Post-inflammatory hyperpigmentation guide: causes, treatment, and prevention

Post-inflammatory hyperpigmentation is the most common pigmentation concern across all skin types — and one of the most frustrating to treat because the underlying mechanics are often misunderstood. Here is the complete evidence-based guide.

What PIH is

The inflammation-melanin connection

PIH results from an abnormal melanocyte response to skin inflammation. The cascade:

Inflammation — from any source: acne, eczema, psoriasis, insect bites, chemical burns, friction, laser treatment, or physical trauma
Cytokine release — keratinocytes release IL-1, TNF-α, prostaglandins, and leukotrienes into the epidermis during inflammation
Melanocyte stimulation — these inflammatory mediators activate adjacent melanocytes, upregulating tyrosinase and increasing melanin synthesis
Melanin deposition — excess melanin accumulates in the epidermis (epidermal PIH) and in some cases is shed into the dermis (dermal PIH) as the epidermis turns over

Key point: PIH is not caused by the original insult directly — it is caused by the inflammatory response to it. Minimizing inflammation (from any cause) is the most important PIH prevention strategy.

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Epidermal vs. dermal PIH

Why the distinction matters for treatment

| Feature | Epidermal PIH | Dermal PIH |
|---|---|---|
| Melanin location | Upper epidermis | Papillary and reticular dermis |
| Color | Brown, tan | Grey, blue-grey, ashen |
| Wood's lamp | Accentuates (appears darker) | Does not accentuate |
| Response to topicals | Responds well | Poor response to topicals |
| Timeline | Months | Years to permanent |
| Treatment | Topical depigmenting agents + retinoids | Laser (Q-switched Nd:YAG, picosecond) |

The Wood's lamp test: A UV lamp that accentuates epidermal melanin (makes brown spots appear much darker) but does not accentuate dermal melanin (grey spots look the same). This is the clinical tool for distinguishing epidermal from dermal PIH — determining whether topical treatment or laser is indicated.

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Why darker skin types are disproportionately affected

Melanocytes in Fitzpatrick IV–VI skin produce more melanin basally and respond to the same inflammatory stimulus with a more robust melanin surge than in lighter skin types. The melanocytes are not overactive in resting state — they are hyperresponsive to inflammatory triggers. This means:

The same acne lesion that leaves no mark in Fitzpatrick I–II skin can leave a month-long dark spot in Fitzpatrick V–VI
Inflammatory skincare treatments (glycolic acid irritation, retinoid purging, laser) carry a higher PIH risk in darker skin
Prevention (reducing inflammation and UV) is proportionally more important

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Treatment hierarchy

Sun protection (non-negotiable foundation)

UV exposure stimulates melanin synthesis independently — it simultaneously darkens existing PIH and prevents topical treatments from working. Every active depigmenting agent on earth is working against UV-induced melanogenesis if SPF is not applied daily.

SPF 30–50+ every morning, regardless of whether the patient goes outside. UVA penetrates glass windows; indoor exposure sustains PIH.

Tinted mineral sunscreen (with iron oxides) provides an additional benefit: it blocks visible light (HEV), which also stimulates melanogenesis in darker skin types — an effect that chemical and untinted mineral filters do not address.

Tranexamic acid (first-line OTC)

PAR-2 pathway inhibition — addresses the keratinocyte-melanocyte signaling crosstalk that drives post-inflammatory melanocyte overstimulation. 2–5% topical, twice daily. Excellent tolerability across all Fitzpatrick types — no PIH risk from the active itself.

Niacinamide (4–10%)

Melanosome transfer inhibition — does not reduce melanin production but prevents its transfer to keratinocytes, reducing visible pigmentation. Highly compatible as a base layer or combination ingredient. Complementary mechanism to tranexamic acid.

Azelaic acid 15–20%

Selective cytotoxicity to hyperactive melanocytes. Particularly valuable for PIH in darker skin types — it specifically targets abnormal melanocyte activity without affecting normally active melanocytes, reducing PIH risk from the treatment itself. Prescription formulations preferred for therapeutic effect.

Kojic acid 1–2%

Tyrosinase copper chelation. Effective but with sensitization risk (1–10%) — if sensitization occurs, substitute tranexamic acid or azelaic acid.

Vitamin C (5–20% L-ascorbic acid or stabilized derivative)

Dopaquinone reduction and antioxidant activity. Morning application while the skin is protected by SPF is the standard integration. Lower standalone potency for established PIH than the above agents, but important for combined prevention + treatment.

Retinoids (tretinoin, adapalene)

Do not directly inhibit melanin synthesis, but accelerate epidermal cell turnover — melanin-containing keratinocytes shed faster, clearing epidermal PIH more rapidly than without retinoid use. Also reduce new PIH formation by normalizing follicular hyperkeratinization. Add retinoid to any PIH regimen as an accelerant.

Retinoid caution in darker skin: Retinoid irritation can trigger new PIH in Fitzpatrick IV–VI skin. Start at low concentration (tretinoin 0.025% or retinol 0.025–0.05%), advance slowly, and combine with niacinamide to reduce irritation.

Professional treatments for resistant PIH

Chemical peels (glycolic 20–30%, salicylic, jessner's) — accelerate epidermal turnover; risk of worsening PIH if irritation-induced inflammation occurs; best performed by experienced providers in darker skin
Laser (Q-switched or picosecond) — for dermal PIH specifically; targets melanin with nanosecond or picosecond pulses; requires experienced operator to avoid paradoxical PIH worsening

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What makes PIH worse

Picking and squeezing active acne lesions → prolongs inflammation → more intense PIH response
UV exposure without SPF → stimulates new melanin synthesis and deepens existing spots
Irritating actives (high-concentration glycolic, retinoid irritation, poorly introduced active) → triggers fresh inflammation in already-healing skin → new PIH layer on existing PIH
Inadequate treatment of the underlying cause — if acne is still actively inflaming new spots, no depigmenting regimen can keep up

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Realistic timelines

Epidermal PIH: With consistent daily SPF + active depigmenting regimen, most cases show meaningful improvement in 8–12 weeks; complete clearance in 3–6 months.

Dermal PIH: Does not respond to topical agents. Laser treatment (Q-switched Nd:YAG 1064 nm is the most Fitzpatrick-safe) can reduce dermal PIH over multiple sessions (4–8 treatments spaced 4–6 weeks apart). Some dermal PIH is permanent without laser.

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