The most important building block in anti-aging skin is protection against UV radiation and now also against environmental pollutants. Topical preparations can slow down skin aging, help repair cellular damage and promote the formation of new collagen. Currently, the focus is on irregular pigmentation, which makes people appear ten years pre-aged.

Like every organ, the skin ages. The genetic ageing of the skin and its natural hormonal status cause what is known as intrinsic skin ageing. Self-determined influencing variables and external influences lead to extrinsic skin ageing. These include environmental factors such as UV radiation, smoking, diesel soot and exhaust fumes, nutrition and lifestyle.

Histological, biochemical and molecular-biological investigations have shown that UV-induced, i.e. extrinsic skin aging has different pathophysiological processes than normal aging. However, environmental factors and intrinsic skin aging add up and together form the picture of aging skin.

Characteristics of the aging skin

The aging skin is atrophic, the height of the interlocking from upper to lower skin flattens. The cell layers of the epidermis are 15 percent thinner, mitotic activity is reduced. The cell volume of the keratinocytes is reduced, while the corneocytes are larger. The intracellular calcium concentration is reduced. Melanocytes and Langerhans cells are reduced. The physical barrier recovers more slowly after exogenous noxae, as does the pH gradient.

The natural moisturizing factors (NMF) also decrease. The lipids in the stratum corneum show a changed ceramide composition and the lipid content is reduced in relation to the water content, which influences permeability. Since the stratum corneum becomes rigid and rigid, the transepidermal water loss is rather lower and the barrier function is increased.

Two UV-related skin cancer types: above lentigo-maligna melanoma on the chin (safety distance for excision marked with a black felt tip pen), below a spinalioma on the cheek.

However, although the lipid content of the aging skin is reduced, highly lipid-soluble substances such as testosterone and estradiol can be absorbed well. In contrast, for relatively hydrophilic substances such as benzoic acid and acetylsalicylic acid, the average absorption time is longer for aging skin. A possible increased passage effect of irritants, for example acids, alkalis and emulsifiers, through the skin appendages is discussed (4). Table 1 shows factors of cellular senescence and their consequences.

One of the most important drivers of extrinsic skin aging is UV light. It not only induces benign changes. The WHO added natural and artificial UV radiation to the list of carcinogenic rays in 2009.

Carcinogenic effects of UV radiation

According to the data available, UVB is responsible for actinic keratoses, which frequently occur in UV-exposed parts of the body and which are considered precancerous, as precancerous stages of spinalioma (epithelial skin tumor). The actinic keratoses can be recognized by crusts on a reddened ground, which loosen again and again, hurt and bleed.

The so-called white skin cancer has a potential metastasis risk of about 2 percent. In black skin cancer, the malignant melanoma, UV radiation is a co-factor, but only in certain types, especially in lentigo maligna melanoma. This melanoma of the elderly occurs in UV-exposed parts of the body such as the forehead, temples, cheeks, back of the hand and forearms.

UVA radiation is also thought to have carcinogenic potential at higher doses. Compared to UVB, long-wave UVA penetrates deeper and promotes skin ageing through various effects on mitochondria, fibroblasts and collagen-building enzymes as well as the formation of free oxygen radicals in the dermis.

With the help of electron spin resonance, the amount of free radicals triggered by UV radiation can be determined. A certain amount of free radicals is necessary, also for vitamin D formation. It is below the individual erythema threshold, i.e. below the UV dose at which a slight reddening of the skin occurs, as in the case of incipient sunburn. Too much UV radiation generates free radicals with cell-damaging effects and lipid peroxidation (2). The term critical radical concentration was coined for this purpose.

At the molecular level, UV radiation triggers DNA damage, which is partially repaired by repair enzymes (DNA repair). In melanoma patients, it was found that damage is also found in the genomic DNA and not only on the transcribed DNA sections.

UVB predominantly induces cyclobutane-pyrimidine dimers and 6-4-photoproducts (false bridges between nucleic acids), while UVA causes oxidative damage in the form of 8-oxoguanine. For these damages the organism possesses nuclear repair enzymes: for the two typical UVB damages the nucleotide excision repair and for the 8-oxoguanine the base excision repair. UVB can also trigger oxidative stress (to a lesser extent than UVA). There is therefore no strict separation between UVA and UVB effects.

DNA repair is subject to an ageing process. This favours the development of tumours on the basis of UV damage.

Damage to the development regulator Notch, which controls the maturation of stem cells depending on the environment and tissue, favours “field cancerisation”, i.e. multiple actinic keratoses and spinaliomas that occur over large areas. In pathogenesis, besides UVB effects, the chronic inflammatory dermal UVA-induced process is also increasingly important because inflammation – and a UV erythema (sunburn) is an inflammation – can be locally carcinogenic.

Since spinaliomas can develop from field cancerization, early and extensive therapy is obvious. Anti-inflammatory local therapies with diclofenac/hyaluronic acid, cytotoxic plant extracts such as ingenol mebutate, immune-stimulating preparations with imiquimod or topical 5-fluorouracil as well as photodynamic therapy have been tested in studies.

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