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The skin of seniors: clinical and histological aspects
- 30min
- May. 2022
- Supported by
While this article only concerns the skin, this limitation is artificial, because particularly on the face, the underlying tissues participate very much in overall facial aging. It is true that for a long time, we were essentially interested in the skin because only its alterations were accessible to non-surgical corrective techniques. The arrival of injectables, botulinum toxin for muscular aging and dynamic wrinkles and products for volumetric filling for ptosis, the atrophy of adipose tissue and the restructuring of the volumes of the face opened a much wider field of action for dermatologists. Facial aging must now be evaluated and treated in its globality.
Appearing to be younger, or at least not too old for as long as possible, has become, because of social constraints, a constant concern for personal well-being, relations with one’s entourage and a necessity in professional life where seniors are being pushed aside earlier and earlier. The correction of facial aging, particularly cutaneous aging, is the most frequent request by aesthetic dermatology patients and is an essential element of perceived age, and the progress and effectiveness of the treatment techniques, of which they are very well informed, encourages them to request these. The skin of each individual ages differently and reflects his/her life history, associated in a variable manner with his/her genetic heritage and the environment to which he/she has been exposed.
Intrinsic skin aging
Chronological aging1
No one escapes from time passing mark: Chronological aging is connected with age and is determined genetically, but it is all the same variable on the basis of the biological clock that is specific for each individual. This concerns the entire body, but it is more easily evaluated on the covered portions of the body, because on the uncovered areas, particularly the face, this is masked by the additional effect of photoaging which is often very clearly dominant. The skin is thinned, wrinkled, dehydrated and often slightly scaly. Because of dermal atrophy, the skin loses its elasticity, forming fine parallel lines (figure 1) and at the level of the larger folds. Among the eldest, the skin is flaccid like clothing that is too large (figure 2).
Because of the loss of dermal density, the small vessels are poorly protected by an insufficient connective tissue environment. At the slightest trauma, this leads to small skin tears associated with purpuric spots that disappear and leave in their place stellar pseudo-scars which are considered to be spontaneous, but in fact result from this. Age is not solely responsible for these initial aspects of dermatoporosis, because photoaging explains the preferential locations for this, the exposed faces of the extremities, particularly the forearm and the back of the hands, and the anteroexternal part of the legs where these are sometimes the source of ulcerations that are difficult to heal. On the other hand, surgical incisions, particularly on the face after the removal of a skin tumour, heal well and the scars rapidly become less visible than with a young subject. The skin of elderly people becomes dehydrated and is irritated more easily. Pruritis is frequent, particularly in winter if the baths or showers are too hot and too long. Benign proliferations are very frequent, sometimes starting with middle age: seborrhoeic keratoses, particularly on the torso but also sometimes on the face, pedunculated papillomas of the large folds, strawberry angiomas and senile blood plaques. However, baso- and spinocellular carcinomas and melanoma are connected with photoaging more than with chronological aging.
The hair and nails also age, the hair becomes grey and then white and then becomes finer and more scarce. Body hair reduces and in the genital regions, the nails grow more slowly, the nails on the hand become thinner with longitudinal striations and become brittle, whereas those on the feet, particularly on the large toes, have the tendency to thicken and are often affected by mycosis.
Biopsy shows a weakening of most of the components of the skin (figure 3): The epidermis is thinner, with the interpapillary ridges effaced. Only the corneal layer, which is composed of dead cells, is slightly thickened. The dermo-epidermal junction is flattened. The dermis is thinned, its density is lessened, the fibroblasts are stunted and the components of the extra-cellular matrix, collagen fibers and particularly hyaluronic acid, is diminished. The fine network that forms the elastic armature of the dermal papillas has completely disappeared.
From the physiopathological point of view, chronological aging is genetically determined and the deficiency of the gene that codes for telomerase is particularly involved. The alterations connected with aging are no longer correctly repaired. The cellular turn over diminishes by 50% between the age of 20 and 70 years.
Hormonal aging1
At menopause, the sudden fall in estrogen leads to the rapid accentuation of signs similar to those of chronological aging for women who have not had hormone replacement therapy. The skin becomes thinner, fades and dries, particularly on the face, which is richer in estrogen receptors. From the histological point of view, there is particularly a reduction in dermal collagen, estimated at 30% during the first 5 years of menopause not subject to hormonal substitution and then 1 to 2%, with a certain amount of parallelism in the reduction of the bone matrix and the risk of osteoporosis. There is also a fall in dermal hyaluronic acid which is responsible for an alteration of cutaneous visco-elasticity.
Other inconveniences are connected with the deficit of estrogen: vasomotor and sudoral flashes, dryness and atrophy of the genital mucous responsible for dyspareunia, and more rarely palmoplantar climacteric keratosis. Finally, with menopause, there is a relative hyperandrogenism, since the androgens, although reduced, are still present and their effects are no longer counterbalanced by those of the female hormones, estrogen and progesterone, which have collapsed. An increase in hair on the face is often noted, and an androgenic type of alopecia. These manifestations normally remain discrete, but they harm the quality of life as they are perceived as a visible loss of femininity. Hormone replacement therapy, if there is not any reason to counter indicate this, may avoid or reduce these manifestations, but this is variable from one woman to the next.
Among men, there is a reduction of androgens, but this is progressive, without a sudden fall and one prefers to speak of an “androgen deficit connected with age.” Aging, particularly cutaneous aging, is also more gradual and slower than with women. Bouts of excess perspiration, comparable to those that accompany vasomotor flashes among women, are however noted.
Conclusion
While the means for the correction of skin aging have progressed much, very effective prevention with regard to extrinsic factors should not be neglected: photoprotection and reasonable exposure to the sun, no tobacco. Cosmetology may, to a certain extent, slow the chronological aging and hormone replacement therapy can prevent or improve the effects of hormonal aging. When photoaging has occurred, surface techniques, lasers, radiofrequency with micro-needles and peelings, which have a more or less invasive character, are used in parallel with the associated effectiveness, depending on the necessity, of vascular lasers or IPL (intense pulsed light), pigment lasers, the destruction or excision of benign or malignant tumors, may be proposed.
Bibliography
- Beylot C. Vieillissement cutané. Vieillissement facial global : orientation thérapeutique. EMC – Cosmétologie et Dermatologie Esthétique 2016;11:1-27.
Link to abstract - Krutmann J et al. The skin aging exposome. J Dermatol Sci 2017;85:152-61.
Link to full publication - Gilchrest BA. Photoaging. J Invest Dermatol 2013;133:E2-6.
Link to full publication - Beylot C. Vieillissement cutané et tabac. Dermatologie Esthétique, supplément de Réalités Thérapeutiques 2014;6:25-30.
Link to abstract
Extrinsic cutaneous aging
This is connected with environmental factors that vary depending on the individuals and which a recent article suggested calling “exposomis.”2
Photoaging (or heliodermy)1
Photoaging clearly predominates over the other types of aging, particularly on the face. But while this is the very standard type of environmental aging, genetics also plays a role since photoaging is much more marked with subjects with fair complexions. The alterations occur essentially on the uncovered parts, but they are generalized with fanatics of tanning.
On the face, the skin is normally thickened, yellowish, covered with deep wrinkles, the follicle orifices are dilated, it has lost its elasticity, and it is flaccid and relaxed. The alteration of the cutaneous texture, its visco-elasticity and its bio-mechanical properties, does not explain everything and the aging of the underlying tissues must not be neglected. In fact, the skin does not undergo ptosis alone, it follows the ptosis of the adipose tissue and goes along with its atrophy (accentuation of the nasogenian folds, alteration of the oval of the face, jowls). The dynamic wrinkles (glabella, crows feet) are the result of photoaging and distending skin which folds on the skin muscles that are contracting continually to compensate for their aging. But there are also wrinkles that are purely connected with photoaging, such as vertical sun-pleating wrinkles of the upper lip that must be distinguished from more oblique dynamic wrinkles, like bar codes, due to the contraction of the orbicular muscle of the lips (figure 4).
Other alterations connected with photoaging: elastoidosis with cysts and comedones in the malar regions, particular among men; sebaceous adenomas; erythrotelangiectatic rosacea; benign smooth solar lentigines of variable size are present among 90% of European-type subjects over the age of 60 years (figure 5); actinic keratoses, whether greya or pink, that are rough and may develop into a spino-cellular cancer (figure 6). As the risk of skin cancer is particularly connected with photoaging, the start of proliferations must be searched for carefully and their tumorous character is not always evident, particularly with regard to basocellular carcinomas or a Dubreuilh melanoma which is not to be confused with a benign lentigo.
On the neck, photoaging is manifested by inter-follicular erythrosis of the neck, which only avoids an area in the shadow of the chin (figure 7) and on the back of the neck among subjects professionally very exposed to the sun (sailors, farmers), by deep, rhomboidal (diamond shaped) wrinkles.
On the extended parts of the limbs, particularly on the back of the hands, the skin is very atrophic, like an onion skin, speckled with solar lentigines. There are also purpuric spots completing the aspect of dermatoporosis, which among the oldest subjects may develop into extended cutaneous tears and deep haematomas that show the extreme fragility of the skin and the dermal vessels and the cutaneous underlayers. On the legs of women, there are often small white spots (guttate hypomelanosis).
The biopsy is characterized by alterations at the upper level of the dermis (figure 8), which corresponds to the level of penetration by UV in the skin (epidermal UVB, epidermal UVA and superficial dermis). The epidermis is thinned, with irregular dispersion of melanin, and some cellular atypia if there are keratoses. But the alteration that most evokes photoaging is the massive actinic elastosis located in the superficial dermis, with abnormal, thickened and fragmented elastic fibres, and it is clear that the bio-mechanical properties of the skin are affected, since there is also a rarefaction of dermal collagen. While remembering that the matter is much more complex, one may consider very schematically that the UVB rays, which are very energetic but only penetrate the epidermis, are responsible for skin cancers, whereas the UVA rays that penetrate the superficial dermis are involved in aging, particularly skin aging. Infrared and visible light penetrate more deeply, to the hypodermis and more discretely participate in skin aging, particularly by increasing the production of metalloprotease-1.
The physiopathology of photoaging is complex3: The deleterious roll of reactive oxygen species is primary and works on a multitude of targets: mutations of nuclear and mitochondrial DNA; activation of the AP-1 transcriptional factor, with a reduction in the synthesis of procollagen and increasing the expression of genes coding for matrix metalloproteinases (MMPS) which degrade the collagen; slight sensitivity of the fibroblasts to the transduction signals of the TGF-β keratinocyte and thus the reduction in their capacity to divide and the collagen that they synthesize; modification of the genetic program of the fibroblasts, particularly those of the papillary dermis, with an increase in the expression of the gene for the elastin responsible for actinic elastosis and an over-expression of the genes of the MMPs that destroy collagen; glycation and rigidification of the fibrillar proteins of the dermis, collagen and elastin; failure of the hyaluronan/CD44 signalization, resulting in a reduction in dermal hyaluronic acid.
But under the action of UVB rays, there is also a direct attack on the DNA. And is the DNA excision and reparation mechanisms are overwhelmed, there is cellular alteration, senescence, apoptosis or cell death, gene mutation p53, the “guardian of the genome”, which may cause skin cancers. Finally, the UV rays reduce the number of Langerhans cells, causing the alteration of the immunosurveillance of the skin and favoring skin cancers.
Skin aging connected with tobacco4
Epidemiological studies attest to the reality of aging connected with tobacco and the risk of early wrinkling which is 4.7 times higher among smokers than non-smokers. A comparison of smoker and non-smoker twins confirms that those who smoke appear much older and wrinkled than their non-smoking twin. Aging connected with tobacco resembles photoaging and increases this: greyish skin, with deep wrinkles and often cysts and comedones. The wrinkles are particularly marked in the circumoral region, especially among women. They are associated to various degrees with wrinkles caused by photoaging, with certain differences, including a more pronounced affect of the lower lip among women smokers (figure 4B), whereas the sun pleating particularly concerns the upper lip.
The use of tobacco also causes difficulties in healing, connected with the harm to the cutaneous arterioles and plastic surgeons are always concerned when they plan a facelift for such patients.
As with the clinical, the histology is close to that of photoaging. This is not surprising, since there are shared physiopathological mechanisms as concerns the alterations of the extracellular matrix of the dermis, with a reduction of the synthesis of collagen, an increase in its degradations under the influence of MMPs, and the abnormal production of elastic material. The harm to the arterioles, first with vasoconstriction, then histological alterations, is more specific for tobacco use. Menopause, which is earlier for women who smoke, is responsible for estrogen deficiency and a reduction in dermal collagen, as in hormonal aging.
And pollution?
The role of pollution in the acceleration of skin aging is suspected, but it is difficult to prove because it is impossible to dissociate it from other dominant intrinsic or extrinsic factors, particularly photoaging. A comparative study in the Ruhr, however, showed among women subject to a high density of fine particles and soot connected with traffic, 20% more pigmented spots on the face than among women from group living in a residential zone, but there was little correlation with wrinkles. Chinese studies also signal an increase in pigmented lesions among subjects affected by pollution.3
Conclusion
While the means for the correction of skin aging have progressed much, very effective prevention with regard to extrinsic factors should not be neglected: photoprotection and reasonable exposure to the sun, no tobacco. Cosmetology may, to a certain extent, slow the chronological aging and hormone replacement therapy can prevent or improve the effects of hormonal aging. When photoaging has occurred, surface techniques, lasers, radiofrequency with micro-needles and peelings, which have a more or less invasive character, are used in parallel with the associated effectiveness, depending on the necessity, of vascular lasers or IPL (intense pulsed light), pigment lasers, the destruction or excision of benign or malignant tumors, may be proposed.
Bibliography
- Beylot C. Vieillissement cutané. Vieillissement facial global : orientation thérapeutique. EMC – Cosmétologie et Dermatologie Esthétique 2016;11:1-27.
Link to abstract - Krutmann J et al. The skin aging exposome. J Dermatol Sci 2017;85:152-61.
Link to full publication - Gilchrest BA. Photoaging. J Invest Dermatol 2013;133:E2-6.
Link to full publication - Beylot C. Vieillissement cutané et tabac. Dermatologie Esthétique, supplément de Réalités Thérapeutiques 2014;6:25-30.
Link to abstract