The aim of this article is to review the experimental knowledge concerning black skin. We point out its histological and physiological features without discussing here the specific pathology of black patients. Under the microscope skin structure is roughly the same in all races, but morphological differences exist, particularly within the epidermis, with potential practical consequences. In comparison with white skin, the black skin stratum corneum is equal in thickness but more compact: about twenty cell layers are observed in blacks versus sixteen layers in whites. The lipid content of black epidermis is also somewhat higher, and this perhaps explains the greater cellular cohesion, hence the difficulty in stripping off the black horny layer. These findings could also explain a slightly inferior permeability of black skin to certain chemicals. The hair of blacks in naturally more brittle and more susceptible to breakage and spontaneous knotting than that of whites. The kinky or wooly form of black hair, the weak intercellular cohesion between cortical cells and the specific hair grooming practices among black people account for these effects. The higher electrical resistance of black skin suggests that the black epidermis would be less hydrated than white epidermis. Anatomically, the amount of sweat glands in black and white skins is identical and varies with climatic changes but not with racial factors. Likewise, sweating is thought to be similar in both races, taking into account the contradictory results from studies, but black subjects withstand humid heat better while whites cope better with dry heat. The second mechanism of thermoregulation, i.e. vasomotor functions, appears to be quite different in black subjects, whereas skin vascularity does not differ from that found in whites. A dissimilar response of black skin to thermal stimulation has also been observed. The differences observed in racial responses to skin vasoconstriction and vasodilatation might have potential pharmacological repercussions. On the whole, sebum production is equal in blacks and whites, even if topographic variations exist: sebum level is higher on the scalp but smaller on the trunk of blacks. In blacks, the sebaceous follicles are evidently sturdier, and racial differences in follicular reactivity to comedogenic substances have been demonstrated. << Pomade acne >> in blacks is a noninflammatory comedonal disease: this hyperkeratotic response strikingly differs from the inflammatory reaction of white skin on follicle disintegration. This suggests a greater resistance of black skin to this type of irritation. However, responses to other chemical irritants are similar in both races. The risk of sensitization is also identical, even if differences exist in the clinical manifestation (blacks easily develop disorders of pigmentation and lichenification). Finally, pigmentation is the most outstanding difference between black and white skin. In black epidermis, the melanosomes are wider and not grouped but individually dispersed in the keratocytes. The arrangement of melanin pigment in the epidermis provides a superior mechanism of photoprotection among blacks. The main site of ultraviolet filtration in whites is the stratum corneum, whereas in blacks it is the malpighian layers. Blacks are less susceptible to acute and chronic actinic damage than whites. As compensation, increased skin pigment reduces the cutaneous production of vitamin D, at least for a single ultraviolet exposure. Howerver the production of vitamin D in blacks approaches that of whites on repeated exposure.
