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Skin Lightening Challenges
By: Zoe Diana Draelos, MD
Posted: February 3, 2009, from the February 2009 issue of GCI Magazine.
Irregular pigmentation of the face is one of the most common signs of photoaging. Pigmentation is due to the uneven production of melanin, a brown pigment produced by melanocytes in the skin. Many different patterns can be seen on the faces of people of different ages. Small localized brown spots in the form of freckles across the cheeks, medically known as lentigenes, usually appear around age 25–30, depending on cumulative sun exposure.
Pigmentation can also present in the form of melasma, a diffuse darkening of the skin over the sides of the forehead, lateral jawline and upper lip. This type of skin darkening is hormone dependent, most commonly seen during pregnancy, around menopause and with the use of oral contraceptives. Lastly, increased facial pigmentation can present as overall darkening in people over age 50 from a combination of melanin pigment and fragmented elastin fibers.
Other factors also influence facial pigmentation, such as gender. Since men do not experience the same hormonal issues as women, increased facial pigmentation from melasma is uncommon. While male testosterone may cause some skin issues, it is female estrogen that produces facial pigmentation. The coarse skin texture of the male face from hair growth camouflages fine freckling that is often seen on the female face. Finally, male facial skin is more resistant to UVA damage due to its increased thickness from the terminal hairs present as a beard on the face. UVA radiation penetrates deeply into the skin, but not as readily into thicker male skin as it does into thinner female skin. Because UVA damage is the primary cause of pigmentary abnormalities, pigment lightening products are more commonly used by females than males.1
There are also differences in skin pigmentation problems based on race. Individuals with darker skin are more prone to skin darkening. This is due to an enhanced ability of darker skin to produce melanin. Pigment may be produced in response to sun exposure, skin disease and skin trauma. It is distinctly more difficult to lighten skin in darker-complected individuals. While pigmentation problems may be more visible in persons with lighter skin, OTC skin lightening preparations are more successful in this population. There is no doubt that the best method of skin lightening is avoiding sun damage. In fact, all OTC skin lightening treatments should include a sunscreen. Sunlight contains visible light and invisible ultraviolet B (UVB) and ultraviolet A (UVA) radiation. Visible light and UVB radiation do not tan the skin. Skin tanning in people of all skin colors is due to UVA radiation. Most sunscreens focus on preventing sunburn, which is due to UVB radiation. They do not prevent tanning, since UVA radiation still strikes the skin. Thus, sunscreens selected for skin lightening purposes should contain UVA photoprotectants such as avobenzone, oxybenzone, zinc oxide and/or titanium dioxide. Topical treatments for facial pigmentation are problematic. A successful treatment must remove existing pigment from the skin, shut down the manufacture of additional melanin pigment and prevent the transfer of existing melanin pigment to the melanosomes. No currently available topical product is able to accomplish all three of these functions. This review article examines various actives for topical skin lightening products on the OTC markets.
The gold standard for topical skin lightening in the United States remains hydroquinone. This substance is controversial, having been removed from the OTC markets in Europe and Asia. Concern arose from reports that oral hydroquinone caused cancer in mice that were fed large amounts of the substance. While oral consumption probably is not related to topical application, hydroquinone remains controversial because it actually is toxic to melanocytes.
Hydroquinone, a phenolic compound chemically known as 1,4 dihydroxybenzene, functions by inhibiting tyrosine, a key substance in melanin pigment production.2 Specificially, it covalently binds to histidine or interacts with copper at the active site of tyrosinase. It also inhibits RNA and DNA synthesis and may alter melanosome formation, thus selectively damaging melanocytes. These activities suppress the melanocyte, causing gradual decrease of melanin pigment production.3