What Is Melasma? Definition and Epidemiology
Melasma (from the Greek melas = black) is an acquired hyperpigmentation disorder characterized by irregular brown-grey pigmentation on the face, neck, or forearms, resulting from excessive stimulation of melanocytes. Because it frequently appears during pregnancy, it is commonly known as the "pregnancy mask" or chloasma. In medical literature, the term chloasma is specifically used for pregnancy-related forms.
In regions where Fitzpatrick skin types III–V predominate — such as Turkey — prevalence ranges from 8–29%; it is approximately 9 times more common in women than in men. In areas with high sun exposure and distinct seasons, such as the Kocaeli/Izmit region, seasonal flares are particularly concentrated in spring and summer.
Melasma is not merely a cosmetic concern: research shows that patients experience loss of self-confidence, social withdrawal, and anxiety. Dermatology Life Quality Index (DLQI) studies consistently place melasma patients in the moderate impairment category. Treatment must therefore be evaluated from both a medical and a psychological perspective.
Biochemistry of Melanogenesis: Why Does Melasma Occur?
Melanogenesis is a complex enzymatic process that takes place in melanocytes and regulates melanin production. The key enzyme, tyrosinase, converts tyrosine to DOPA and dopaquinone, initiating the synthesis of both eumelanin (black-brown) and pheomelanin (yellow-red). Melanin pigments produced in melanocytes are transferred to surrounding keratinocytes via organelles called melanosomes.
In melasma pathogenesis, the number of melanocytes does not increase; rather, existing melanocytes become hyperactivated. The principal mechanisms driving this hyperactivation are: UV-B-induced DNA damage and increased melanocortin (alpha-MSH); oestrogen-mediated induction of tyrosinase through melanocyte receptors; and mast cell activation with stem cell factor (SCF) release.
Causes and Triggers of Melasma
The main factors that initiate melanocyte hyperactivation are as follows:
- UV radiation exposure: The most critical and universal trigger. UVA (320–400 nm) and UVB (280–320 nm) rays stimulate melanocytes and increase melanin synthesis. Because visible light (including blue light) and infrared radiation can also trigger melanogenesis, mineral sunscreens are preferred.
- Hormonal changes: Oestrogen and progesterone increase sensitivity to melanocortin. Pregnancy, oral contraceptives (especially those with high oestrogen content), and hormone replacement therapy (HRT) are the primary hormonal triggers.
- Genetic predisposition: A history of melasma in first-degree relatives is a strong risk factor; HLA and MC1R gene variants are under investigation.
- Thyroid dysfunction: Several studies have identified a significant association between thyroid disease and melasma, particularly Hashimoto thyroiditis.
- Phototoxic and photoallergic agents: Fragrances, certain botanical extracts (bergamot oil), tetracycline, and amiodarone can act as triggers.
- Heat exposure: Infrared radiation and chronic heat exposure (including occupational sources) can increase melanogenesis; physical barrier protection is therefore important in addition to chemical sunscreen.
Clinical Types of Melasma: Wood Lamp and Dermoscopy Assessment
The depth of pigment within the skin is the single most critical factor determining treatment success. A comparison of diagnostic tools:
| Type | Pigment Location | Wood Lamp Finding | Dermoscopy | Treatment Response |
|---|---|---|---|---|
| Epidermal | Stratum basale and spinosum | Borders become accentuated | Brown reticular network | Good (80–90%) |
| Dermal | Papillary dermis, macrophages | Borders unchanged | Grey-blue dots | Poor (20–30%) |
| Mixed | Both layers | Partially accentuated | Brown + grey-blue mixed | Moderate (50–60%) |
Sunscreen: The Non-Negotiable Foundation of Every Protocol
No melasma treatment protocol can succeed without the use of a broad-spectrum (UVA+UVB) SPF 50+ sunscreen — this is our recommendation with the highest level of clinical evidence. Physical (mineral) filters, zinc oxide and titanium dioxide, are considered superior to chemical filters for melasma because they reflect not only UV radiation but also visible light and infrared radiation.
Sunscreen should be applied as the final step of the morning skincare routine and reapplied every 2 hours when outdoors. A wide-brimmed hat (10 cm+), UV-protective sunglasses, and physical shading provide additional barriers. These precautions are especially critical during high UV-index days in the Izmit/Kocaeli area from May to September.
Topical Treatment Options: Comparison by Level of Evidence
| Agent | Concentration | Mechanism of Action | Evidence Level | Key Note |
|---|---|---|---|---|
| Hydroquinone | 2–4% | Tyrosinase inhibition, melanocyte cytotoxicity | A (highest) | Ochronosis with >6 months use; drug holiday required |
| Azelaic acid | 10–20% | Selective tyrosinase inhibition | A | Safe in pregnancy (Category B); well tolerated |
| Tranexamic acid | 2–5% (topical) | Plasminogen → tyrosinase signalling pathway inhibition | A | Excellent safety profile; oral form also effective |
| Tretinoin | 0.025–0.1% | Epidermal turnover, melanosome dispersion | B | Contraindicated in pregnancy; used at night |
| Niacinamide | 4–5% | Inhibition of melanosome–keratinocyte transfer | B | Highly suitable for combination use; anti-inflammatory |
| Kojic acid | 1–4% | Copper chelation → tyrosinase inhibition | B | Contact dermatitis risk; safer in combination formulas |
Clinical Chemical Peeling and Seasonal Planning
Chemical peeling is applied in addition to topical treatment or when topical response is insufficient. Appropriate peeling agents for melasma include:
- Glycolic acid (20–70%): The most potent and most studied agent in the AHA group; removes melanin-laden keratinocytes from the surface. Superficial to medium-depth peel.
- Mandelic acid (30–50%): Penetrates the skin slowly due to its large molecular weight; preferred for darker skin tones (Fitzpatrick IV–V) because of a lower post-inflammatory hyperpigmentation (PIH) risk.
- Kojic acid + glycolic acid combination: Synergistic brightening effect acting on both melanin synthesis and epidermal turnover.
- Modified Jessner's solution: Combination of resorcinol, lactic acid, and salicylic acid; effective in pigmented skin types.
- Salicylic acid (20–30%): BHA; dual benefit especially when acne and melasma co-exist.
Seasonal planning is critically important: In regions such as Kocaeli/Izmit where sun exposure peaks in spring and summer, clinical chemical peeling should only be scheduled between October and March. Peeling performed during summer dramatically increases the risk of PIH.
Tranexamic Acid: A Versatile and Safe Option
Tranexamic acid (TXA), originally developed to inhibit fibrinolysis, has become a first-line choice in melasma treatment over the past decade. It stands out for its multiple routes of administration and safety profile:
- Oral TXA (250 mg/day): Systemic effect; placebo-controlled studies have demonstrated a significant reduction in the MASI (Melasma Area and Severity Index) score. Caution is required in patients with risk factors for deep vein thrombosis (DVT); a physician prescription is mandatory.
- Topical TXA (2–5%): The safest route of administration; systemic absorption is minimal and local tolerability is high.
- Intradermal TXA mesotherapy: Direct injection into the dermis achieves high local concentrations; faster and more pronounced responses are reported compared with topical application. At Virtuana Clinic, this method is a standard component of treatment protocols.
Laser Treatments: When to Use and When to Avoid
The role of laser in melasma treatment remains a nuanced subject. Incorrect parameter or indication selection can worsen pigmentation by inducing post-inflammatory hyperpigmentation (PIH). Current best practice is as follows:
| Laser Type | Mechanism | Role in Melasma | PIH Risk |
|---|---|---|---|
| Q-switched Nd:YAG 1064 nm | Selective photothermolysis | Very low energy only; high recurrence risk | Moderate–High |
| Picosecond laser | Ultra-short pulse, minimal thermal damage | Resistant epidermal melasma; promising results | Low–Moderate |
| IPL (Intense Pulsed Light) | Broad-spectrum light | Generally not recommended; risk of pigment activation | High |
| Fractional laser (CO2 / Erbium) | Ablation + collagen induction | Contraindicated; very high PIH risk | Very High |
Long-Term Management Strategy for Melasma
Melasma is a chronic condition with a high tendency to relapse; lasting success requires a "manage and protect" rather than a "treat and stop" approach. The long-term plan developed collaboratively with our patients at Virtuana Clinic consists of the following components:
- Sunscreen discipline: Every day, in every season; mineral SPF 50+ combined with physical barriers (hat, sunglasses).
- Trigger control: Reviewing the type of hormonal contraceptive used, avoiding phototoxic products, and reducing chronic heat exposure.
- Maintenance topical therapy: After the active treatment phase, a "maintenance protocol" is continued at reduced concentrations (e.g., 2% hydroquinone → niacinamide + azelaic acid).
- Seasonal scheduling of aesthetic procedures: Peeling and laser treatments are planned for autumn and winter; invasive procedures are avoided in spring and summer.
- Regular dermatological follow-up: Check-ups every 3–6 months; treatment response is monitored with MASI scoring and photographic comparison.
Differential Diagnosis: Conditions That Can Mimic Melasma
Facial pigmentation is not always melasma. A definitive diagnosis must be made after excluding the following conditions:
- Post-inflammatory hyperpigmentation (PIH): Follows acne, eczema, or trauma; lesions are irregular with less-defined borders and are associated with a history of inflammation.
- Solar lentigo (age spot/sun spot): Circumscribed, round pigment deposit; shows a photo-distribution pattern; characteristic "fingerprint" appearance on dermoscopy.
- Nevus of Ota: Unilateral, grey-blue pigmentation; congenital; located in the distribution of the trigeminal nerve.
- Addison's disease: Diffuse hyperpigmentation associated with cortisol deficiency and systemic symptoms; endocrinology consultation is essential.
- Contact dermatitis hyperpigmentation: Post-phototoxic or photoallergic reaction; a history of relevant exposure is the distinguishing feature.
At Virtuana Clinic, diagnosis is confirmed with Wood lamp examination and dermoscopy before a personalized treatment protocol is prepared.
Assessing Melasma Severity: The MASI Score
The MASI (Melasma Area and Severity Index) is a standardized tool that numerically scores the clinical severity of melasma. The face is divided into four regions (forehead, right/left cheek, chin); for each region, the area extent and pigmentation intensity are scored separately. The total score ranges from 0 to 48. This gold-standard measure for monitoring treatment efficacy is applied routinely throughout our treatment processes at Virtuana Clinic.
Melasma Treatment Protocol at Virtuana Clinic
Virtuana Clinic (Izmit/Kocaeli) offers a systematic approach to melasma treatment from initial diagnosis through to long-term management. At the first consultation, Fitzpatrick skin type classification is performed; lesion depth is determined with Wood lamp and dermoscopy; and the MASI score is calculated to document a baseline assessment. The topical treatment protocol (combinations of hydroquinone, azelaic acid, tranexamic acid, retinoids, and niacinamide) is customized for each patient. When indicated, clinical chemical peeling (scheduled in autumn/winter) or intradermal tranexamic acid mesotherapy is added. Sunscreen education and seasonal care planning are integral parts of treatment; progress is monitored with 3-monthly follow-up appointments.
This article is for informational purposes only. Please consult a qualified physician for treatment decisions.