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The sources of pigment that cause hyperpigmentation of the skin range from endogenous products such as melanin and hemosiderin to exogenous agents such as tattoo dyes, ingested metals, and drugs. In some instances, these agents combine to produce hyperpigmentation. For example, in argyria- and chlorpromazine-related hyperpigmentation, silver particles along with melanin and drug metabolites plus melanin, respectively, contribute to dyschromasia. Ultraviolet (UV) rays often enhance pigmentation, so sun-exposed skin shows more intense discoloration. When the epidermis is heavily melanized, pigment incontinence may result in upper dermal melanization as well. Disorders of hypopigmentation and depigmentation are caused mainly by damage to and dysfunction of epidermal melanocytes (Figs. 15-1 and 15-2). In some congenital diseases (eg, piebaldism), melanocytes are absent, and in other conditions (eg, idiopathic guttate hypomelanosis) the melanocytes are dysfunctional with rudimentary dendritic processes. The circulation of blood through the superficial capillary plexus may influence the skin color, as evidenced by nevus anemicus. Both hyper- and hypopigmentations may be congenital or hereditary, postinflammatory, or induced by chemicals and foreign materials.


Disorders of pigmentation.


Disorders of hyperpigmentation. CALM = café-au-lait macule.

Melanocytes from all sites (skin, hair bulb, eyes) produce melanosomes that in the normal process mature into electron-dense stage IV melanosomes in dark-skinned individuals. The maturation is arrested at stage I or II in fair-skinned whites (Fig. 15-3). In leukodermic conditions, various dysfunctions of tyrosinase or damage to melanocytes produce fewer pigmented melanosomes or a decrease in their number (Figs. 15-4 and 15-5), changes that are more visible in dark skin. Hyperactivity of melanocytes results in various hyperpigmented conditions, and in such disorders, lesions are again more striking in dark than in light skin. In some conditions, the transfer of melanosomes from normal melanocytes to the surrounding basal keratinocytes is disturbed, causing an uneven light color of the lesion (eg, nevus depigmentosus) or hyperpigmentation in some instances (eg, Peutz-Jeghers syndrome). In many hyperpigmented conditions (eg, lentigo simplex and solar lentigines), the rete ridges are elongated, and an aggregation of melanocytes and pigment occurs (Fig. 15-6).


An epidermal melanocyte is actively synthesizing melanosomes. Stage 1 melanosome contains amorphous, nebulous material. In stage 2, cristae are formed, and melanin begins to deposit on them. In stage 3, melanin polymers become denser, and in stage 4, the increased density masks the underlying structure of cristae.


Vitiligo. (A) Depigmentation involving the neck in a characteristic periorificial and periocular distribution. (B) A Melan-A immunostain at the edge of a vitiligo lesion. Depigmented skin shows a loss of melanocyte.

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