THE AGEING SKIN.
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The generally held view is that as skin ages it develops characteristic physiological signs (i.e. wrinkles, pigment alteration, thinning). It is now known that this is not normal ageing but pathological changes mainly due to ultraviolet light exposure. Obviously some conditions will occur from unavoidable environmental exposure, genetics and the effects of disease etc., but normal ageing produces surprisingly few skin changes.
The exposure to sunlight,
however, produces very deleterious effects with numerous pathological
conditions including keratoses, squamous cell carcinoma, basal cellThe Ageing Process.
carcinoma and
malignant melanoma. Less life-threatening effects include wrinkling and hyper-
and hypopigmentation. Thus there is very little evidence that the skin ‘ages’
apart from the effects ofgenetics,
environment and disease.
EPIDERMIS
The changes to the epidermis as a person gets older are minimal and subtle. The skin may become thinner, especially where it has been exposed to sunlight, and oxygen consumption may be slightly decreased. Metabolic processes appear unchanged.
DERMIS
The changes in collagen are qualitative more than quantitative. There is some decrease in thickness, especially in light-exposed skin, but the main changes include increases in the cross-links on the collagen with some deterioration in fibre organization. The flexibility of the skin is due to the dermal collagen and there is minor deterioration with age.
However, it is very marked in the pathological state known as the ‘transparent skin syndrome’. With respect to age and keratinocytes, it is clear that ageing skin epithelializes more slowly after injury and that the thinner epidermis (mainly due to UV light exposure) provides a diminished barrier function.
There is an age-related reduction in the skin’s immunosurveillance system; keratinocytes, Langerhans cells, epidermotrophic lymphocytes, etc. In addition there is an age-related increased risk of photocarcinogenesis in habitually sunexposed and photo-aged skin (see ‘UV light’, below). One must not forget, however, that wounds heal well in normal elderly people.
ULTRAVIOLET (UV)
LIGHT
The dangerous components of UV light are the shorter wavelengths, the effects being initially erythema (sun-burn), increased thickness of the stratum corneum and increased melanocytes (hence a sun tan). Repeated exposure, especially with ‘burning’, results in pathological effects including the skin cancers. This is important because advertising still tells us that ‘brown is beautiful’ and that sun tans are ‘healthy’. The sideeffects of accelerated skin ageing and the potential dangers are not mentioned as prominently.
Early pathological changes include yellowing and the formation of wrinkles (though excess wrinkles
probably have a genetic component). A few people get depigmentation and obvious superficial ‘broken’ blood vessels - telangiectasia. The backs of the hands can develop keratotic nodules as well as the face. The skin around the eyes may show yellow plaques Dubreuilh’s elastoma. The thick, deeply lined ‘crazy-
paving’ type skin on the back of sun-exposed necks has the wonderful name of cutis rhomboidalis nuchae of jadassohnl. Other sun-induced changes include keratoacanthoma, basal cell carcinoma and squamous cell carcinoma. The most dangerous is the malignant melanoma which has now become so common in Australia that doctors have been doing ‘rounds’ on the beaches, examining people and giving advice. Very little is known about skin changes and age in the black population.
TRANSPARENT SKIN
SYNDROME
People with transparent skin syndrome have skin which looks and feels like tissue paper, especially on the backs of the hands and forearms (Fig 2.1). The skin is loose and wrinkled and the underlying structures are seen easily. This type of skin has very poor elastic (i.e. tensile) properties. Histologically there is a thin dermis.
This is probably a pathological condition and not an ageing process. Interestingly it is associated with osteo porosis and hence collagen abnormalities may be implicated. The skin ‘tears’ easily and is difficult to suture. It skin also bleeds and bruises easily. A similar finding is found in patients who have taken steroids (‘steroid atrophy’) and in patients with rheumatoid arthritis. The condition could possibly be related to other ‘lax-skin’ conditions which are increasingly being diagnosed in non-pure forms. Transparent skin may also have white pseudoscars (thought to be due to episodes of minor trauma) and has an increased tendency to senile purpura
SENILE PURPURA
Many elderly people develop bruising, especially over the hands and arms, without having the full-blown
transparent skin syndrome. It is presumed that they still have less elastic collagen and hence blood vessels are less well tethered and are more easily ruptured by minor trauma. The purpura stays longer because reabsorption is much slower. Other vascular changes include the appearance ofa few spider naevi and an occasional splinter haemorrhage under the fingernails (traumatic in origin). The most common skin lesion noted is the small red Campbell de Morgan spot, a benign lesion seen most often on the trunk and abdomen. T
HAIR
Grey hair is genetically determined (autosomal dominant) and is far less traumatic than the loss of hair (again genetically determined in men). Both men and women lose their hair with age, men simply lose it sooner, faster and more comprehensively! Male vanity and the media have determined that enormous sums are being spent to stop and reverse this most benign of ageing processes.
PRURITUS
This is so common in the elderly that the term ‘senile pruritus’ is well known. However, it is again pathology rather than normal ageing that is more important in the etiology, diagnosis and treatment.
Drugs
Blood disorders (e.g. polycythaemia rubra vera, anaemia) Malignant disease (e.g. lymphomas) Liver and kidney disease (esp. with jaundice and uraemia) Dryness (exacerbated by washing, detergent residues in clothes, temperature) Infestations (scabies, lice) Skin disorders (eczema, lichen planus, pre-pemphigoid) Incontinence (the effects of urine and faeces).
GROWTH FACTORS
Growth factors are peptides with mainly stimulating effects on cell proliferation. They are named after the target cell or source that led to their discovery (e. g. epidermal growth factor, EGF). Within this rapidly expanding Held there are some areas of special interest. Donor age seems to influence the proliferative capacity and lifespan of cells in culture, and there is a diminished in vitro response and impaired growth factor processing by cells with increasing age. Age appears to influence growth factor production by cells.
The physical changes in skin associated with ageing (thinner epidermis, altered dermis with reduced
amounts of extracellular matrix proteins, collagen and elastin) may have significance with growth factors. It has been suggested that there may be possible interaction and stabilization of growth factors in the extracellular matrix. The matrix may even protect growth factors from degradation or provide long-term storage.
ANTI-AGEING MEASURES
Because the superficial effects of ‘ageing’ are so visible it is not surprising - in a youth-obsessed culturethat a whole industry has developed to keep people looking younger. More could _be achieved simply by avoiding sunlight. Most creams are useless apart from their camouflage effect. However isotretinoin (used to treat severe acne) does cause ‘peeling’ in normal skin, erasing the finest of the wrinkles. More dramatic is the use of plastic surgery, and ‘face-lifts’ are becoming increasingly popular. People should be warned, however, that repeat procedures may lead to the umbilicus becoming an unusual beauty-spot on the chin! Many manufacturers of facial skin creams and suntan lotions are now including anti-UVA (photo ageing) sun blocks. The economic if not health message is getting across.
There is increasing evidence that free radical damage is part of the ageing process. The role of antioxidants including vitamins C and E, selenium and beta-carotene remain speculative.
Mercyvill.
