How do wrinkles appear on the face?

How are wrinkles formed?

Over time, the skin changes both in its structure and its function. These alterations, often imperceptible at first, eventually lead to the formation of wrinkles. How and why do these lines appear on the skin’s surface? Let us explore the various mechanisms that drive wrinkle development.

Published on January 20, 2026, updated on January 20, 2026, by Pauline, Chemical Engineer — 7 min of reading

What is the mechanism of wrinkle formation?

The wrinkles correspond to visible changes in the surface of the skin, resulting from progressive and profound transformations of the structure of the skin. Classically, we distinguish dynamic wrinkles, or expression lines, linked to repeated facial muscle contractions, and static wrinkles, which persist even at rest and reflect a lasting alteration of the cutaneous tissues. Although their onset is multifactorial, their formation primarily relies on a progressive imbalance between the synthesis, organisation and degradation of the components of the extracellular matrix.

Among the most striking changes observed in ageing skin are quantitative and structural alterations of collagen fibres. In young skin, the collagen is abundant, densely packed and organised into intact fibrils, providing optimal mechanical support to the skin. With age, these fibres gradually become fragmented, thickened and disorganised, weakening the dermal architecture. Furthermore, the TGF-β pathway, which stimulates the production of collagen and other structural components, becomes progressively impaired, leading to reduced collagen synthesis and accentuating dermal density loss.

This phenomenon arises from a twofold imbalance: an increase in collagen degradation coupled with a decrease in its synthesis, resulting in a net loss of collagen in the dermis.

The degradation of collagen is largely mediated by matrix metalloproteinases (MMPs), a family of enzymes capable of cleaving extracellular matrix proteins. Some MMPs, notably MMP-1, initiate fragmentation of type I and III collagen fibres, which predominate in human skin. Once these fibres are fragmented, other MMPs take over to continue their breakdown. Several studies have indeed shown an overall increase in MMP expression with age, without a proportionate rise in their natural inhibitors, the TIMPs. This is particularly the case in the work carried out by QUAN and colleagues, who examined skin biopsies from 12 volunteers aged 25 to 30 and another 12 volunteers over 80 years old.

(A) Élévation de plusieurs MMPs chez les personnes âgées (80 ans et plus) comparée à la peau humaine jeune (25 à 30 ans) – (B) Aucun changement dans l’expression de l’ARNm des TIMPs. — (A) Increased levels of multiple MMPs in elderly individuals (80 years and over) compared with young human skin (25 to 30 years) – (B) No change in TIMP mRNA expression.
Source: QUAN T. & al. Age‐related reduction of dermal fibroblast size upregulates multiple matrix metalloproteinases as observed in aged human skin in vivo. British Journal of Dermatology (2017).

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Wrinkles therefore develop as a result of the continuous, uncompensated degradation of the dermal matrix.

This mechanism is closely linked to the increase in oxidative stress, notably via the activation of intracellular signalling pathways that stimulate the production of MMPs by fibroblasts and keratinocytes. Indeed, free radicals play a key role in wrinkle formation. When produced in excess, they activate intracellular signalling cascades, notably the MAP kinase pathway, leading to the activation of transcription factors such as AP-1 and NF-κB. These then stimulate the expression of MMPs involved in the degradation of collagen and elastin, another structural fibre of the dermis. Elastin also undergoes several modifications over time. Sun exposure particularly causes an accumulation of disorganised, non-functional elastic fibres, resulting in a loss of skin elasticity.

Exposure to sunlight is one of the leading factors in skin ageing due to the substantial oxidative stress it generates. Applying sunscreen daily is therefore a key measure to prevent skin ageing.

Moreover, fibroblasts, the primary cells responsible for producing the dermal matrix, rely heavily on their mechanical interactions with the surrounding collagen. In youthful skin, these interactions enable fibroblasts to maintain an elongated shape and optimal metabolic activity. As the extracellular matrix progressively fragments, fibroblast adhesion is impaired. These cells adopt a more contracted morphology, associated with a reduced capacity to synthesise collagen and an increased production of MMPs, which directly contributes to the structural degradation of the dermis.

Finally, glycosaminoglycans (GAGs) and proteoglycans, such as hyaluronic acid, play a role in hydration, cohesion and the mechanical properties of the skin. With age, their distribution, structure and interactions with the extracellular matrix evolve. These modifications can impair the dermis’s ability to retain water, absorb mechanical stresses and maintain a supportive environment for cells. These alterations contribute to the progressive loss of volume, suppleness and resilience of the skin, indirectly contributing to wrinkle formation.

Résumé des principaux mécanismes à l'origine de la formation des rides. — Summary of the principal mechanisms underlying wrinkle formation.
Source: PARK K.-C. & al. Molecular mechanisms of dermal aging and antiaging approaches. International Journal of Molecular Sciences (2019).

In very concrete terms, what processes are at work in the formation of wrinkles?

Wrinkles form as a result of modification of the balance between the production and degradation of the skin’s supportive structures. Over time, within the dermis, collagen and elastin fibres, which govern skin suppleness and elasticity, become fewer, more fragmented and less well organised. This alteration is linked to increased degradation by certain enzymes, together with decreased synthesis by fibroblasts. At the same time, oxidative stress disrupts the cellular signals involved in extracellular matrix renewal and weakens cell-environment interactions. The skin then gradually loses its ability to resist mechanical stresses and to regain its original shape, leading to the appearance of wrinkles on its surface.