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Clinical dermatology: retinoids & other treatments--25 years.

For the third of our anniversary issues, I have chosen two previous articles in an area which has particular interest for me: and to date, the message on photodamage remains much the same. The Gallery for this issue offers a selection of warty and scaling disorders, one showing notable improvement in response to topical calcipotriol.

The first article, 'Facing the future with photodamage', is a brief exposition of the pathophysiology and clinical features of the chronic damage caused by long-term overexposure to solar ultraviolet radiation. It is worthwhile expanding on this theme and attempting to relate the tissue changes of solar elastosis to the clinical phenomena seen in photoageing.

Lines and wrinkles

Solar elastosis results in the destruction of the coherent mechanically strong and protective fibrous network of dermal collagen, and the substitution of an amorphous gel-like elastotic material. There can be little doubt that these alterations account for the general lack of firmness, and the 'droopiness', of photodamaged skin, but do they also cause wrinkling? There is no clear answer to this question. Despite numerous studies on the nature of lines and wrinkles, a clear explanation for their presence is still not forthcoming. Numerous tools and techniques have been used to study wrinkles--histological, ultrastructural, histochemical, epidemiological, biophysical and mathematical. Interestingly, it is not only dermatologists, cosmetic scientist and plastic surgeons who have been involved in the study of wrinkles but clothing and paper manufacturers, geologists and mathematicians have also all contributed to work on wrinkles.

According to the US National Institutes of Health National Library, in mid-April this year, there were 8811 entries under the search terms "wrinkles skin", of which 1695 were reviews. Perhaps not unexpectedly, 4243 of these came up under the search terms "wrinkles treatment".

Histologically, there are no special features, and there is no accumulation of elastotic change around the wrinkle site. Some have talked about areas of epidermal atrophy but certainly there are no dramatic histological findings in wrinkles. Most wrinkles occur at skin sites subject to the greatest and most frequent skin movement--the corners of the mouth, the sides of the eyes and the cheeks are the sites of predilection. Wrinkles may develop because of the failure of the damaged dermis to undertake the restitutive phase after an initial extension. Kligman regarded wrinkles as "configurational change" resulting from "mechanical stresses acting on lax excessive skin especially in actinically damaged areas".

Cutis rhomboidalis nuchae

Also known as 'sailor's skin', this disorder is seen on the back of the neck in fair-skinned outdoor workers such as farm labourers and sailors. The rhomboidal furrows on the back of the neck are easily recognised but poorly explained. Presumably the furrows are a result of the altered mechanical qualities of affected skin in an area which is constantly on the move, and are quite analogous to wrinkles.

Reddened cheeks, telangiectasia and purpura

A significant proportion of the elderly have reddened cheeks and are thought by many lay folk to be brimming with health because of this appearance. It seems that it is in fact a sign of photodamage. Apart from the observation that those apple-red cheeks are often seen in farmers and 'rugged outdoor types', we do not know what determines whether this sign develops or not. The explanation for the redness appears to be the passive dilatation of the subpapillary venous plexus due to loss of perivascular supporting collagen, with substitution by degenerate incoherent elastotic tissue. The passive vasodilatation results in 'pooling' of the blood, accounting for the red colour. It also accounts for the coolness to the touch because the volume flow will be decreased rather than increased as in inflammation. The dilatation of individual large venules (telangiectasia) is cosmetically most unpopular and due to the same problem of mechanical failure of the supporting function of perivascular collagen. The crimson patches on the backs of the hands and the forearms of the elderly are known inappropriately as senile purpura. Solar purpura would be a better name, since they seem to be due to minor traumata to the superficial vasculature of skin affected by elastosis, because of the loss of protective perivascular collagen.

The deleterious effects of elastosis on the mechanical and protective qualities of the dermal connective tissue do not stop at red cheeks, telangiectasia and purpura. Rosacea may, in part, also be due to the persistent dilatation caused by photodamage. The early stages of rosacea certainly resemble the condition of weathering, and histologically the two disorders are identical. A reasonable hypothesis is that the later stages of rosacea, characterised as they are by inflammation, are in some way due to diffusion of mediators and/or cytokines from the compromised endothelium of vasculature containing pooled blood.

Senile comedones

Blackheads are common on the ageing face and some are indisputably the result of photodamage. The condition known eponymously as Favre and Racouchot disease, in which clusters of large comedones appear on a thickened plaque over the malar region or elsewhere around the orbit, seems to always be accompanied by severe photodamage. The giant comedones seen over the upper back and occasionally on the face are also associated with photodamage, and I suspect that they are passively allowed to dilate with the keratinous debris because of the loss off perifollicular dermal support--exactly analogous to the situation with the microvasculature. The common blackheads found scattered over the faces of the elderly do not seem to be associated with photodamage in the same consistent way.

Conditions associated with elastosis

Citrine skin

The term citrine skin has been used to describe the background, yellowish discoloration frequently observed in severely photodamaged individuals. Apart from accompanying severe photodamage, and by implication somehow the result of solar elastosis, there is little available information on the nature of this physical sign. Nonetheless it would seem reasonable to suggest that the yellowish tint is due to a difference in the way elastotic skin reflects back incident light.

Triradiate or stellate scars

These curious scar-like lesions occur mostly on the extensor surface of the forearms on a background of severely photodamaged skin. An explanation for their presence is usually offered by their owners, and some may well have started out as minor injuries. The majority of these odd angulated scars, however, appear to arise spontaneously and, as they always occur in the midst of a markedly elastotic dermis, may owe their origins in some way to this degenerate tissue.

The cause of solar elastosis

What do we know of the cause of solar elastosis?

Work from Uitto and colleagues from Philadelphia established that UVR switches on the elastin-promoter gene in fibroblasts, resulting in the synthesis of large amounts of disorganised elastic tissue. In addition to the deposition of this degenerate and disorganised elastic staining material there is a reduction in the amount of collagen present in affected skin. It has been shown that solar UVR stimulates the release of factors which activate proteases (including stromolysin, gelatinase and collagenase). The reduction in collagen is aggravated by a reduction in the rate of collagen synthesis after solar damage. The net result of the loss of collagen and its substitution by a degenerate elastotic substance in photodamaged skin is to markedly alter the physical properties and mechanical function of this part of the skin. This, I believe, is responsible for most of the clinical sequelae observed.

Non-UVR causes of elastotic degenerative change

Agencies other than sun can cause similar alterations to the dermal connective tissue, including x-rays, infrared irradiation from focal heating sources and cigarette-smoking. Is there a specific final common pathway for these different causes of elastosis? Currently there is no answer to this question. A histological study of the condition of erythema ab igne, which results from chronic focal overheating of the skin, showed that elastotic change occurred throughout the depth of the dermis--presumably reflecting the depth of penetration of the infrared rays. Similarly, with x-ray burns, the depth of the elastosis depends on the degree of penetration of the x-irradiation. There have now been several studies published to show that cigarette smokers have more wrinkles than control non-smokers, presumably on the basis of an increased amount of elastotic degeneration--but the mechanism involved is obscure.

Treatment for solar elastosis

The answer to the question posed by the article, 'Must one suffer to be beautiful' depressingly remains "Yes". We still do not have a way of separating the desirable regenerative stimulatory actions of the topical retinoids from their annoying irritative effects. Even with the physical techniques to improve the appearance of ageing, there is a price to pay, of a variable amount of discomfort. Whether the technique be a chemical peel, microdermabrasion or laser resurfacing, there is a degree of soreness, peeling and crusting that follows. The practitioner who provides a treatment for the photoaged face without any 'suffering' will be popular indeed.
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Article Details
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Title Annotation:Editorial
Author:Marks, Ronald
Publication:Clinical Dermatology
Date:Sep 1, 2009
Previous Article:Matrix metalloproteinase-21 expression is associated with keratinocyte differentiation and upregulated by retinoic acid in HaCaT cells.
Next Article:Facing the future with photodamage.

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