Melasma Is Not Just “Too Much Melanin” — The Skin Biology Behind Recurrent Pigmentation

What is melasma, exactly?

Melasma is an acquired disorder of hyperpigmentation, usually appearing as symmetrical brown or grey-brown patches on sun-exposed facial skin.

It is more common in women and particularly common in people with medium to deeper skin tones. Pregnancy, hormonal exposure, family history and light exposure are well recognised associations.

But modern research has changed the way dermatology describes the condition. The older explanation — “melanocytes are making too much pigment” — is incomplete.

Reviews now describe changes in the epidermis, basement membrane and upper dermis, including vascular changes, mast-cell activity, solar elastosis and senescent fibroblasts. In other words, melasma is a disorder of the skin microenvironment, not just one overactive cell type. At EC Clinic in Dublin, that starts with a doctor-led skin consultation rather than a treatment package.

How does a visible dark patch form in the first place?

To understand melasma, it helps to follow the pigment from signal to surface.

Step 1: a trigger creates a signal. Ultraviolet radiation, visible light, inflammation and hormonal signalling can all increase melanogenic signals in susceptible skin.

Step 2: keratinocytes and other cells “talk” to melanocytes. Keratinocytes are the main cells in the epidermis. After light exposure or inflammation, they release signalling molecules that can stimulate nearby melanocytes. Pigmentation is therefore a conversation between cells.

Step 3: the melanocyte switches on melanin production. Inside the melanocyte, several biochemical pathways regulate pigment production. Tyrosinase is a key enzyme involved in converting the amino acid tyrosine through steps that ultimately produce melanin.

Step 4: pigment is packaged. Melanin is packaged inside small cellular structures called melanosomes.

Step 5: melanosomes are delivered to keratinocytes. Melanocytes have branching extensions called dendrites. Through these, melanosomes are transferred into neighbouring keratinocytes. The melanin then sits above the keratinocyte nucleus like a microscopic umbrella, helping protect DNA from radiation.

That protective system is normal. Melasma is what happens when the signalling and tissue environment keep driving pigment production in a focal, persistent way.

Why does melasma keep coming back after I lighten it?

Because the visible pigment is only one layer of the problem.

Peer-reviewed reviews describe several changes in melasma skin:

• hyperactive melanocyte signalling
• increased or redistributed melanin in epidermis and sometimes dermis
• basement-membrane disruption
• solar elastosis, a sign of chronic photodamage
• increased vascularisation
• mast-cell activity
• senescent fibroblasts and altered dermal signalling

This helps explain why a treatment can reduce colour and still leave the biological environment ready to reactivate.

If the skin remains highly light-exposed, inflamed or hormonally stimulated, pigment production can begin again.

Recurrence is not proof that treatment “did nothing.” It is part of the natural history of a chronic pigment disorder.

What is the role of visible light? I thought only UV mattered.

UV remains central, but visible light matters too, particularly in pigmentation-prone skin.

Research has shown that high-energy visible light can stimulate pigmentation through photoreceptors and melanogenic pathways. UVA1 — the longer-wave portion of UVA — also contributes to pigment and dermal change.

This matters because visible light is not captured perfectly by the simple idea “I wore SPF, therefore all light was blocked.” Some patients with melasma benefit from photoprotection strategies designed for visible light as well as UV.

The clinical point is not to create fear of daylight. It is to recognise that melasma management often requires more consistent photoprotection than someone treating an occasional sun spot.

Are hormones the cause of melasma?

Sometimes they are an important contributor. They are rarely the whole explanation.

Melasma is strongly associated with pregnancy and can occur or worsen with hormonal exposures in susceptible patients. Oestrogen and progesterone signalling can influence melanogenesis.

But an association does not mean every woman with melasma needs a hormone panel, needs to stop contraception or has a gynaecological disorder.

If pigmentation appeared during pregnancy, perimenopause or after a hormonal treatment change, that history is relevant. It may influence the conversation. It does not automatically dictate the treatment.

This is where having gynaecology and aesthetics in the same clinic can be useful: hormonal history is considered without turning every skin problem into “hormonal imbalance.”

Does heat make melasma worse?

Heat is frequently reported as a trigger by patients, and inflammation can influence melanogenic pathways. But the evidence is more complex than the evidence for ultraviolet and visible light.

The practical approach is individual: if heat exposure repeatedly worsens your pigmentation, we take that pattern seriously. We do not need to invent a universal rule for every patient.

What I would avoid is aggressively inflaming melasma-prone skin in the hope that “more treatment” must mean “more result.” In pigmentation, more inflammation can mean more pigment.

Is every brown patch on the face melasma?

No, and this is why diagnosis comes before the treatment menu.

Other possibilities include:

• post-inflammatory hyperpigmentation, which follows acne, dermatitis, injury or procedures
• solar lentigines, often called sun spots
• pigmentation from medication or inflammation
• benign lesions with their own biology
• lesions that require dermatology assessment because their pattern is atypical or changing

A treatment appropriate for one diagnosis may be ineffective or inappropriate for another.

The question I prefer is not “What laser removes dark spots?” It is “What is this pigment, and what keeps producing it?”

Why can aggressive laser or peeling make melasma worse?

Because pigment-producing cells respond to inflammation.

Many procedures work by creating controlled injury. In the right condition, right skin type and right settings, this can be useful. But melasma is already a pigment-reactive disorder. If a procedure creates excessive inflammation, post-inflammatory hyperpigmentation or rebound melasma can follow.

This is especially important in richer skin tones, where the risk of post-inflammatory pigmentation is higher.

It is not that procedures are “bad.” It is that indication, energy, depth, density, timing and skin type matter. Where resurfacing belongs in a plan at all, it is selective — see our page on CO2 laser resurfacing for how that modality is used at EC Clinic when clinically appropriate.

A clinic that has only one device will often see every pigmentation problem as a reason to use that device. A medical consultation should work in the opposite direction: diagnose first, then choose whether a device belongs in the plan at all.

What are the evidence-based principles of melasma treatment?

The exact treatment is individual, but the strategy usually has several layers.

1. Photoprotection. This is foundational. If light keeps activating the pathway, every other treatment is working uphill.

2. Reduce avoidable triggers and inflammation. That can include reviewing irritating skincare, unnecessary procedures or personal patterns that repeatedly worsen the pigment.

3. Use appropriate topical medical therapy where indicated. Topical treatments can reduce melanogenesis through different pathways. Because public advertising of prescription-only medicines is restricted in Ireland, this article discusses treatment categories rather than promoting prescription products by brand.

4. Use procedures selectively. Peels, resurfacing and other procedures can play a role in carefully selected cases, but they are not automatically first-line and not automatically better than topical management.

5. Plan for maintenance. Melasma often needs long-term management. A realistic plan includes what happens after the visible improvement, not only how to create it.

Is autumn the best time to treat melasma in Ireland?

Autumn can be a practical treatment window because average UV exposure falls and patients are less likely to have intense holiday sun exposure.

But “Irish autumn” does not mean “no UVA.” UVA is present through cloud and can pass through glass. Visible light is also still present.

So autumn changes the risk environment, not the biology of melasma. It can make certain procedures easier to plan safely, but photoprotection remains part of the treatment throughout the year. Our guide to why autumn and winter are the best time for laser skin treatments in Ireland covers the seasonal UV side of that calendar.

Why does skin type change the plan?

Melanin is protective, but pigment-rich skin also has a stronger tendency to respond to inflammation with hyperpigmentation.

That means a patient with a higher Fitzpatrick skin type may need:

• more conservative procedural settings
• more careful preparation
• longer intervals between treatments
• more emphasis on barrier control and photoprotection
• realistic discussion of post-inflammatory hyperpigmentation risk

There is no single “melasma protocol” that should be applied to every face.

What does a good melasma consultation actually look like?

It begins with diagnosis and history, not a treatment package.

I want to know:

• when the pigment began
• whether pregnancy or hormonal change coincided with it
• whether acne, dermatitis or a procedure came first
• what treatments have already been tried
• whether the pigment worsens with sun, heat or inflammation
• what your skin does after spots, burns or procedures
• what skincare and photoprotection you actually use

Then we examine the pattern and decide whether this looks like melasma, another form of hyperpigmentation, or something that should be assessed by dermatology.

That is a much more valuable first appointment than simply selling the strongest treatment available.

Medically reviewed by Dr. Eliana Castañeda, Obstetrician-Gynaecologist and Aesthetic Specialist · 14 September 2026

— Dr. Eliana Castañeda
Obstetrician-Gynaecologist and Aesthetic Specialist · Medical Director, EC Clinic Dublin