Journal
ANNALES DE DERMATOLOGIE ET DE VENEREOLOGIE
Volume 139, Issue -, Pages S125-S129Publisher
MASSON EDITEUR
DOI: 10.1016/S0151-9638(12)70123-0
Keywords
Hyperpigmentation; Skin Color; Melanin; Melanosomes; Melanocytes
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The varieties of nornnal skin color in humans range from people of-no color-(pale white) to-people of color-(light brown, dark brown, and black). Skin color is a blend resulting from the skin chromophores red (oxyhaemoglobin), blue (deoxygenated haemoglobin), yellow-orange (carotene, an exogenous pigment), and brown (melanin). Melanin, however, is the major component of skin color; it is the presence or absence of melanin in the melanosomes in melanocytes and melanin in keratinocytes that is responsible for epidermal pigmentation, and the presence of melanin in macrophages or melanocytes in the dermis that is responsible for dermal pigmentation. Two groups of pigmentary disorders are commonly distinguished: the disorders of the quantitative and qualitative distribution of normal pigment and the abnormal presence of exogenous or endogenous pigments in the skin. The first group includes hyperpig-mentations, which clinically manifest by darkening of the skin color, and leukoderrnia, which is characterized by lightening of the skin. Hypermelanosis corresponds to an overload of melanin or an abnormal distribution of melanin in the skin. Depending on the color, melanodermia (brown/black) and ceruloderma (blue/grey) are distinguished. Melanodermia correspond to epidermal hypermelanocytosis (an increased number of melanocytes) or epidermal hypermelanosis (an increase in the quantity of melanin in the epidermis with no modification of the number of melanocytes). Ceruloderma corresponds to dermal hypermelanocytosis (abnormal presence in the dermis of cells synthesizing me(anins); leakage in the dermis of epidermal melanin also exists, a form of dermal hypermelanosis called pigmentary incontinence. Finally, dyschromia can be related to the abnormal presence in the skin of a pigment of exogenous or endogenous origin. (C) 2012 Elsevier Masson SAS. All rights reserved
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