Melasma: Why It Happens and How We Treat It

Reviewed by Dr Matete Mathobela – Specialist Dermatologist
Founder of MD DermOutlet and MD Cosmeceuticals by Matete Derma

Read more about Dr Matete Mathobela →

Medical Disclaimer

This article is for educational purposes only and does not replace individual medical advice. Melasma can resemble other causes of facial pigmentation. Persistent, unusual, asymmetrical or changing pigmentation should be appropriately assessed before treatment.

Introduction

Melasma treatment can be challenging because melasma is not simply a problem of excess pigment. It is a complex, chronic pigmentation condition influenced by melanocyte activity, light exposure, hormones, inflammation, blood vessels and changes within the dermis.

Melasma is often described simply as a condition in which the skin produces too much pigment.

We now know that explanation is incomplete.

Melasma involves increased melanocyte activity, but research has also identified changes involving sun-damaged dermal tissue, senescent fibroblasts, the basement membrane, blood vessels, mast cells, oxidative stress and inflammatory signalling.

This helps explain something many people with melasma already know:

Melasma can improve — and then come back.

It also explains why treatment is rarely as simple as finding one “brightening” cream.

Modern melasma management may combine photoprotection, pigment-regulating skincare, retinoids, antioxidants, tranexamic acid and, in selected patients, procedures such as chemical peels, laser or radiofrequency microneedling.

The important question is therefore not simply:

“What fades pigmentation?”

It is:

“Which part of melasma are we trying to treat?”

2-Minute Read

• Melasma is more than excess melanin.
• UV radiation and visible light can stimulate pigmentation and contribute to recurrence.
• Melanocytes, blood vessels, mast cells, fibroblasts, oxidative stress and the basement membrane may all be involved.
• Pigmentation ingredients such as Melasyl™, thiamidol, 4-n-butylresorcinol, SebiWhite®, niacinamide, peptides and retinoids target different parts of the pigmentation pathway.
• Tranexamic acid may influence pigment production as well as vascular and inflammatory pathways.
• Tinted photoprotection containing iron oxides is particularly important for visible-light-induced pigmentation.
• Licochalcone A, Melasyl™ and Polypodium leucotomos/Fernblock® provide additional approaches to some of the biological or pigmentary consequences of light exposure.
• Chemical peels can address epidermal pigment and turnover, while newer TCA-based biorevitalising systems may provide additional remodelling effects.
• Selected laser/light treatments may address pigment, vascularity and aspects of the abnormal dermal environment.
• RF microneedling is particularly interesting because of emerging evidence involving senescent fibroblasts and basement-membrane repair.
• Melasma is chronic and recurrence is common, so maintenance matters.

In a Nutshell: Melasma Is a Multi-Pathway Condition

The important point is that two treatments may improve melasma while doing completely different jobs.

What Is Melasma?

Melasma is an acquired hyperpigmentation disorder characterised by brown to grey-brown patches, usually occurring symmetrically on sun-exposed areas of the face.

Common sites include the cheeks, forehead, upper lip, nose and chin.

It is particularly common in women and people with intermediate to higher skin phototypes, although anyone can develop melasma.

Hormonal factors—including pregnancy and hormonal medication—can contribute in susceptible individuals, but hormones alone do not explain the condition.

Light exposure is particularly important. Ultraviolet radiation stimulates melanogenesis and contributes to photoageing, while visible light can also produce persistent pigmentation, particularly in melanocompetent skin.

Why Does Melasma Happen?

Melasma-affected skin is biologically different from nearby unaffected skin.

Melanocytes Become More Active

Melanocytes are the cells responsible for producing melanin.

In melasma, they respond to multiple signals coming from light exposure and the surrounding epidermal and dermal environment.

Even melanogenesis itself offers several possible treatment targets:

This is why the term “brightening ingredient” is far too broad.

The Dermis Is Involved

Melasma-affected skin often demonstrates solar elastosis and other evidence of chronic photodamage.

Of particular interest are senescent fibroblasts.

These cells have stopped dividing but remain biologically active. They can release factors such as stem-cell factor, hepatocyte growth factor, keratinocyte growth factor and VEGF that influence melanocytes, blood vessels and the surrounding extracellular matrix.

This may help explain why removing superficial pigment does not necessarily remove the biological tendency to develop melasma.

The Basement Membrane Can Be Disrupted

The basement membrane separates the epidermis from the dermis.

Chronic photodamage and increased matrix metalloproteinase activity may contribute to basement-membrane disruption in melasma.

Histological studies have also described melanocytes protruding downward towards the dermis, sometimes referred to as pendulous melanocytes.

This again demonstrates why melasma cannot always be treated as purely superficial pigmentation.

Blood Vessels Are Part of the Picture

Melasma lesions may demonstrate increased vascularity and increased signalling involving mediators such as VEGF and endothelin-1.

There is also evidence of communication between vascular endothelial cells, fibroblasts and melanocytes.

This is clinically relevant because patients with visible vascular features on dermoscopy may represent a subgroup in whom vascular-targeted treatment becomes particularly interesting.

Mast Cells May Contribute

Mast cells are inflammatory cells capable of releasing mediators that influence melanogenesis, vascular changes and extracellular-matrix remodelling.

Their increased presence in melasma provides another link between:

photodamage → inflammation → dermal/vascular changes → melanogenesis

Oxidative Stress Matters

UV and visible-light exposure can generate reactive oxygen species.

Oxidative stress contributes to cellular damage, photoageing and melanogenic signalling.

This gives antioxidants a rational role in melasma management—but antioxidant defence is not automatically the same as physically blocking visible light.

Targeting Melanin: Not All Pigmentation Ingredients Work the Same Way

Melasyl™: A Different Way to Target Pigment

Melasyl™, or 2-mercaptonicotinoyl glycine (2-MNG), does not work like a conventional tyrosinase inhibitor.

It interacts with reactive melanin precursors before they become incorporated into mature pigment.

It therefore provides a useful example of why modern pigmentation treatment should not be reduced to finding the strongest tyrosinase inhibitor.

4-n-Butylresorcinol

4-n-Butylresorcinol inhibits both tyrosinase and tyrosinase-related protein-1 and has clinical evidence in hyperpigmentation.

Multi-pathway formulations may combine it with other mechanisms. For example, one formulation may combine butylresorcinol, alpha-arbutin, kojic acid, tranexamic acid, niacinamide, undecylenoyl phenylalanine and a pigment-regulating peptide.

The value is not simply having many ingredients. It is that the ingredients intervene at different stages of pigmentation.

Pigment-Regulating Peptides

“Peptides” should not be treated as one single pigmentation ingredient because their mechanisms and clinical evidence vary.

For example, the peptide Pro-Lys-Glu-Lys (PKEK) has been studied in South African participants with Fitzpatrick phototypes V–VI and melasma or PIH, with improvement in skin-tone evenness.

The evidence for each peptide should therefore be considered individually rather than assuming all pigment peptides are equivalent.

Retinoids Still Matter

Retinoids increase epidermal turnover, help disperse epidermal pigment and can complement other pigment-regulating treatments.

They are also part of established combination therapy for melasma.

However, excessive irritation is counterproductive.

More peeling does not mean more effective melasma treatment.

Why Tranexamic Acid Is Particularly Interesting

Tranexamic acid (TXA) is not simply another pigment inhibitor.

It inhibits the plasminogen/plasmin pathway, which helps explain its effect on melanogenic signalling after UV exposure.

Its relevance may extend further:

TXA has been studied topically, intradermally and orally.

Oral tranexamic acid is not a cosmetic supplement and should not be self-prescribed.

Its systemic antifibrinolytic effects mean thromboembolic risk and contraindications need to be assessed.

Support Your Melasma Routine at Home
A consistent home routine is an important part of long-term melasma management. Explore dermatologist-selected pigmentation skincare, including targeted serums, moisturisers and daily photoprotection available from MD DermOutlet.

Shop Melasma & Pigmentation Skincare

Melasma Photoprotection: It Is About More Than SPF

For melasma, SPF alone does not tell the full photoprotection story.

A comprehensive approach considers UVB, UVA, visible light and the biological consequences of light exposure.

Iron Oxides

Tinted sunscreens containing iron oxides are particularly useful because they attenuate visible light itself.

Clinical studies in melasma have shown better pigmentation outcomes when visible-light protection is added to strong UV protection.

Colour match also matters: a sunscreen only works if enough is applied consistently.

Licochalcone A

Licochalcone A provides a different form of defence.

Experimental and in-vivo research shows that it can reduce high-energy-visible-light-induced oxidative stress.

It is used in selected Eucerin photoprotective formulations for this reason.

Licochalcone A and iron oxides should not be considered interchangeable. Iron oxides attenuate visible light, whereas Licochalcone A helps counter some of the oxidative biological consequences of exposure.

They can therefore complement each other.

Melasyl™ and Visible-Light-Induced Pigmentation

Melasyl provides another strategy.

Human controlled studies have found that 2-MNG can reduce pigmentation induced by repeated HEVL exposure.

It does not physically block visible light. Instead, it interferes with the pigment that would otherwise be produced downstream from that light exposure.

Where Does Fernblock® Fit?

Fernblock® is a standardised Polypodium leucotomos extract used as an oral photoprotective adjunct.

Its proposed benefits include antioxidant, anti-inflammatory and broader photobiological effects, and Polypodium leucotomos has also been studied as an adjunct in melasma treatment.

I consider it an additional layer of photoprotection—not an oral replacement for sunscreen.

What About Other Antioxidants?

Vitamin C, vitamin E, ferulic acid and resveratrol still have roles because oxidative stress is relevant to melasma.

However, an antioxidant should not automatically be described as a visible-light blocker.

Daily Photoprotection Matters
Melasma management does not stop with treatment. Daily broad-spectrum photoprotection—and, where appropriate, protection against visible light—is one of the most important steps for reducing recurrence.

Shop Sunscreens & Photoprotection

Chemical Peels for Melasma: More Than Exfoliation

Chemical peels can help melasma by promoting controlled epidermal renewal and removal of pigment-containing keratinocytes. However, modern TCA-based systems may provide effects beyond conventional exfoliation.

Conventional Chemical Peels

Glycolic, salicylic, mandelic and conventional TCA peels primarily help by promoting controlled epidermal turnover and reducing pigment-containing keratinocytes.

TCA also causes protein coagulation and, depending on concentration and treatment depth, stimulates regeneration extending beyond simple surface exfoliation.

In darker phototypes, depth and inflammation need particularly careful control because excessive chemical injury may provoke PIH.

PRX-T33: More Than a Conventional TCA Peel

PRX-T33 combines 33% TCA, hydrogen peroxide and kojic acid.

It is better described as a TCA-based biorevitalisation treatment than as a traditional frosting/peeling procedure.

From a melasma perspective, the attraction is that the treatment potentially combines pigment regulation with regenerative stimulation, rather than relying exclusively on removal of epidermal pigment.

BioRePeelCl₃: TCA Plus a Multi-Component Biorevitalising System

BioRePeelCl₃ is a biphasic TCA-based treatment. The facial formulation incorporates 35% TCA alongside alpha-, beta- and polyhydroxy acids and additional amino-acid, vitamin and biorevitalising components.

BioRePeel is therefore better understood as a multi-component resurfacing and biorevitalising treatment rather than simply an exfoliating peel.

Are PRX-T33 and BioRePeel Better Than Conventional Peels?

Not automatically.

Different peel systems have different advantages, and established superficial peels still have evidence in melasma.

The most appropriate treatment depends on skin phototype, barrier status, depth and pattern of pigmentation, previous reactions and other treatments being used.

The principle remains:

enough controlled stimulation to improve pigmentation without generating unnecessary inflammation.

Could a Chemical Peel Be Part of Your Melasma Plan?
Chemical peels can help target superficial pigmentation and support skin renewal, but the type and strength of peel should be selected according to your skin type, pigmentation pattern and risk of post-inflammatory hyperpigmentation.

Explore Chemical Peel Treatments

Laser and Light Treatment: Targeting More Than Melanin

Laser treatment for melasma requires careful patient selection because excessive heat or inflammation can trigger rebound pigmentation or post-inflammatory hyperpigmentation, particularly in darker skin phototypes.

However, our evolving understanding of melasma provides a broader rationale for laser and light treatment than simply targeting pigment.

Melasma may involve increased melanin, abnormal vascularity, photoaged dermal tissue, basement-membrane disruption and senescent fibroblasts.

Different energy-based treatments can therefore target different components of the condition.

Why Target the Vascular Component?

Melasma lesions may demonstrate increased blood-vessel number, size and density, together with increased vascular signalling.

This matters because blood vessels are not simply an incidental finding.

Senescent fibroblasts can release VEGF, promoting neovascularisation, while vascular endothelial cells can release mediators such as endothelin-1, which stimulate melanocytes.

This provides a biological rationale for vascular-directed treatment:

reduce abnormal vascular signalling → potentially reduce one source of melanocyte stimulation

This may be particularly relevant in patients whose melasma demonstrates visibly widened vessels on dermoscopy.

What About the Dermal Component?

Laser treatment may also be relevant to the abnormal dermal environment found in melasma.

Senescent fibroblasts can release melanogenic, inflammatory and vascular mediators, while chronic photodamage contributes to basement-membrane abnormalities and solar elastosis.

The current pathogenesis literature therefore proposes selected fractional and remodelling laser therapies as one way of addressing some of these deeper abnormalities.

This is an important distinction:

some lasers primarily target pigment or vessels, while others may exert their effects partly through dermal remodelling.

Where Does Aerolase Neo Elite® Fit?

In my practice, Aerolase Neo Elite® is one laser option that may be considered for appropriately selected patients with melasma.

It uses a 1064 nm Nd:YAG wavelength with a 650-microsecond pulse duration.

Rather than viewing treatment simply as “breaking up pigment”, its potential relevance can be considered across several targets:

This gives Aerolase a potential role in addressing pigment, vascular features and the dermal environment as part of a broader melasma treatment strategy.

Laser is not appropriate for every patient. Skin phototype, pigment depth, vascular features, previous treatment response, PIH tendency, barrier status and concurrent treatments all influence whether it is appropriate.

Laser and light therapies can be useful options for selected or treatment-resistant melasma, but outcomes vary considerably between devices and protocols.

For this reason, I view laser as a selected adjunct rather than a stand-alone cure.

Considering Laser Treatment for Melasma?
Laser treatment for melasma needs careful patient selection, particularly in darker skin tones where excessive inflammation can worsen pigmentation. At our dermatology practices, laser treatment may be considered as part of an individualised melasma treatment plan.

Explore Laser Treatments

RF Microneedling and Senescent Fibroblasts

RF microneedling has a particularly interesting pathogenesis-based rationale because it targets the dermis while limiting epidermal injury.

Research has demonstrated increased senescent fibroblasts in melasma lesions, and RF treatment has been associated with:

A 2026 systematic review identified 12 clinical studies and found consistent improvement in melasma severity or melanin measures, with histological evidence of reduced dermal senescence markers and partial restoration of basement-membrane integrity.

This gives RF microneedling one of the clearest examples of pathogenesis-directed procedural treatment:

rather than simply targeting melanin, we may also be modifying part of the abnormal dermal environment that keeps stimulating melanocytes.

RF microneedling may therefore be considered for appropriately selected patients, but it is not a universal first-line treatment or permanent cure.

Building a Practical Melasma Treatment Plan

The pathogenesis is complicated, but a patient’s daily routine does not need to be.

Depending on the patient, additional options may include topical or oral TXA, oral Polypodium leucotomos, chemical peels, selected laser treatment or RF microneedling.

Multi-ingredient formulations may also be useful when their mechanisms genuinely complement one another.

For example, one pigmentation formulation may combine butylresorcinol, alpha-arbutin, kojic acid, TXA, niacinamide, SebiWhite® and a pigment-regulating peptide, while another may combine mandelic acid with pigment regulators, antioxidants and barrier-supporting lipids such as ceramides and cholesterol.

The principle is:

complementary mechanisms + good tolerability + consistent use

—not the longest possible ingredient list.

When Should We Consider In-Room Treatment?

Procedural treatment may be considered when topical treatment alone is inadequate, the diagnosis is secure and the skin is stable enough to tolerate intervention.

Procedures do not replace daily photoprotection, maintenance skincare and management of ongoing triggers.

Why Does Melasma Keep Coming Back?

Treatment may reduce visible pigmentation without eliminating the underlying susceptibility.

This is why I prefer to talk about melasma control and maintenance, rather than promise permanent clearance.

What Can Make Melasma Worse?

Common contributors include inadequate photoprotection, visible-light exposure, hormonal triggers, irritating skincare, over-exfoliation, inappropriate or overly aggressive procedures, poor treatment adherence and stopping maintenance therapy immediately after improvement.

One principle is particularly important in darker skin:

Do not create inflammation while trying to treat pigmentation.

Dermatologist’s Perspective

When I treat melasma, I don’t see it simply as brown pigment that needs to be removed.

I ask:

What is likely driving the pigmentation in this patient?

Is melanogenesis the dominant problem?

Is there substantial photodamage?

Are vascular features visible?

Is the barrier already irritated?

Does the patient develop PIH very easily?

Are UVA and visible light being adequately addressed?

Could a topical programme be enough, or is there a reason to consider TXA, a peel, laser or RF microneedling?

And perhaps most importantly:

How much treatment can this particular skin tolerate without inflammation becoming another driver of pigmentation?

Two patients with melasma may therefore leave with very different treatment plans.

Understanding the pathogenesis allows us to move beyond simply treating the colour we can see and towards addressing the biological processes helping to maintain it.

Frequently Asked Questions

Can melasma be cured permanently?

Melasma is generally considered a chronic, relapsing condition.

It can often be substantially improved and controlled, but recurrence is common. Long-term photoprotection and maintenance therapy are therefore important.

What is the best ingredient for melasma?

There is no universally best ingredient.

Options include hydroquinone, thiamidol, 4-n-butylresorcinol, Melasyl™, azelaic acid, arbutin, kojic acid, TXA, retinoids, niacinamide, SebiWhite® and selected pigment-regulating peptides.

The best choice depends on the patient and overall treatment plan.

Is Melasyl™ the same as a tyrosinase inhibitor?

No.

Melasyl acts by interacting with reactive melanin precursors rather than primarily inhibiting tyrosinase.

Do I need a tinted sunscreen for melasma?

Tinted sunscreens containing appropriate pigments such as iron oxides can provide additional protection against visible-light-induced pigmentation.

This can be particularly relevant in melasma and darker phototypes.

Does Licochalcone A protect against visible light?

Licochalcone A has evidence showing protection against HEVIS-induced oxidative stress.

It should not be considered identical to iron oxides.

Iron oxides attenuate visible light, whereas Licochalcone A helps counter some of the oxidative biological consequences of exposure.

Can Fernblock® or Polypodium leucotomos replace sunscreen?

No.

Polypodium leucotomos is best considered an adjunctive oral photoprotective strategy.

It does not replace adequately applied broad-spectrum topical sunscreen or visible-light protection.

Does tranexamic acid only reduce melanin production?

No.

TXA acts through the plasminogen/plasmin pathway and may also influence vascular and inflammatory pathways implicated in melasma.

Can oral tranexamic acid be taken for melasma?

Oral TXA may be considered in appropriately selected patients but requires medical assessment because of its systemic antifibrinolytic activity and thrombotic considerations.

Do chemical peels help melasma?

Yes, particularly by promoting controlled epidermal turnover.

However, newer TCA-based systems such as PRX-T33 and BioRePeelCl₃ have a broader formulation rationale than conventional exfoliation alone.

They are still adjuncts rather than cures.

What is the difference between PRX-T33 and a traditional TCA peel?

Traditional TCA produces controlled chemical injury and visible peeling according to concentration and depth.

PRX-T33 combines 33% TCA, hydrogen peroxide and kojic acid in a formulation designed to provide biorevitalising TCA stimulation with less conventional epidermal caustic injury.

Can Aerolase treat melasma?

Aerolase Neo Elite is a 650-microsecond 1064 nm Nd:YAG platform that may be considered in selected melasma patients.

Its potential relevance includes pigment, vascular features and dermal remodelling as part of a broader treatment strategy.

It is not appropriate for every patient and should not be considered a permanent cure.

Does RF microneedling help melasma?

Emerging evidence is encouraging.

RF microneedling is particularly interesting because studies have demonstrated improvement in pigmentation alongside reductions in dermal senescence markers and partial restoration of basement-membrane integrity.

How long does melasma treatment take?

Response varies according to severity, phototype, triggers, adherence, treatment selection and photoprotection.

I prefer to assess whether pigmentation is progressively improving while the skin remains able to tolerate the treatment, followed by an appropriate maintenance plan.

Final Thoughts

Our understanding of melasma has moved far beyond the idea of simply having “too much melanin.”

Melasma involves interactions between melanocytes, keratinocytes, fibroblasts, blood vessels, mast cells, the basement membrane, oxidative stress and environmental light exposure.

This explains why successful management may involve several complementary strategies rather than relying on one pigment treatment.

The aim is not to target every pathway in every patient. It is to identify which pathways and triggers appear most clinically relevant, select treatments that complement one another, minimise unnecessary inflammation and maintain the results.

For me, that is the central message of modern melasma management:

Treat the biology behind the pigmentation—not only the pigment we can see.

Not Sure Where to Start With Your Melasma?
Melasma does not look or behave the same in everyone. A dermatologist can assess your pigmentation pattern, contributing factors and skin type before deciding whether your plan should focus on skincare, prescription treatment, chemical peels, laser, RF microneedling or a combination approach.

Book a Dermatology Consultation

Suggested Related Articles

• Hyperpigmentation: A Dermatologist’s Guide
• How to Layer Skincare Products Correctly
• Aerolase Nd:YAG Laser: A Dermatologist’s Guide
• Where to Buy Authentic Dermatologist-Recommended Skincare in South Africa

References

1. Ali L, Al-Niaimi F. Pathogenesis of Melasma Explained. International Journal of Dermatology. 2025;64:1201–1212.
   Read the full article
2. Masub N, Nguyen JK, Austin E, Jagdeo J. The Vascular Component of Melasma: A Systematic Review of Laboratory, Diagnostic, and Therapeutic Evidence. Dermatologic Surgery.
   Read the vascular melasma systematic review
3. Lai D, Zhou S, Cheng S, et al. Laser therapy in the treatment of melasma: a systematic review and meta-analysis.
   Read the laser systematic review and meta-analysis
4. Kumar N, et al. The Efficacy and Safety of Radiofrequency Microneedling for Melasma: A Systematic Review and Qualitative Evidence Synthesis. 2026.
   Read the RF microneedling systematic review
5. Castanedo-Cazares JP, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial.
   View the study on PubMed
6. Piffaut V, et al. Topical prevention from high-energy-visible-light-induced pigmentation by 2-mercaptonicotinoyl glycine, but not by ascorbic acid antioxidant: two randomized controlled trials.
   View the HEVL and 2-MNG study on PubMed
7. Mann T, et al. High-energy visible light at ambient doses and intensities induces oxidative stress of skin: protective effects of Licochalcone A in vitro and in vivo.
   View the Licochalcone A study on PubMed
8. Goh CL, et al. Polypodium leucotomos extract as an adjunct to sunscreen in the treatment of melasma.
   View the Polypodium leucotomos melasma research on PubMed