Skin colour and pigmentation

Also known as: skin color, pigmentation, melanin, melanogenesis, tanning, carotene, Fitzpatrick skin type

Skin colour results from three pigments — melanin produced by melanocytes, dietary carotene, and haemoglobin in dermal blood — modified by skin thickness and blood flow.

Overview

Melanin is the dominant pigment. Brown-black eumelanin absorbs UV radiation and scavenges free radicals efficiently; red-yellow pheomelanin (sulphur-containing) is less protective and can generate reactive oxygen species under UV. Melanogenesis in melanosomes is catalysed by tyrosinase (tyrosine → DOPA → dopaquinone). Human skin colour varies mainly with the number, size and dispersal of melanosomes and the eumelanin:pheomelanin ratio — people of all ancestries have similar numbers of melanocytes. In darker skin, large melanosomes are dispersed singly in keratinocytes and degraded slowly; in lighter skin, smaller melanosomes are clustered and degraded quickly.

Tanning has two phases: immediate pigment darkening (minutes; UVA oxidises existing melanin) and delayed tanning (from ≈48–72 h; UVB-induced DNA damage activates p53 in keratinocytes, increasing POMC/α-MSH, which acts on melanocyte MC1R to increase melanin synthesis and transfer). UV also thickens the stratum corneum.

Carotene, a fat-soluble yellow-orange plant pigment, accumulates in the stratum corneum and subcutaneous fat — most visible on the palms and soles. Haemoglobin in the superficial dermal vessels imparts pinkness, more visible in lightly pigmented skin: oxyhaemoglobin is bright red, deoxyhaemoglobin dark bluish-red. The Fitzpatrick scale classifies skin types I (always burns, never tans) to VI (never burns, deeply pigmented).

Function

Photoprotection of keratinocyte and dermal DNA by melanin

Balance between UV protection and cutaneous vitamin D synthesis

Visible indicator of oxygenation, perfusion and liver function

Regulation

α-MSH and ACTH (via MC1R and cAMP), UV radiation (p53–POMC), endothelin-1 and SCF (KIT ligand) from keratinocytes; oestrogen and progesterone (pregnancy pigmentation).

Clinical significance

Cyanosis, jaundice, pallor

Blue (deoxyhaemoglobin ≥≈50 g/L in capillaries), yellow (bilirubin >≈40–50 µmol/L, sclerae first) and pale (anaemia or vasoconstriction) skin are among the commonest physical signs; carotenaemia yellows the skin but spares the sclerae.

Albinism and vitiligo

Albinism: normal melanocytes, absent melanin synthesis (tyrosinase defect). Vitiligo: autoimmune loss of melanocytes. Both increase sunburn risk in affected skin; under a Wood (UV) lamp vitiligo patches fluoresce bright white.

Hyperpigmentation

Addison disease (ACTH excess), haemochromatosis ("bronze diabetes"), pregnancy (melasma, linea nigra), café-au-lait macules (neurofibromatosis type 1 — ≥6 macules), post-inflammatory hyperpigmentation, drugs (amiodarone, minocycline).