SKIN CARE


TABLE 1: RETINOID USES IN COSMETIC AND DERMATOLOGICAL SKIN CARE TREATMENTS Retinoids


Functions/mechanism of action Retinol (all-trans retinol)


Retinoic acid (all-trans retinoic acid, tretinoin)


Retinyl esters (retinyl acetate and palmitate)


Retinaldehyde


Adapalene (naphthalenecarboxylic acid)


Tazarotene


Inhibits collagenase and MMP expression; stimulates collagen type 1 and GAG synthesis


Stimulates the process of epidermal cell proliferation, accelerates the elimination of sebum remaining in ducts, therefore reducing inflammation in sebaceous glands; loosens connections among cells in stratum corneum and inhibits keratosis


First converts to retinol by cleavage of the ester bond, then con- verts into retinoic acid, stimulates the epidermal cell proliferation, regulates the sebum


First oxidises to retinoic acid by retinaldehyde dehydrogenases (e.g. RALDH2) or some enzymes of the CYP family and then stimulates the epidermal cell proliferation


Changes gene expression and mRNA synthesis; a strong


modulator of keratinisation of hair follicle cells, modifies keratinocyte metabolism, increases their proliferation, and thus has a keratolytic effect


Receptor-specific retinoid regulates down markers of keratinocyte differentiation, keratinocyte proliferation and inflammation


of living (nucleated) cells that are constantly producing new cells) as well as to a small extent, into the dermis and marginally to the subcutaneous tissue. In the case of retinol applied topically,


there is an interaction with specific nuclear receptors. Retinol makes the connections between epidermal cells more loose and facilitates keratosis. What is more, it enhances epidermis turn-over and accelerates proliferation of the basal layer of epidermal cells and the stratum corneum. In keratinocytes, proliferation AP-1 transcription factor, exposed to various stimulants, growth factors and cytokines, plays a major role. In retinol-treated aged human skin, AP-1 complex is comprised of c-Jun/c-fos and c-Jun transcription factor was increased.13


elastin fibres) and promotes angiogenesis.14 Some studies indicate that retinol also enhances production of elastin fibres.15 Moreover, the retinol inhibits matrix MMPs and enhances synthesis of tissue inhibitors of MMPs (TIMPs).16 Changes within collagen and elastin fibres


Due to the fact that retinoids


exert anti comedogenic effects, they regulate the process of shedding within sebaceous glands ducts. Most importantly, retinoids decrease activity of enzymes participating in lipogenesis and block differentiation and cellular divisions of sebocytes.13


Moreover,


they reduce discoloration of the skin, reduce its pigmentation by about 60% and contribute to a proper distribution of melanin in the skin. Topically applied retinoids also influence the function of melanocytes, providing regular arrangement of melanin in the epidermis. They also block transport of melanin to epidermal cells and diminish the activity of stimulated melanocytes. An increase in the synthesis and activity of tyrosinase, disturbances in subsequent steps of melanogenesis or a decrease in the number of melanocytes is related to inhibition of melanogenesis. Retinoids are also commonly known as


biologically active anti-ageing molecules. Retinol stimulates fibroblasts to synthesise collagen fibres (stimulates the activity of fibroblasts and increases their number), improves skin elasticity (removes degenerated


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are associated with photoageing. It leads to occurrence of wrinkles and loss of the skin firmness and elasticity. Collagen fibre atrophy is caused by an increased expression of collagenases (MMP-1), gelatinases (MMP-2) and stromelysin-117, as well as enhanced expression of elastase and MMP-9 associated with degradation of elastin fibres. Retinol counteracts the development of pre- cancerous conditions as a result of hampering the activity of atypical cells, which has been proved by the results of studies.18


ECM-


producing cells in the skin are activated by retinol and cause its production in the aged skin. The activation of fibroblast production is stimulated through TGF-β/connective tissue growth factor (CTGF), including immunostaining of TGF-β1, which is the regulator of ECM homeostasis, is increased by retinol.19


secreted by the skin, retinoids reduce the tendency to form blackheads.20


Acne, inflammation, excessive keratosis


Acne vulgaris, psoriasis, chronically photodamaged skin, photoprotection from sunlight


bioactive form among retinoids applied topically to the skin. Tretinoin increases the epidermal cellular turnover, it also causes dispersion of melanin granules. Its inhibition of MMPs results from blocking AP-1, not upregulating TIMP1. The most commonly used tretinoin concentration in anti-acne therapy varies from 0.01% to 0.4%. It comes in the form of gel or cream applied topically. Retinoic acid may have different formulas: gel (0.01%, 0.25%), cream (0.025%, 0.05%, 0.1%), new technology microspheres (0.04%, 0.1%), solution (0.05%), and emollient (0.05%).22 Retinol is most frequently used in


By reducing the amount of sebum Excessive


degradation of the stratum corneum and keratosis of hair follicles is associated with vitamin A deficiency. Regulation of secretion within sebaceous gland ducts make retinoids produce an anticomedogenic effect. Retinoids decrease the activity of enzymes participating in lipogenesis. Moreover, they block cellular division of sebocytes and differentiation.21


are widely used externally in the treatment of acne, psoriasis, excessive dryness, skin keratosis and hair and nail disorders.14,21


Application in cosmetology & dermatology Tretinoin (all trans-retinoic acid) is the most


cosmeceutical treatment. It is very stable in product formulations and well tolerated. It provides better effects than retinoic acid applied in equivalent doses. Retinoic acid is approximately 20 times more powerful than retinol. Firstly, retinol is converted to retinoic acid through a two-step oxidation process. Retinol has an ability to bind to the retinoic acid receptors. The process begins when free retinol is combined with a specific cytoplasmic protein that binds retinol. The resultant complex is a substrate for retinol dehydrogenase, an enzyme that catalyses the conversion of retinol to retinaldehyde. Retinaldehyde is oxidised to retinoic acid by retinaldehyde oxidase.24 Retinol is known to improve the skin texture, dyspigmentation, dryness and fine lines. The optimal concentration to balance the skin irritation against effectiveness has not been determined. Retinol concentration in the cosmetic product is between 0.0015% and 0.3%.25 Retinal is the aldehyde formulation of


They


vitamin A, i.e. the oxidised form of retinol. It is used in cosmeceuticals; however, its efficacy in the skin treatment is limited. Similarly, to retinyl esters, it is a stable derivative of vitamin A but it only mildly improves wrinkles and the skin texture. As compared to retinoic acid, it is less irritating and well tolerated. It is used to improve signs of photoageing.26


October 2021 PERSONAL CARE


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Application in cosmetic & dermatological treatment Anti-wrinkle treatments, improvement of


texture, dyspigmentation, dryness, and fine lines


Acne, psoriasis, chronic inflammation of hair follicles and sebaceous glands


Antioxidant, wrinkles, stabilising properties Stabilising properties, wrinkles, texture


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