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Hyperpigmentation and Skin of Color

By: Jennifer Linder, MD
Posted: August 23, 2010, from the September 2010 issue of Skin Inc. magazine.

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Melanocyte stimulating hormone (MSH) is triggered and released. Within the melanocyte, a chain of events is activated that begins with the enzyme tyrosinase being released from the rough endoplasmic reticulum (RER) and acting on the amino acid tyrosine to convert it to L-DOPA.

Then, tyrosinase binds with copper and acts on L-DOPA, converting it into melanosomes. These melanosomes are packets of pigment that can either be eumelanin (brown/black pigment) or pheomelanin (orange/red pigment). Dark skin tends to have more eumelanin. This more vigorous type of melanin contributes to the increased occurrence of hyperpigmentation in darker skin.

Those with fairer skin, and especially red hair, will predominantly have pheomelanin. The final color of a person’s skin will be slightly different based on the ratio of eumelanin to pheomelanin, as well as the quantity of sustained UV exposure to which their skin is subjected.

The melanosomes produced are then transported along the dendrites, or arms, of the melanocyte and transferred into the keratinocyte. They then congregate in an umbrellalike pattern over the nucleus to protect the DNA within the cell, resulting in visible hyperpigmentation. Protease-activated receptor-2 (PAR-2) is the receptor located in the keratinocytes that regulates whether or not the melanosomes that arrive at the keratinocyte are phagocytized—consumed or taken in. The keratinocytes in skin of color contain more of these PAR-2 receptors, increasing the amount of phagocytized melanosomes by keratinocytes.

Additionally, PAR-2 receptors are increased in number by UV exposure, which may explain the predisposition of darker skin to be more responsive to melanogenesis. All types of hyperpigmentation can affect any person, regardless of race, although this PAR-2 expression and upregulation makes it more prevalent in clients with darker skin.

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