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Skin lesions

Ageing skin

Objectives

  • Distinguish intrinsic ageing from photoageing.
  • Revise basic physics and photobiology relating to ultraviolet radiation.
  • List the six different Skin Types.
  • Understand the reasons for sun protection and describe how to achieve it.

Key points

Characteristics of UVR include:

  • UVR: UVC (200-290 nm), UVB (290-320nm) and UVA (320-400nm).
  • UVR is at its greatest when the sun is overhead.

Important characteristics of skin exposed to UVR include:

  • UVR damages nucleic acids eventually resulting in skin cancer.
  • Acute effects of UVR are erythema, melanisation, vitamin D production and skin thickening.
  • Skin Types are classified according to how easily it burns and tans (the fairest, Type 1 to the darkest, Type 6).
  • Immune response includes cytokine and neuropeptide release, reduction of Langerhans cell function, reduction of histamine release and tolerance.
  • Chronic effects of UVR (photoageing) changes are dryness, skin thinning, easy bruising, solar keratoses and skin cancer.
  • Sun protective factor (SPF) is the ratio of the time for the skin to burn with a sunscreen when exposed to UVR compared without the sunscreen.

Introduction

Skin changes with age. Some of this ageing is intrinsic and some is extrinsic ageing due to environmental exposure, mainly photoageing.

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.

Naevi

Naevi are benign proliferations of cells within the tissue of origin. They may be congenital (birthmarks) or acquired. Although congenital naevi affect only a small percentage of infants, nearly everyone develops acquired naevi such as moles, skin tags, seborrhoeic keratoses and vascular lesions. Some of these will be described in other sections of this module.

Ultraviolet radiation

UVR is arbitrarily split into UVC (200-290 nm), UVB (290-320nm) and UVA (320-400nm). Solar UVC does not pass through the ozone layer so is not present on the earth’s surface.

The electromagnetic spectrum

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 on a clear day compared with a cloudy day, according to the time of day

UVR in different seasons, according to the time of day

Measurements of UVR at Waikato Hospital in 1989


The biological effects of light on normal skin

UVR causes biological effects on various tissues when it is absorbed. Injury to nucleic acids results in abnormal structures such as 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. 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.

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.

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
Type 6
Black

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.

Immune response

UVR results in profound alterations of both local and systemic immune responses

Chronic response to exposure to UVR

Sun damage (photoageing) includes:

Thin skin: transparent and wrinkled

Furrows due to muscle movement and loss of subcutaneous fat

Senile purpura


Skin cancers require a double-hit to DNA. They are induced by:

Photoprotection

The best protection from sun damage is to stay indoors. If outside, then protection from directly incident light can be obtained by seeking shade: trees, verandas, and umbrellas.

As much skin as possible should be covered with densely woven darkly coloured clothing.

Clothing as sun protection

Apply sunscreen to all uncovered skin liberally. Reapply after half an hour to ensure an even coating soaks into the skin, and then follow the instructions on the container. These generally advise reapplication 2-hourly and after bathing.

Sun protective factors (SPF) are a useful guide to the efficacy of a sunscreen. In New Zealand most manufacturers adhere to the requirements of a voluntary Australian and New Zealand Standard in which the labelled SPF can be up to 50+. The SPF is calculated from in-vivo testing, and is the ratio of the time for the skin to burn when exposed to solar simulating UVR with the sunscreen compared without the sunscreen. Thus white skin that normally burns in 10 minutes will burn in 150 minutes (2 1/2 hours) with SPF 15 sunscreen however often it is reapplied. In general, sunscreens are much less effective than predicted by their SPF number as they are applied significantly less thickly than is tested and are rubbed, sweated or washed off.