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Hyperpigmentation and Skin of Color

Jennifer Linder, MD September 2010 issue of Skin Inc. magazine
Hyperpigmentation and Skin of Color

Much of the world’s population is considered Fitzpatrick type IV–VI. (See Fitzpatrick Scale.) By 2050, according to the U.S. Census Bureau in 2000, 50% of Americans will be of darker-skinned racial backgrounds. One of the most common skin conditions in higher Fitzpatrick clients is hyperpigmentation. Although many of the popular treatments performed on a regular basis on Caucasians may be well-tolerated by clients with darker skin, special considerations need to be taken to ensure positive treatment outcomes for such clients. A deeper understanding of the causes of hyperpigmentation, and of the myriad of ingredients available for its treatment, will help spa professionals develop highly effective therapies for all of their clients, regardless of ethnicity.

Beyond black and white

Within any ethnic background, a variety of Fitzpatrick skin types can be identified. Darker skin can commonly be seen in Hispanics, Latinos, Africans, African-Americans, Caribbeans, Native Americans, Pacific Islanders, East Indians, Pakistanis, Eskimos, Koreans, Chinese, Vietnamese, Filipinos, Japanese, Thai, Cambodians, Malaysians, Indonesians and Aleuts, according to dermatologist Pearl Grimes, MD.1 With this broad global representation in mind, spa professionals should expect to see an increase in clients of one or mixed racial backgrounds with darker skin.

The most apparent difference in the skin of those from different ethnicities is, of course, the color, although there are also differences in skin thickness, vascularity, and predispositions to certain skin conditions and diseases. Hyperpigmentation can occur due to UV exposure, cutaneous trauma or hormonal fluctuations. Studies by dermatologist Susan Taylor in 2005 demonstrate that up to 86% of women of Latino, Asian and African descent are concerned about skin discolorations.2

Melanogenesis and skin color

Melanin is the complex molecule that is responsible for the pigment in the body; specifically eyes, hair and skin. Melanin works to protect by reducing the penetration of UV rays into the skin and, even more importantly, into the nuclei of cells where DNA resides. Those with both dark and light skin have the same number of melanocytes—the cells responsible for melanogenesis or melanin production—although their level of responsiveness differs. Clients whose genetic heredity is that of global regions with extreme UV exposure have melanocytes that will, out of protective necessity, instigate the process of melanin deposition much more quickly than someone with lighter skin. Some clients with mixed genetic heritage may have lighter skin, but still have a greater predisposition for hyperpigmentation than a typical Fitzpatrick skin type I or II.

As a result of inflammation or hormonal fluctuations, the following process is stimulated.

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.

Gentle treatment options

Many of the ingredients that are used to treat hyperpigmentation can be topically irritating. Therapeutic ingredients must be selected with care when treating clients with darker skin to avoid causing undue irritation that will worsen the condition rather than improve it.

To avoid stimulating pigment deposition, it is wise to use lower percentages of ingredients in blends to prevent melanogenesis, rather than one ingredient at a high percentage that could potentially be surface-stimulating. Hydroquinone is very effective at the low over-the-counter (OTC) percentage of 2%, especially when used in concert with other effective ingredients, such as lactic, kojic, ascorbic and azelaic acids, just to name a few. Care must be taken when using hydroquinone at 4% or higher on darker skin, as these are more irritating and can trigger post-inflammatory hyperpigmentation. See Melanogenesis Inhibitors Appropriate for Darker-skinned Clients to identify which ingredients to look for when working with Fitzpatrick skin types IV–VI.

Prevention

One of the most important steps in any daily care regimen or professional treatment is that of sun protection. A broad-spectrum moisturizer with an SPF of 30 or greater should be applied to all exposed areas every day and after any professional treatment. Although darker skin has more natural protection against UV exposure, this critical step cannot be omitted. With an understanding of the more reactive state of the melanocytes in clients with darker skin, along with blends of gentle, beneficial melanogenesis-inhibiting ingredients, great success can be achieved in treating Fitzpatrick type IV–VI clients.

REFERENCES

1. PE Grimes, Aesthetics and Cosmetic Surgery for Darker Skin Types, Lippincott Williams & Wilkins, Philadelphia, 2008 (pp 15–26)

2. test.neton-line.com/EMAIL/eNewsletters/Public/0207.html (Accessed Jul 11, 2010)

3. S Badreshia-Bansal and ZD Draelos, Insight into Skin Lightening Cosmeceuticals for Women of Color, J of Drugs in Dermatology 6 1 32–39 (2007)

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Retail Tips: Hyperpigmentation and Skin of Color

For successful spa retail: Blends of melanogenesis-inhibiting ingredients should be incorporated into daily care regimens for clients working to reduce hyperpigmentation.

Some successful spa treatment options: Gentle, blended chemical peels that increase cell turnover and remove surface-darkened cells without the excessive inflammation that can stimulate melanin production can be of great benefit. Although such blended peels will speed the improvement of skin discoloration, it is critical that clients with dark skin or mixed racial heritage are not treated with highly active peel solutions or laser treatments that can incur excessive inflammation and lead to post-inflammatory hyperpigmentation. Overly aggressive peels (medium and deep) can not only cause additional hyperpigmentation, but can also stimulate the formation of keloids, the excess growth of scar tissue at the site of a healed skin injury. A series of superficial peels is the safest option for higher Fitzpatrick clients. The typical frequency of treatment for hyperpigmentation is every three weeks, and can involve the following peeling agents: Jessner’s solutions, alpha hydroxy acids (AHA), beta hydroxy acids (BHA), trichloroacetic acid (TCA) and retinoids.

Melanogenesis Inhibitors Appropriate for Darker-Skinned Clients

Arbutin—A potent antioxidant that is found naturally in cranberries, wheat, pears, and blueberry and bearberry leaves, arbutin is thought to be less cytotoxic than hydroquinone. It inhibits the activity of tyrosinase, inhibits melanosome maturation and converts to hydroquinone in the skin, allowing for a controlled release, resulting in less irritation than hydroquinone.

Azelaic acid—Naturally sourced from cultures of Pityrosporum ovale, grain products, castor beans or by the oxygenation of oleic acid, found in milk, azelaic acid has an antiproliferative and cytotoxic effect on melanocytes while sparing surrounding healthy cells. It also inhibits tyrosinase activity, DNA synthesis and mitochondrial activity.

Hydroquinone—Hydroquinone is typically engineered in a lab, but can be found naturally in wheat, berries, coffee and tea. It works by inhibiting DNA and RNA synthesis, suppressing the binding of copper and tyrosinase, decreasing the formation of melanosomes, increasing the degradation of melanosomes and inducing melanocyte-specific cytotoxicity.

Kojic acid—Derived from rice, soy and mushrooms, kojic acid may cause irritation in some skin types, although less frequently than with hydroquinone. It inhibits melanogenesis by chelating the copper bound to tyrosinase, rendering it useless. It also decreases the number of melanosomes and dendrites, and is useful in treating hyperpigmentation due to its ability to inhibit nuclear factor-kappa B (NF-kB) activation in keratinocytes, mitigating inflammatory response.

L-ascorbic acid (vitamin C)—Derived from many botanical sources such as citrus fruit and corn, L-ascorbic acid is an anti-inflammatory and antioxidant agent that stimulates collagen production and converts dopaquinone back to L-DOPA, preventing melanin formation.

Lactic acid—Derived from sour milk and sugars, lactic acid works as a moisturizer and antimicrobial agent. It increases the exfoliation of melanin-filled keratinocytes and suppresses the formation of tyrosinase.

Licorice extract—Licorice extract can be naturally derived or engineered. It inhibits tyrosinase activity of melanocytes without cytotoxicity, UV-B–induced hyperpigmentation and erythema, and has strong anti-inflammatory properties.

Morus bombycis root extract (mulberry)—A potent antioxidant and anti-inflammatory agent that inhibits the L-DOPA oxidase activity of tyrosinase, studies show a 50% reduction in tyrosinase activity following an application of Morus bombycis root extract.3

Phenylethyl resorcinol—An engineered resorcinol derivative, phenylethyl resorcinol is an antioxidant that has demonstrated results comparable to kojic acid and hydroquinone without any potential for topical irritation. It works by inhibiting the conversion of tyrosinase to L-DOPA.

Retinoids (vitamin A)—Retinoids stimulate collagen, elastin and glycosaminoglycan production and inhibit tyrosinase activity, decrease the amount of melanosomes produced, inhibit the transfer of melanin from melanocytes to keratinocytes, and enhance the penetration of actives through the stratum corneum.

Undecylenoyl phenylalanine—Another engineered ingredient, undecylenoyl phenylalanine prevents the synthesis the melanocyte-stimulating hormone (MSH).

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