How Chemical Peels Work

A chemical peel applies an acid (or a phenol) to the skin to create a controlled, depth-limited injury. The acid wounds tissue to a level you choose; the skin then heals from that insult, and it is the healing — re-epithelialization of the epidermis and, at deeper levels, dermal collagen remodeling — that produces the brighter, smoother, more even result. The acid is the trigger; the biology is the treatment.

The mechanism: injury, then a repair cascade

Every peel works the same way at the level of principle. The agent disrupts the skin to a defined depth, the disrupted tissue is shed or resorbed, and the wound-healing response rebuilds it. Three things happen in sequence:

1. Exfoliation / corneocyte disruption. Acids reduce corneocyte cohesion or denature surface protein, removing the outer, often dyspigmented and disorganised layers.
2. Re-epithelialization. A fresh epidermis regenerates from the adnexal reservoir — the keratinocytes lining hair follicles and sweat-gland ducts. Because adnexal structures survive superficial and medium injury, the epidermis can fully reconstitute. This is also why depth that destroys those reservoirs is the threshold where scarring risk climbs.
3. Dermal remodeling. When injury reaches the dermis, the wound-healing cascade upregulates fibroblast activity, neocollagenesis and reorganisation of the dermal matrix over weeks to months — the basis of textural and fine-line improvement from medium and deep peels.

Coagulant versus metabolic acids

It is clinically useful to split peeling agents by how they injure, because it predicts how the peel behaves on the chair.

• Coagulant (keratocoagulant) agents — trichloroacetic acid (TCA) is the archetype — work by protein denaturation. They precipitate epidermal and dermal proteins, producing the visible white frost as denatured keratin. Depth is tightly coupled to concentration and the number of layers, and the frost gives you a real-time depth readout.
• Metabolic / keratolytic acids — the alpha-hydroxy acids (glycolic, lactic, mandelic) — do not primarily coagulate protein. They reduce corneocyte adhesion and thin the stratum corneum, and at the cellular level they signal accelerated epidermal turnover. Most metabolic peels never frost; they are time- and pH-dependent and usually require neutralisation to stop.
• Salicylic acid (a beta-hydroxy acid) is lipophilic and keratolytic, concentrating in sebaceous units; the white film it leaves is pseudofrost (precipitated salicylic acid), not protein coagulation — a distinction that matters when you read endpoints.

This split is why "the acid on the label" tells you less than clinicians expect: a 70% glycolic and a 25% TCA injure by different mechanisms and are titrated by different variables.

What actually determines the effect

Two peels using the same molecule can behave completely differently. The effect is governed by a small set of controllable variables:

For AHAs in particular, free-acid value and pH — not the labelled percentage alone — determine real potency: a partially neutralised 50% glycolic can be gentler than a fully free 30%. For TCA, concentration and coat count dominate. Across all agents, priming and degreasing standardise the barrier so that the same protocol lands at the same depth on the next patient.

Why this matters first in skin of color

Mechanism is identical across phototypes, but the cost of overshooting depth is not. In Fitzpatrick IV–VI skin, melanocytes are labile and readily triggered by inflammation, so an injury deeper than intended is the principal driver of post-inflammatory hyperpigmentation (PIH). The clinical consequence is conservative: in darker skin you favour controllable, shallow-to-moderate mechanisms (metabolic AHAs, mandelic, lower-strength TCA), prime the skin, and treat depth as something to limit, not maximise. The biology of injury-and-repair is your tool; restraint is how you keep it safe.

Key takeaway

A peel does not work by "dissolving" skin. It works by injuring tissue to a chosen depth and letting the healing response rebuild it better. Understand the mechanism (coagulant vs metabolic), control the depth (agent, concentration, free acid/pH, time, layering, priming), and you control both the result and the risk — which is exactly what the rest of Foundations builds on.