From visible to invisible: how does our skin age?

The skin is not immune to the passage of time and undergoes a series of transformations. The skin ageing combines two processes: intrinsic ageing, determined by genetic programming, and extrinsic ageing, driven by external aggressions such as UV rays, pollution and tobacco, which induce oxidative stress.

These various factors lead to a progressive reduction in the synthesis of collagen and elastin, a loss of skin hydration and an accumulation of oxidative damage that disrupts the structure and cohesion of the skin. In the dermis, fibroblasts synthesising collagen and elastin in the extracellular matrix become less active and produce fewer supporting fibres. In the epidermis, keratinocyte renewal slows, while blood circulation becomes impoverished, reducing the supply of nutrients and oxygen to the tissues.

While cutaneous ageing is a natural process, its severity is largely determined by our lifestyle and the quality of our environment.

Skin ageing is a comprehensive and progressive process affecting all the structures of the skin – epidermis, dermis and hypodermis – and modifying its appearance and biological functions. Its manifestations vary from one individual to another depending on genetics, lifestyle and the phototype, but overall they remain broadly similar.

The formation of wrinkles.

The wrinkles are undoubtedly the most emblematic sign of skin ageing. They reflect a progressive deterioration of the skin’s supportive structures and a natural shift in its cellular activity. Over time, the dermo-epidermal junction flattens, cell renewal slows, and collagen and elastin fibres become disorganised. These structural changes lead to a loss of elasticity, a reduced resistance to mechanical stress and an increased tendency for visible furrow formation.

On the surface, the earliest wrinkles often present as fine lines fine and shallow. They primarily result from dehydration of the stratum corneum. Over time, these fine lines evolve into deeper, more pronounced wrinkles anchored in the dermis, owing to reduced collagen levels and extracellular matrix degradation. Expression lines, meanwhile, appear in areas of repeated movement, such as the forehead, the eye contours and of the lips, and become permanent as the skin loses its ability to spring back. Finally, the so-called gravitational wrinkles, associated with loss of tone and skin laxity, progressively alter facial volumes, particularly in the cheeks and jawline.

Note The appearance of wrinkles is also strongly influenced by sun exposure, which causes actinic elastosis, that is, an accumulation of altered elastin fibres in the dermis.

Cutaneous laxity.

The skin laxity is another visible and progressive manifestation of skin ageing. It results from a loss of tension in the deep structures of the dermis and hypodermis, which normally maintain tissue cohesion and firmness. With age, fibroblast activity declines. This reduction in collagen and elastin fibre production is accompanied by fragmentation of existing networks, rendering the skin less dense, thinner and less capable of resisting gravity. The tissue ptosis phenomenon, that is their sagging under gravity, becomes perceptible: the cheekbones sink, the facial contour blurs and jowls begin to form.

This laxity is not purely mechanical. It is also associated with a reduction in the subcutaneous muscle mass and a redistribution of facial fat. After the menopause, the decline in oestrogens exacerbates this loss of firmness, since these hormones normally stimulate collagen synthesis and maintain dermal thickness. Moreover, exposure to UV radiation and pollution accelerates the enzymatic breakdown of dermal fibres via the activation of metalloproteinases, amplifying the loss of tone.

Drier skin.

The skin gradually loses its ability to maintain hydration. This drying reflects various structural and functional changes. In the superficial layers of the skin, the reduction of the natural moisturising factor (NMF) reduces the skin’s capacity to retain water. Concurrently, sebum production by the sebaceous glands decreases, especially after menopause, resulting in a loss of the hydrolipidic film protective on the skin’s surface. Furthermore, over time, the content of intercellular lipids, particularly ceramides, becomes depleted, weakening the barrier function and promoting water loss.

In the dermis, the decline in hyaluronic acid also contributes to skin dehydration. This hygroscopic molecule, capable of retaining up to 1,000 times its weight in water, becomes less abundant over time, directly impacting skin hydration and contributing to the appearance of dehydration lines. These various processes explain the sensation of tightness, roughness and occasional flaking observed in mature skin.

A more lacklustre complexion.

With age, the skin gradually loses its natural radiance and the complexion becomes duller. This change is largely due to the slowing of cellular turnover, a biological process in which keratinocytes, accounting for around 80% of epidermal cells, form in the basal layer and progressively migrate to the stratum corneum.

In a young adult, this complete cycle takes approximately 28 days, ensuring a regular renewal of the skin’s surface. In mature skin, the cellular renewal slows down. Keratinocytes renew less rapidly, and dead cells accumulate on the epidermal surface. This results in a thickening of the stratum corneum and a decreased ability of the skin to reflect light, contributing to a duller and less uniform appearance.

Dull complexion is a subtle yet noteworthy sign of skin ageing, reflecting a decline in cellular activity.

An enlargement of the pores.

At first glance, it may seem paradoxical that the pores become more visible with age, even though sebum production gradually diminishes. However, skin ageing alters the skin’s structure and elasticity, affecting the appearance of pores. Enlarged pores are characterised by an uneven skin surface, an abnormal dermo-epidermal junction and an altered extracellular matrix. As we age, this matrix breaks down and loses its capacity to support the skin’s tissues, contributing to pore enlargement. A study conducted by KITAHARA and his team on 138 volunteers of various ages confirmed that the degradation of skin structure is closely linked to both age and pore size.

The appearance of pigmented spots.

With age, the skin becomes increasingly prone to pigmented spots, known as solar lentigines or age spots. These marks mainly appear on sun-exposed areas such as the face, hands and décolleté, and reflect an irregular distribution of melanin within the skin. From a mechanistic perspective, skin ageing leads to a progressive depletion of epidermal melanocytes. Paradoxically, the remaining melanocytes become locally hyperactive and produce melanin in a disorganised manner in response to oxidative damage and repeated UV exposure, resulting in the formation of localised brown spots.

Increased stiffness of blood vessels.

Skin blood vessels tend to become increasingly rigid over time, a phenomenon that contributes to the appearance of visible signs of ageing such as telangiectasias and diffuse redness. This stiffening is associated with several factors, notably the progressive loss of perivascular connective support and the thickening of vascular walls, which reduce their ability to dilate and contract normally. Vascular stiffening is particularly evident on the face and legs, where small dilated vessels can appear as red or purple lines and forming stellate angiomas.

The appearance of petechia.

In the elderly, it is very common to observe the appearance of petechiae, also called senile purpura, which are manifested by small red or violaceous spots on the skin, often on the arms or legs. This phenomenon mainly results from the progressive atrophy of dermal tissues and the weakening of the walls of small blood vessels, which become more fragile with age. Even slight trauma or pressure can then cause small subcutaneous hemorrhages, visible on the surface of the skin. Although these spots are generally benign, they clearly illustrate the skin weakening associated with aging and the decrease in the mechanical strength of the epidermis and dermis.

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