How do wrinkles appear on the face?

How do wrinkles form?

Over time, skin evolves both in its structure and its function. These changes, often invisible at first, eventually manifest as wrinkles. How and why do these marks form on the skin’s surface? Let’s decode the various mechanisms that lead to wrinkle formation.

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 skin surface, resulting from progressive and profound changes in the structure of the skin. They are classically classified as dynamic, or expression, wrinkles, linked to repeated facial muscle contractions, and static wrinkles, which persist even at rest and reflect lasting deterioration of skin tissue. Although their emergence is multifactorial, their formation primarily relies on a progressive imbalance between the synthesis, organization, and degradation of extracellular matrix components.

Among the most striking changes observed in the aging skin are the quantitative and structural changes of collagen fibers. In young skin, the collagen is abundant, dense, and organized into intact fibrils, providing optimal mechanical strength to the skin. With age, these fibers gradually become fragmented, thicker, and disorganized, weakening the dermal architecture. Moreover, the TGF-β pathway, which stimulates the production of collagen and other structural components, is progressively impaired with age, leading to a reduction in collagen synthesis, accentuating the loss of dermal density.

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

Collagen degradation is largely mediated by matrix metalloproteinases (MMPs), a family of enzymes capable of cleaving extracellular matrix proteins. Some MMPs, notably MMP-1, initiate the fragmentation of type I and III collagen fibers, which are predominant in human skin. Once these fibers are fragmented, other MMPs take over to continue their degradation. Several studies have indeed reported an overall increase in MMP expression with age, without a proportional rise in their natural inhibitors, the TIMPs. This is particularly illustrated by the work of QUAN and his team, who studied 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) Elevated levels of multiple MMPs in elderly individuals (80 years and older) compared to young human skin (25–30 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 thus form as a result of a continuous, uncompensated degradation of the dermal matrix.

This mechanism is closely linked to an increase in oxidative stress, notably through activation of intracellular signaling pathways that stimulate MMP production by fibroblasts and keratinocytes. Indeed, free radicals play a key role in wrinkle formation. When produced in excess, they activate intracellular signaling cascades, notably the MAP kinase pathway, leading to activation of transcription factors such as AP-1 and NF-κB. These, in turn, stimulate the expression of MMPs involved in the degradation of collagen and elastin, another structural fiber of the dermis. Elastin itself also undergoes several changes over time. Sun exposure, in particular, causes an accumulation of disorganized, nonfunctional elastic fibers, resulting in a loss of skin elasticity.

Sun exposure is one of the leading factors of skin aging due to the significant oxidative stress it induces. Applying sunscreen daily is therefore a key measure to prevent skin aging.

Furthermore, fibroblasts, the main cells responsible for producing the dermal matrix, depend closely on their mechanical interactions with surrounding collagen. In young skin, these interactions enable fibroblasts to maintain an elongated shape and optimal metabolic activity. With the progressive fragmentation of the extracellular matrix, fibroblast adhesion is impaired. These cells adopt a smaller morphology, associated with a reduced ability to produce 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, contribute to the hydration, cohesion, and mechanical properties of the skin. With age, their distribution, structure, and interactions with the extracellular matrix change. 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 promoting 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).

More concretely, which processes are at work in the formation of wrinkles?

Wrinkles form as a result of the alteration of the balance between the production and degradation of the skin’s supporting structures. Over time, within the dermis, collagen and elastin fibers that determine skin suppleness and elasticity become fewer in number, more fragmented, and less well organized. This change is associated with increased enzymatic breakdown and reduced synthesis by fibroblasts. Concurrently, oxidative stress disrupts the cellular signals involved in extracellular matrix renewal and weakens interactions between cells and their environment. The skin then gradually loses its ability to withstand mechanical stress and to return to its original shape, leading to the appearance of wrinkles on its surface.