Hyperpigmentation is one of the most difficult challenges skin health professionals face. The broad and varied base of patients that seek treatment for this frustrating condition make it necessary for the clinician to have a deep understanding of its etiology. Outstanding and consistent results can be achieved by approaching treatment from two angles: topical treatment and patient education. Ensure that the professional treatments you perform and the daily care products you recommend address the melanogenesis process at multiple points. Be certain you take the time to properly educate each patient about their role in the success or failure of their treatment outcome. Doing these things will lead to the fast, dramatic results both you and your client desire.
What happens in the skin
Hyperpigmentation is the deposit of melanin (pigment) due to a process called melanogenesis. This process encompasses the production of pigment and its duplication in the skin. It is the end result of inflammatory insults. Regardless of the source of the inflammation—UV exposure, hormonal triggers or cutaneous inflammation, such as heat or trauma—this activity of the melanocytes is designed to protect the skin cells’ DNA from damage and mutation.
After the initial inflammatory response or hormonal fluctuation, the melanocyte’s stimulating hormone is released. Within the melanocyte, a chain of events is then triggered:
• The enzyme tyrosinase is released
from the rough endoplasmic reticulum (RER).
• Tyrosinase acts on the amino acid tyrosine
to convert it to L-DOPA.
• Tyrosinase then binds with copper and acts on the L-DOPA, converting it to DOPAquinone.
• DOPAquinone stimulates the release of melanin, which is packaged into melanosomes.
• These melanosomes are transported along the dendrites (arms) of the melanocyte and transferred into the keratinocyte, creating an umbrella-like pattern to protect the DNA within the cell, resulting in hyperpigmentation.
Types of hyperpigmentation
UV-induced hyperpigmentation is a result of UV exposure and can be caused by the sun, tanning beds and fluorescent and ambient lighting. It is identifiable by its appearance as diffused spots that are evenly distributed around the face. This type of hyperpigmentation can also be referred to as actinic hyperpigmentation.
Hormonally induced hyperpigmentation is typically referred to as melasma, and it is caused by hormone fluctuations. The term melasma comes from the Greek word “melas,” which means black. It is commonly associated with a fluctuation of hormones (pregnancy, oral contraceptives, thyroid dysfunction, menopause or hormone replacement therapy), and will worsen with UV exposure. It typically appears as large symmetrical patches with jagged borders that form around the jawline, upper lip, cheeks and forehead. The exact cause of melasma is unknown, but it is widely believed to be a result of an increase in the formation and distribution of melanosomes (packets of melanin pigment) among the keratinocytes, along with increased branching of melanocytic dendrites. Research also indicates that the elevated estrogen levels that result from pregnancy and birth control pills increase both the number of melanocytes and the activity of tyrosinase. Conversely, studies indicate that the androgen dominance that occurs during menopause is responsible for an increase in tyrosinase activity.
Post-inflammatory hyperpigmentation (PIH) is a result of skin irritation, inflammation or abrasion. It is identified as a darkened area left behind at the sites of trauma. It is common in patients fighting acne, dermatitis, psoriasis and eczema, and can also be caused by bug bites.
Regardless of the cause or type of hyperpigmentation you are working to treat, there are four common strategies that must be followed: gently exfoliate the skin, increase cell turnover, inhibit melanogenesis and protect the skin from UV exposure and other inflammatory insults. There are multiple ways to achieve each of these goals, but when creating treatment plans you must employ multiple products in the professional setting, as well as in the patient’s daily care regimen. There simply is not one single “miracle product” that will clear and prevent this common condition.
Benefits of superficial chemical peels
The melanin deposited in the skin due to hyperpigmentation will appear darker to the naked eye as it rises toward the stratum corneum on its way to being shed. Part of a successful treatment plan is to remove these darker impacted cells to keep the appearance of the pigmented area to a minimum—even as you are working to increase cell turnover and lift deeper pigment to the surface. It is wise to perform a superficial peel twice a week to keep the unwanted pigment from re-depositing onto the surface. Although this is a normal way of lifting pigment, a better way is to gently remove the stratum corneum before it has a chance to become visibly darker to the patient. They will likely be happier and remain more compliant with your predetermined plan if you follow this method.
Because inflammation is the direct trigger of hyperpigmentation, gentle exfoliation is crucial. If aggressive methods are employed, the condition will worsen rather than improve. Avoid high percentage straight acid peels and any mechanical methods, like harsh scrubs or loofahs. It is important to make your hyperpigmentation patients aware of this so that they are not inadvertently undoing the positive progress you help them achieve by irritating their skin at home.
Proven melanogenesis inhibition
Because melanogenesis is a process with many interconnected reactions, effective treatment is achieved by using topicals that contain ingredients that are proven to interrupt melanin production at multiple points.
• Retinoids, such as retinoic acid, retinol and retinaldehyde inhibit tyrosinase to suppress hyperpigmentation, enhancing cell turnover. Retinol is typically used in cosmeceutical preparations, as it is successfully converted to retinoic acid within the skin. This is especially important for patients with sensitive skin, as prescription retinoic acid can be highly stimulating on some skin types. This overstimulation could instigate melanogenesis.
• Azelaic acid inhibits tyrosinase activity and suppresses the proliferation of melanocytes.
• Glycolic acid is the most active and beneficial of the Alpha-Hydroxy-Acids (AHA) used in skin care for treating skin hyperpigmentation. Studies have shown glycolic acid to be the most effective fruit acid for cosmetic application. It has the smallest molecular structure of all AHAs, thus possesses the greatest penetration potential. Inside the cell, it stimulates the collagen and elastin fibers in the dermis, improving the appearance of wrinkles, fine lines and other forms of sun damage.
Avoiding UV-induced damage
Daily use of broad spectrum sun protection with an SPF of at least 30 is critical for all patients throughout the year. It is especially important for those fighting hyperpigmentation, as the inflammation resulting from UV exposure is a direct cause of melanogenesis. As a result of new sunscreen labeling regulations by the Food and Drug Administration, products can only be labeled “broad spectrum” after passing a rigorous critical wavelength test, so it is now easier to identify effective sunscreens.
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