloderma) [2, 5]. But, despite the variety of causes leading to this pathology, in most cases, hyperpigmentation develops against the background of skin damage as a result of ultraviolet radiation (solar, senile lentigo) and increased melanin synthesis by UV rays against the background of endocrine pathology (melasma, chloasma). Everyone knows the complex mechanism of pigment formation, the most important of which is the stage of conversion of tyrosine into DOPA under the influence of tyrosinase. Reducing the appearance of pigmentation can be achieved by suppressing the synthesis of tyrosinase by inhibiting the pigment itself, as well as by acting on DOPA-chromium tautamyrase, which promotes the transition of chromium into melanin precursors. These effects can be achieved through the use of mesotherapy cocktails, which include aminoethylphosphinic acid, vitamins C and B3. The main properties of these components are based on the normalization of the tyrosinase synthesis process, anti-inflammatory and lightening effects. Omega (3, 6 and 9), quercetin, and some components from the group of polyphenols (for example, galic and chlorogenic acids) also remain indispensable in solving this problem [1]. An important stage in the treatment of hyperpigmentation is the elimination of pigment accumulation in the epidermal layer of the skin. The choice of method for this treatment is based on the level of social activity of the client, the existing phototype and the regenerative ability of the skin. For this purpose, chemical peels (phenolic, TCA, resorcinol, retinoic acid or retinol, thioglycolic, phytic and mandelic acids), hardware abrasion (carbonic, laser), microdermabrasion, BBL and IPL therapy are successfully used [11]. To provide a cytostatic effect on melanocytes, topical hydroquinone is used in a concentration of 1% to 4%. In addition to a wide range of well-known contraindications, this component has some application features. Due to the photosensitivity of hydroquinone, it should be applied at night with additional use of sunscreen during the day. The duration of therapy with topical hydroquinone at a concentration of more than 3% should not exceed 6 months, as there is a risk of developing atrophies and unwanted persistent dyschromia in the form of alternating hyper- and hypopigmentation of the skin [5]. To inhibit tyrosinase, inhibit the synthesis of the DOPA-chromium tautomerase enzyme, normalize the distribution of melanosomes, suppress the synthesis of endothelin-1, and the keratolytic effect in products for daily topical application, the necessary components are: ginthesic acid, plant extracts (mulberry, lemon, licorice, etc.), azelaic acid acid, aloesin, N-acetycysteine, arbutin, aminoethylphosphinic, kojic and retinoic acids [4, 7]. <img alt="" src="https://pro.bhub.com.ua/cosmetology/upload/files/m1.jpg" style="width: 500px; height: 683px;" /> Facial skin melasma as a result of photodamage in a 28-year-old patient However, an important step when working with a client who suffers from UV-induced hyperpigmentation is not only the correct treatment protocol, choosing home care and explaining the importance of using sunscreens. It is necessary to explain to him the specifics of the development of the pathology and its tendency to become chronic, since the patient’s inflated expectations are a frequent reason for false, but so convincing conclusions about the complete ineffectiveness of the therapy. Literature: 1. Bosset S., Barre P., Chalon A., Kurfurst R., Bonte F., Andre P., Perrier P., Disant F., Le Varlet B., Nicolas JF Skin aging: clinical and histopathological study of permanent and reducible wrinkles. Eur J Dermatol 2002; 12: 247-52. 2. Bulletin of Dermatology and Venereology 58 No. 5, 2014 1. Zins JE, Moreira-Gonzalez A. Cosmetic procedures for the aging face. Clin Geriatr Med 2006; 22: 709-28. 3. Webster GF Common skin disorders in the elderly. Clin Cornerstone 2001; 4: 39-44. 4. Berneburg M., Plettenberg H., Krutmann J. Photoaging of human skin. Photodermatology, Photoimmunology &amp; Photomedicine 2000; 16: 239-44. 5. Berneburg M., Gattermann N., Stege H., Grewe M., Vogelsang K., Ruzicka T., Krutmann J. Chronically ultraviolet-exposed human skin shows a higher mutation frequency of mitochondrial DNA as compared to unexposed skin and the hematopoietic system. Photochem Photobiol 1997; 66: 271–5. 6. Yano K., Kadoya K., Kajiya K. et al. Ultraviolet B irradiation of human skin induces an angiogenic switch that is mediated by upregulation of vascular endothelial growth factor and by downregulation of thrombospondin-1. Br J Dermatol 2005; 152: 115-21. 7. Ravanat JL et al. Direct and indirect effects of UV radiation on DNA and its components. J. Photochem. Photobiol. B 2001, 63. 8. Courdavault S. et al. Repair of the three main types of bipyrimidine DNA photoproducts in human keratinocytes exposed to UVB and UVA radiations. DNA Repair 2005; 4: 836–844. 9. Grether-Beck S., Oliazola-Horn S., Schmitt H., Grewe M., Jahncke A., Johnson JP, Briviba K., Sies H., Krutmann J. Activation of transcription factor AP-2 mediates ultraviolet A radiation- and singlet oxygen-induced expression of the human intercellular adhesion molecule-1 gene. Proc Natl Acad Sci USA 1996; 93: 14586–91. 10. Xu Y., Shao Y., Voorhees JJ et al. Oxidative inhibition of receptortype protein-tyrosine phosphatase kappa by ultraviolet irradiation activates epidermal growth factor receptor in human keratinocytes. J Biol Chem 2006; 281: 27 389–97. 11. Levine RL, Stadtman ER Oxidative modification of proteins during aging. Exp Gerontol. 2001 Sep; 36 (9): 1495–502. 12. Berneburg M., Grether-Beck S., Kurten V., Ruzicka T., Briviba K., Sies H., Krutmann J. Singlet oxygen mediates the UVA-induced generation of the photoaging-associated mitochondrial common deletion. J Biol Chem 1999; 274: 15 345—9. First published: Cosmetologist No. 3-4, 2020

Treatment of photodamaged skin and selection of sunscreens