DermNet provides Google Translate, a free machine translation service. Note that this may not provide an exact translation in all languages
Skin changes with age. Some of this is intrinsic and some is extrinsic ageing due to environmental exposure, mainly photoageing. Smoking and other pollutants also age the skin, causing delayed healing after injury and enhancing facial lines.
Intrinsic ageing results in thinning of the epidermis and dermis, structural defects and immunological failure. These features are exaggerated in photo-aged skin, accompanied by lines, colour changes and neoplasia.
Photoageing is due to the effects of ultraviolet radiation (UVR) on the skin. The influence of visible light or infrared radiation is comparatively minor unless thermal burns arise.
UVR is arbitrarily split into UVC (200-290 nm), UVB (290-320nm) and UVA (320-400nm). UVA is further divided into UVAI (340-400 nm) and UVAII (320-340 nm). Solar UVC does not pass through the ozone layer so is not present on the earth's surface.
UVR is at its greatest on the earth's surface when the sun is vertically overhead as it passes through thinner atmosphere than when the sun is at a greater angle. Thus:
There is also greater total UV:
Variation is greater for UVB than for UVA.
The global solar ultraviolet index (UVI) describes the level of solar UVR at the Earth's surface and ranges from 1 to 11+.
UVR causes biological effects on various tissues when it is absorbed. Injury to nucleic acids results in abnormal structures such as cyclobutane dimers and adducts. There are several repair mechanisms in normal individuals but their malfunction results in the development of aging changes and skin cancer.
The acute response of the skin to exposure to UVR has rapid onset (minutes to days) and short duration (hours to weeks).
Erythema mainly results from UVB i.e. wavelengths <320nm. It arises from dilation of the superficial blood vessels produced by cytokines. Solar-induced erythema is delayed by a few hours after exposure. Delayed tanning is noticeable two days after exposure and most intense a week afterwards. It is due to melanogenesis and distribution of melanin to keratinocytes throughout the epidermis. UVA and even visible radiation may cause melanogenesis, but UVB is the most effective in initiating it.
Further exposure to UVR causes less damage:
UVB converts precursors in the skin into vitamin-D. The liver, then the kidneys, change vitamin-D into calcitriol (1,25 dihydroxycholecalciferol), which is required for calcium homeostasis.
Skin cancers are due to progressive mutations in DNA. They are induced by:
Fitzpatrick skin phototypes 1 to 6 are used to classify the effect of sun exposure on an individual's skin. Types 1 and 2 are at high risk of skin cancer, particularly when exposed to intense sunlight.
|Type 1:||Very fair. Burns easily, doesn't tan|
|Type 2:||Fair. Burns easily, tans lightly|
|Type 3:||Olive. Burns somewhat, tans readily|
|Type 4:||Light brown. Burns rarely, tans well|
|Type 5:||Dark brown. Doesn't burn, tans deeply|
UVR results in profound alterations of both local and systemic immune responses:
Sun damage (photoageing) includes:
Glogau skin types refer to the degree of photoageing:
Determine Fitzpatrick skin phototype in 20 patients over 60 years of age. Compare this to their Glogau skin type.
Information for patients
See the DermNet NZ bookstore
© 2020 DermNet New Zealand Trust.
DermNet NZ does not provide an online consultation service. If you have any concerns with your skin or its treatment, see a dermatologist for advice.