From visible to invisible: how does our skin age?

Skin does not escape the passage of time and undergoes a series of transformations. The skin aging combines two processes: intrinsic aging, programmed by genetics, and extrinsic aging, which depends on various external aggressors, such as UV rays, pollution, and tobacco, all of which generate oxidative stress.

These various factors result in a progressive decrease in the synthesis of collagen and elastin, a loss of skin hydration and an accumulation of oxidative damage that disrupt the skin’s structure and cohesion. In the dermis, fibroblasts synthesizing the collagen and elastin of the extracellular matrix become less active and produce fewer supporting fibers. In the epidermis, keratinocyte renewal slows down, while blood circulation diminishes, reducing the supply of nutrients and oxygen to the tissues.

Although skin aging is a natural process, its degree largely depends on our lifestyle habits and the quality of our environment.

Cutaneous aging is a comprehensive, progressive process that affects all layers of the skin – the epidermis, dermis, and hypodermis – altering its appearance and biological functions. Its manifestations vary from person to person depending on genetics, lifestyle, and phototype, yet overall they remain largely consistent.

The formation of wrinkles.

The wrinkles are undoubtedly the most emblematic sign of skin aging. They reflect a progressive deterioration of the skin’s supporting structures, as well as a natural evolution of its cellular activity. Over time, the dermal-epidermal junction flattens, cell turnover slows, and collagen and elastin fibers become disorganized. These structural changes lead to a loss of elasticity, a reduced resistance to mechanical stresses and an increased tendency to form visible lines.

On the surface, the first wrinkles often appear as fine lines that are shallow. They primarily arise from dehydration of the stratum corneum. Over time, these fine lines turn into more pronounced wrinkles anchored in the dermis due to collagen reduction and extracellular matrix breakdown. Expression lines emerge in areas of repeated movement, such as the forehead, the eye contours and the lips, and become permanent as the skin loses its ability to spring back. Finally, so-called gravitational wrinkles, linked to loss of tone and skin laxity, gradually reshape facial volume, particularly around 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 fibers in the dermis.

Skin laxity.

The skin laxity is another visible and progressive manifestation of skin aging. It results from a loss of tension in the deep structures of the dermis and hypodermis, which normally provide tissue cohesion and firmness. With age, fibroblast activity decreases. This reduction in collagen and elastin fiber production is accompanied by fragmentation of existing networks, rendering the skin less dense, thinner, and less capable of resisting gravity. The phenomenon of tissue ptosis, that is, their gravitational sagging, then becomes perceptible: the cheekbones descend, the facial oval blurs, and jowls form.

This loosening is not solely mechanical. It is also related to the reduction of subcutaneous muscle mass and the redistribution of facial fat. After menopause, the drop in estrogen further accentuates this loss of firmness, since these hormones normally stimulate collagen synthesis and maintain dermal thickness. Moreover, exposure to UV rays and pollution accelerates enzymatic degradation of dermal fibers via the activation of metalloproteinases, amplifying the loss of tone.

Drier skin.

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

At the dermal level, the decrease 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 fine lines. These various processes explain the sensation of tightness, roughness, and sometimes flaking observed in mature skin.

A duller complexion.

With age, the skin gradually loses its natural radiance and the complexion becomes duller. This change is largely related to the slowing of cell renewal, a biological process by which keratinocytes, which account for about 80% of epidermal cells, form in the basal layer and progressively migrate to the stratum corneum.

In a young adult, this full cycle takes about 28 days, ensuring a regular renewal of the skin’s surface. In mature skin, the cellular renewal slows. Keratinocytes renew more slowly, and dead cells accumulate on the epidermal surface. This leads to a thickening of the stratum corneum and a reduction in the skin’s ability to reflect light, contributing to a duller, less even complexion.

A dull complexion is a subtle yet significant sign of skin aging, revealing a decrease in cellular activity.

Pore dilation.

At first glance, it may seem paradoxical that the pores become more noticeable with age, even though sebum production gradually decreases. However, skin aging affects the structure and elasticity of the skin, which impacts the appearance of pores. Enlarged pores are characterized by an uneven skin surface, an abnormal dermo-epidermal junction, and a altered extracellular matrix. Yet, as we age, this matrix breaks down and loses its ability to support skin tissues, contributing to pore enlargement. A study conducted by KITAHARA and colleagues 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 primarily appear on sun-exposed areas such as the face, hands, and décolletage, and indicate an irregular distribution of melanin in the skin. From a mechanistic perspective, cutaneous aging leads to a gradual loss of epidermal melanocytes. Paradoxically, the remaining melanocytes become locally hyperactive and produce melanin in a disorganized manner in response to oxidative damage and repeated UV exposure, leading to the formation of localized brown spots.

A stiffening of the blood vessels.

Skin blood vessels tend to become progressively stiffer, a phenomenon that contributes to the visible signs of aging such as telangiectasias and diffuse redness. This stiffening is linked to several factors, including the gradual loss of perivascular connective support and the thickening of vascular walls, which diminish their ability to dilate and contract normally. Vessel stiffening is particularly evident on the face and legs, where small dilated vessels can appear as red or purple lines and form 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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