Pigmentation Treatment: Melasma and Hyperpigmentation

Skin pigmentation (hyperpigmentation) is a multifactorial condition in which melanin production increases in localised areas — driven by sun exposure, hormonal changes, inflammation and genetic predisposition acting together. Treatment started without a correct diagnosis usually fails, and the wrong laser or an overly aggressive peel can make the pigment darker. Lasting results depend on identifying the type and depth of the pigmentation, a personalised combination protocol and disciplined sun protection.

How Does Pigmentation Develop?

Skin colour is determined by melanin, produced by melanocytes in the basal layer of the epidermis. Synthesised through a chain of reactions led by the enzyme tyrosinase, melanin is packaged into melanosomes and transferred to surrounding keratinocytes. Normally this system protects the skin from ultraviolet damage; when melanocytes are excessively and irregularly stimulated, pigment production rises locally and a visible spot appears.

Ultraviolet light is the strongest trigger — but not the only one. Visible light (particularly high-energy blue light), heat (ovens, saunas, post-epilation warmth), oestrogen and progesterone (pregnancy, oral contraceptives, hormone therapy), inflammation (acne, eczema, friction, chemical or thermal burns) and certain photosensitising medications all increase melanocyte activity. Genetic predisposition determines who actually develops pigmentation in response to these triggers.

The critical distinction for treatment is the depth of the pigment. Epidermal (superficial) pigment responds well; pigment that has reached the dermis is far more resistant, and the realistic goal there is significant lightening rather than complete clearance.

Types of Pigmentation and Differential Diagnosis

Melasma (chloasma): Symmetrical, irregularly bordered brown-grey patches on the cheeks, forehead, nasal bridge and upper lip. Far more common in women; triggered by pregnancy ("mask of pregnancy"), oral contraceptives and hormone therapy. Extremely sensitive to heat and light, chronic, and prone to relapse — managed as an ongoing condition rather than a one-off cure.

Solar lentigo (sun spots, age spots): Sharply demarcated light-to-dark brown spots on the face, backs of the hands, forearms, shoulders and décolletage, caused by cumulative UV damage. Usually become prominent after 40 and respond best of all to treatment.

Post-inflammatory hyperpigmentation (PIH): The dark mark left behind after acne, eczema, psoriasis, insect bites, epilation, burns or an aesthetic procedure. Much more pronounced in darker skin (Fitzpatrick III–VI). It can fade spontaneously over months once the inflammation stops; the process can be accelerated.

Ephelides (freckles): Genetically determined small spots in fair-skinned individuals that darken with sun and fade in winter.

Other presentations: drug-induced pigmentation, Riehl's melanosis (following cosmetic contact dermatitis), periorbital hyperpigmentation (dark circles) and dermal melanocytoses all require different approaches.

Important warning: not every dark spot is a simple pigment spot. Asymmetry, irregular borders, colour variation, a diameter over 6 mm, rapid growth, bleeding or itching all require dermatoscopic evaluation. Confirming a lesion is benign before starting any cosmetic procedure is the first and non-negotiable step of pigmentation treatment.

Diagnosis: Establishing Depth and Trigger

Wood's lamp examination helps determine whether the pigment is epidermal or dermal: epidermal pigment becomes more prominent under Wood's light, dermal pigment does not contrast in the same way. Dermatoscopy assesses pigment network structure, vascular components and suspicious lesions. Fitzpatrick skin type is recorded, as it directly determines which peel strength or laser parameters are safe.

The history screens for triggers: pregnancy and childbirth, hormonal medication, thyroid function, iron and ferritin, vitamin D, cosmetics in use, occupational heat exposure and photosensitising drugs. No treatment lasts while the trigger remains in place.

Treatment Steps

1. Sun and light protection — the foundation. Broad-spectrum (UVA+UVB) SPF 50+ applied every morning and reapplied every 2–3 hours. In melasma, tinted/mineral sunscreens containing iron oxide are preferred because they also block visible light and have outperformed pure UV filters in clinical studies. Hats, sunglasses and avoiding heat sources are integral. Without sun protection, every other treatment is wasted.

2. Topical therapy. Tranexamic acid, azelaic acid, niacinamide, vitamin C, retinoids, kojic acid and arbutin suppress melanin synthesis at different steps. Hydroquinone is a powerful depigmenting agent but must be used only under medical supervision, for limited periods and intermittently — prolonged use risks exogenous ochronosis. Combination preparations (retinoid + depigmenting agent + anti-inflammatory) clearly outperform any single agent.

3. Chemical peels. Superficial peels based on glycolic, mandelic, salicylic or lactic acid accelerate the shedding of pigment-laden keratinocytes and improve penetration of topical agents. Concentration must match skin type, applied as a series 2–4 weeks apart. In darker skin an aggressive peel can replace the treated spot with fresh PIH — hence the "slow and low-dose" principle.

4. Mesotherapy and microneedling. Depigmenting mesococktails containing tranexamic acid, glutathione, vitamin C, niacinamide and hyaluronic acid are delivered directly to the target layer by intradermal injection or microneedling. The microchannels created by needling both increase active-ingredient delivery and stimulate collagen renewal, improving overall skin tone. See our mesotherapy article for details.

5. Systemic antioxidant support. In selected cases IV glutathione and high-dose vitamin C protocols support topical therapy by lowering oxidative stress and suppressing tyrosinase activity. These are a complementary component of the combination, never a standalone pigmentation treatment.

6. Lasers and light systems. For epidermal pigment such as solar lentigines and freckles, Q-switched/picosecond lasers and IPL deliver striking results. Melasma is different: high-energy treatments frequently cause rebound — returning darker than before. Low-energy "laser toning" sessions are therefore planned only after topical and systemic groundwork, at carefully spaced intervals.

7. Oral therapy. In resistant melasma, low-dose oral tranexamic acid may be used for a limited period under medical supervision after screening for thromboembolic risk. Polypodium leucotomos extract and oral antioxidants provide photoprotective support.

Why Are Some Spots Treatment-Resistant?

There are four common reasons: dermal pigment location, an ongoing trigger (continued hormone use, unprotected sun exposure, heat), fresh inflammation caused by aggressive procedures, and poor adherence. Melasma in particular runs a chronic course, flaring in summer and improving in winter in many patients. Treatment is therefore designed as long-term management, not a cure.

Course, Results and Maintenance

The plan starts with home care (sun protection plus topicals) after examination and trigger screening. Clinical procedures — peels, mesotherapy, microneedling — are typically scheduled as 4–8 sessions 2–4 weeks apart. Visible lightening starts at weeks 6–8; clear results appear at months 3–6. For solar lentigines, 70–90% clearance is a realistic target; in melasma, 50–70% lightening with relapse kept under control counts as success. Seasonal maintenance sessions and uninterrupted sun protection preserve the gain.

Who Is Not a Candidate?

Retinoids, hydroquinone and oral tranexamic acid are not used during pregnancy or breastfeeding; azelaic acid, niacinamide and sun protection are the safe options in that period. Active skin infection, an active herpes outbreak, open wounds, isotretinoin use within the last 6 months (a waiting period is required before peels and ablative procedures), a tendency to keloid formation, uncontrolled autoimmune disease and freshly tanned skin must all be assessed before any procedure.