No Sulfates, No Parabens, and the “No-Poo” Method: A New Patient Perspective on Common Shampoo Ingredients

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No Sulfates, No Parabens, and the “No-Poo” Method: A New Patient Perspective on Common Shampoo Ingredients
In Collaboration with the Skin of Color Society
Author(s)
Abigail Cline, MD, PhD
Laura N. Uwakwe, MD
Amy J. McMichael, MD

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.1 Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.2,3


It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,4 which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.4

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.5 Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.6 The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al7 showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.8 A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.9 However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.9 Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.10 Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.11 Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,13 but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.5 Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P0), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.6 Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).6 Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.5 Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.14 Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.15 A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.4 A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.4,5

 

 

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.16 Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.18 They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.18 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.19 Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer16; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”20 They extended this statement to include isopropylparaben and isobutylparaben in a later review.21 In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.22 This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”23 However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,16 and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.24

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.25 Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.17

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.16 Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.16

 

 

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.5 Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).16 However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.16

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.28 It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.31 Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.30 Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.28 The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.30 The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.33 Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.28 However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.33 Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.34 Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.34

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.38 Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.38

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

References
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  9. Tekbas¸ ÖF, Uysal Y, Og˘ur R, et al. Non-irritant baby shampoos may cause cataract development. TSK Koruyucu Hekimlik Bülteni. 2008;1:1-6.
  10. Cater KC, Harbell JW. Prediction of eye irritation potential of surfactant-based rinse-off personal care formulations by the bovine corneal opacity and permeability (BCOP) assay. Cutan Ocul Toxicol. 2006;25:217-233.
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  12. Rastogi SC. Headspace analysis of 1,4-dioxane in products containing polyethoxylated surfactants by GC-MS. Chromatographia. 1990;29:441-445.
  13. 1,4-Dioxane. IARC Monogr Eval Carcinog Risks Hum. 1999;71, pt 2:589-602.
  14. Trueb RM. Dermocosmetic aspects of hair and scalp. J Investig Dermatol Symp Proc. 2005;10:289-292.
  15. D’Souza P, Rathi SK. Shampoo and conditioners: what a dermatologist should know? Indian J Dermatol. 2015;60:248-254.
  16. Sasseville D, Alfalah M, Lacroix JP. “Parabenoia” debunked, or “who’s afraid of parabens?” Dermatitis. 2015;26:254-259.
  17. Krowka JF, Loretz L, Geis PA, et al. Preserving the facts on parabens: an overview of these important tools of the trade. Cosmetics & Toiletries. http://www.cosmeticsandtoiletries.com/research/chemistry/Preserving-the-Facts-on-Parabens-An-Overview-of-These-Important-Tools-of-the Trade-425784294.html. Published June 1, 2017. Accessed December 20, 2017.
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  19. Hossaini A, Larsen JJ, Larsen JC. Lack of oestrogenic effects of food preservatives (parabens) in uterotrophic assays. Food Chem Toxicol. 2000;38:319-323.
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  30. O’Lenick T. Anionic/cationic complexes in hair care. J Cosmet Sci. 2011;62:209-228.
  31. Gavazzoni Dias MF, de Almeida AM, Cecato PM, et al. The shampoo pH can affect the hair: myth or reality? Int J Trichology. 2014;6:95-99.
  32. Goodman H. The acid mantle of the skin surface. Ind Med Surg. 1958;27:105-108.
  33. Korting HC, Kober M, Mueller M, et al. Influence of repeated washings with soap and synthetic detergents on pH and resident flora of the skin of forehead and forearm. results of a cross-over trial in health probationers. Acta Derm Venereol. 1987;67:41-47.
  34. Tarun J, Susan J, Suria J, et al. Evaluation of pH of bathing soaps and shampoos for skin and hair care. Indian J Dermatol. 2014;59:442-444.
  35. Corbett JF. The chemistry of hair-care products. J Soc Dyers Colour. 1976;92:285-303.
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Dr. Cline is from Augusta University Medical Center, Georgia. Drs. Uwakwe and McMichael are from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina.

Drs. Cline and Uwakwe report no conflict of interest. Dr. McMichael is a consultant for Johnson & Johnson and Procter & Gamble. She also is an investigator for and has received research grants from Procter & Gamble.

Correspondence: Amy J. McMichael, MD, Department of Dermatology, Wake Forest Baptist Medical Center, 4618 Country Club Rd, Winston-Salem, NC 27104 ([email protected]).

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Cutis - 101(1)
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Cutis
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Hair & Nails
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Skin of Color
Author(s)
Abigail Cline, MD, PhD
Laura N. Uwakwe, MD
Amy J. McMichael, MD
Author(s)
Abigail Cline, MD, PhD
Laura N. Uwakwe, MD
Amy J. McMichael, MD
Author and Disclosure Information

 

Dr. Cline is from Augusta University Medical Center, Georgia. Drs. Uwakwe and McMichael are from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina.

Drs. Cline and Uwakwe report no conflict of interest. Dr. McMichael is a consultant for Johnson & Johnson and Procter & Gamble. She also is an investigator for and has received research grants from Procter & Gamble.

Correspondence: Amy J. McMichael, MD, Department of Dermatology, Wake Forest Baptist Medical Center, 4618 Country Club Rd, Winston-Salem, NC 27104 ([email protected]).

Author and Disclosure Information

 

Dr. Cline is from Augusta University Medical Center, Georgia. Drs. Uwakwe and McMichael are from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina.

Drs. Cline and Uwakwe report no conflict of interest. Dr. McMichael is a consultant for Johnson & Johnson and Procter & Gamble. She also is an investigator for and has received research grants from Procter & Gamble.

Correspondence: Amy J. McMichael, MD, Department of Dermatology, Wake Forest Baptist Medical Center, 4618 Country Club Rd, Winston-Salem, NC 27104 ([email protected]).

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In Collaboration with the Skin of Color Society
In Collaboration with the Skin of Color Society

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.1 Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.2,3


It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,4 which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.4

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.5 Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.6 The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al7 showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.8 A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.9 However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.9 Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.10 Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.11 Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,13 but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.5 Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P0), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.6 Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).6 Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.5 Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.14 Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.15 A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.4 A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.4,5

 

 

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.16 Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.18 They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.18 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.19 Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer16; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”20 They extended this statement to include isopropylparaben and isobutylparaben in a later review.21 In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.22 This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”23 However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,16 and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.24

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.25 Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.17

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.16 Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.16

 

 

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.5 Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).16 However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.16

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.28 It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.31 Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.30 Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.28 The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.30 The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.33 Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.28 However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.33 Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.34 Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.34

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.38 Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.38

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.1 Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.2,3


It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,4 which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.4

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.5 Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.6 The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al7 showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.8 A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.9 However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.9 Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.10 Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.11 Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,13 but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.5 Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P0), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.6 Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).6 Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.5 Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.14 Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.15 A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.4 A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.4,5

 

 

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.16 Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.18 They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.18 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.19 Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer16; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”20 They extended this statement to include isopropylparaben and isobutylparaben in a later review.21 In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.22 This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”23 However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,16 and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.24

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.25 Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.17

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.16 Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.16

 

 

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.5 Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).16 However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.16

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.28 It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.31 Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.30 Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.28 The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.30 The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.33 Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.28 However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.33 Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.34 Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.34

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.38 Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.38

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

References
  1. The global shampoo market 2014-2019 trends, forecast, and opportunity analysis [press release]. New York, NY: Reportlinker; May 21, 2015.
  2. Is the ‘no shampoo’ trend healthy or harmful? Mercola website. Published January 16, 2016. Accessed December 8, 2017.
  3. Feltman R. The science (or lack thereof) behind the ‘no-poo’ hair trend. Washington Post. March 10, 2016. https://www.washingtonpost.com/news/speaking-of-science/wp/2016/03/10/the-science-or-lack-thereof-behind-the-no-poo-hair-trend/?utm_term=.9a61edf3fd5a. Accessed December 11, 2017.
  4. Bouillon C. Shampoos. Clin Dermatol. 1996;14:113-121.
  5. Trueb RM. Shampoos: ingredients, efficacy, and adverse effects. J Dtsch Dermatol Ges. 2007;5:356-365.
  6. Bondi CA, Marks JL, Wroblewski LB, et al. Human and environmental toxicity of sodium lauryl sulfate (SLS): evidence for safe use in household cleaning products. Environ Health Insights. 2015;9:27-32.
  7. Green K, Johnson RE, Chapman JM, et al. Preservative effects on the healing rate of rabbit corneal epithelium. Lens Eye Toxic Res. 1989;6:37-41.
  8. Sodium lauryl sulphate. Healthy Choices website. http://www.healthychoices.co.uk/sls.html. Accessed December 8, 2017.
  9. Tekbas¸ ÖF, Uysal Y, Og˘ur R, et al. Non-irritant baby shampoos may cause cataract development. TSK Koruyucu Hekimlik Bülteni. 2008;1:1-6.
  10. Cater KC, Harbell JW. Prediction of eye irritation potential of surfactant-based rinse-off personal care formulations by the bovine corneal opacity and permeability (BCOP) assay. Cutan Ocul Toxicol. 2006;25:217-233.
  11. Birt DF, Lawson TA, Julius AD, et al. Inhibition by dietary selenium of colon cancer induced in the rat by bis(2-oxopropyl) nitrosamine. Cancer Res. 1982;42:4455-4459.
  12. Rastogi SC. Headspace analysis of 1,4-dioxane in products containing polyethoxylated surfactants by GC-MS. Chromatographia. 1990;29:441-445.
  13. 1,4-Dioxane. IARC Monogr Eval Carcinog Risks Hum. 1999;71, pt 2:589-602.
  14. Trueb RM. Dermocosmetic aspects of hair and scalp. J Investig Dermatol Symp Proc. 2005;10:289-292.
  15. D’Souza P, Rathi SK. Shampoo and conditioners: what a dermatologist should know? Indian J Dermatol. 2015;60:248-254.
  16. Sasseville D, Alfalah M, Lacroix JP. “Parabenoia” debunked, or “who’s afraid of parabens?” Dermatitis. 2015;26:254-259.
  17. Krowka JF, Loretz L, Geis PA, et al. Preserving the facts on parabens: an overview of these important tools of the trade. Cosmetics & Toiletries. http://www.cosmeticsandtoiletries.com/research/chemistry/Preserving-the-Facts-on-Parabens-An-Overview-of-These-Important-Tools-of-the Trade-425784294.html. Published June 1, 2017. Accessed December 20, 2017.
  18. Routledge EJ, Parker J, Odum J, et al. Some alkyl hydroxy benzoate preservatives (parabens) are estrogenic. Toxicol Appl Pharmacol. 1998;153:12Y19.
  19. Hossaini A, Larsen JJ, Larsen JC. Lack of oestrogenic effects of food preservatives (parabens) in uterotrophic assays. Food Chem Toxicol. 2000;38:319-323.
  20. Cosmetic Ingredient Review. Final report on the safety assessment of methylparaben, ethylparaben, propylparaben and butylparaben. J Am Coll Toxicol. 1984;3:147-209.
  21. Cosmetic Ingredient Review. Final report on the safety assessment of isobutylparaben and isopropylparaben. J Am Coll Toxicol. 1995;14:364-372.
  22. Scientific Committee on Consumer Products. Extended Opinion on the Safety Evaluation of Parabens. European Commission website. https://ec.europa.eu/health/ph_risk/committees/04_sccp/docs/sccp_o_019.pdf. Published January 28, 2005. Accessed December 20, 2017.
  23. Scientific Committee on Consumer Products. Opinion on Parabens. European Commission website. http://ec.europa.eu/health/scientific_committees/consumer_safety/docs/sccs_o_041.pdf. Revised March 22, 2011. Accessed December 20, 2017.
  24. European Commission. Commission Regulation (EU) No 258/2014 of 9 April 2014 amending Annexes II and V to Regulation (EC) No 1223/2009 of the European Parliament and of the Council on cosmetic products. EUR-Lex website. http://eur-lex.europa.eu/legal-content/EN/TXT/?uri=uriserv:OJ.L_.2014.107.01.0005.01.ENG. Accessed December 20, 2017.
  25. American Cancer Society. Antiperspirants and breast cancer risk. https://www.cancer.org/cancer/cancer-causes/antiperspirants-and-breast-cancer-risk.html#references. Revised October 14, 2014. Accessed January 2, 2018.
  26. MacMillan A. Cutting back on shampoo? 15 things you should know. Health. February 25, 2014. http://www.health.com/health/gallery/0,,20788089,00.html#should-you-go-no-poo--1. Accessed December 10, 2017.
  27. The ‘no poo’ method. https://www.nopoomethod.com/. Accessed December 10, 2017.
  28. Fong, D, Gaulin C, Le M, et al. Effectiveness of alternative antimicrobial agents for disinfection of hard surfaces. National Collaborating Centre for Environmental Health website. http://www.ncceh.ca/sites/default/files/Alternative_Antimicrobial_Agents_Aug_2014.pdf. Published August 2014. Accessed December 10, 2017.
  29. Is baking soda too harsh for natural hair? Black Girl With Long Hair website. http://blackgirllonghair.com/2012/02/is-baking-soda-too-harsh-for-hair/2/. Published February 5, 2012. Accessed December 12, 2017.
  30. O’Lenick T. Anionic/cationic complexes in hair care. J Cosmet Sci. 2011;62:209-228.
  31. Gavazzoni Dias MF, de Almeida AM, Cecato PM, et al. The shampoo pH can affect the hair: myth or reality? Int J Trichology. 2014;6:95-99.
  32. Goodman H. The acid mantle of the skin surface. Ind Med Surg. 1958;27:105-108.
  33. Korting HC, Kober M, Mueller M, et al. Influence of repeated washings with soap and synthetic detergents on pH and resident flora of the skin of forehead and forearm. results of a cross-over trial in health probationers. Acta Derm Venereol. 1987;67:41-47.
  34. Tarun J, Susan J, Suria J, et al. Evaluation of pH of bathing soaps and shampoos for skin and hair care. Indian J Dermatol. 2014;59:442-444.
  35. Corbett JF. The chemistry of hair-care products. J Soc Dyers Colour. 1976;92:285-303.
  36. McMichael AJ, Hordinsky M. Hair Diseases: Medical, Surgical, and Cosmetic Treatments. New York, NY: Taylor & Francis; 2008:59-72.
  37. Allardice A, Gummo G. Hair conditioning: quaternary ammonium compounds on various hair types. Cosmet Toiletries. 1993;108:107-109.
  38. Larson D, Jacob SE. Tea tree oil. Dermatitis. 2012;23:48-49.
References
  1. The global shampoo market 2014-2019 trends, forecast, and opportunity analysis [press release]. New York, NY: Reportlinker; May 21, 2015.
  2. Is the ‘no shampoo’ trend healthy or harmful? Mercola website. Published January 16, 2016. Accessed December 8, 2017.
  3. Feltman R. The science (or lack thereof) behind the ‘no-poo’ hair trend. Washington Post. March 10, 2016. https://www.washingtonpost.com/news/speaking-of-science/wp/2016/03/10/the-science-or-lack-thereof-behind-the-no-poo-hair-trend/?utm_term=.9a61edf3fd5a. Accessed December 11, 2017.
  4. Bouillon C. Shampoos. Clin Dermatol. 1996;14:113-121.
  5. Trueb RM. Shampoos: ingredients, efficacy, and adverse effects. J Dtsch Dermatol Ges. 2007;5:356-365.
  6. Bondi CA, Marks JL, Wroblewski LB, et al. Human and environmental toxicity of sodium lauryl sulfate (SLS): evidence for safe use in household cleaning products. Environ Health Insights. 2015;9:27-32.
  7. Green K, Johnson RE, Chapman JM, et al. Preservative effects on the healing rate of rabbit corneal epithelium. Lens Eye Toxic Res. 1989;6:37-41.
  8. Sodium lauryl sulphate. Healthy Choices website. http://www.healthychoices.co.uk/sls.html. Accessed December 8, 2017.
  9. Tekbas¸ ÖF, Uysal Y, Og˘ur R, et al. Non-irritant baby shampoos may cause cataract development. TSK Koruyucu Hekimlik Bülteni. 2008;1:1-6.
  10. Cater KC, Harbell JW. Prediction of eye irritation potential of surfactant-based rinse-off personal care formulations by the bovine corneal opacity and permeability (BCOP) assay. Cutan Ocul Toxicol. 2006;25:217-233.
  11. Birt DF, Lawson TA, Julius AD, et al. Inhibition by dietary selenium of colon cancer induced in the rat by bis(2-oxopropyl) nitrosamine. Cancer Res. 1982;42:4455-4459.
  12. Rastogi SC. Headspace analysis of 1,4-dioxane in products containing polyethoxylated surfactants by GC-MS. Chromatographia. 1990;29:441-445.
  13. 1,4-Dioxane. IARC Monogr Eval Carcinog Risks Hum. 1999;71, pt 2:589-602.
  14. Trueb RM. Dermocosmetic aspects of hair and scalp. J Investig Dermatol Symp Proc. 2005;10:289-292.
  15. D’Souza P, Rathi SK. Shampoo and conditioners: what a dermatologist should know? Indian J Dermatol. 2015;60:248-254.
  16. Sasseville D, Alfalah M, Lacroix JP. “Parabenoia” debunked, or “who’s afraid of parabens?” Dermatitis. 2015;26:254-259.
  17. Krowka JF, Loretz L, Geis PA, et al. Preserving the facts on parabens: an overview of these important tools of the trade. Cosmetics & Toiletries. http://www.cosmeticsandtoiletries.com/research/chemistry/Preserving-the-Facts-on-Parabens-An-Overview-of-These-Important-Tools-of-the Trade-425784294.html. Published June 1, 2017. Accessed December 20, 2017.
  18. Routledge EJ, Parker J, Odum J, et al. Some alkyl hydroxy benzoate preservatives (parabens) are estrogenic. Toxicol Appl Pharmacol. 1998;153:12Y19.
  19. Hossaini A, Larsen JJ, Larsen JC. Lack of oestrogenic effects of food preservatives (parabens) in uterotrophic assays. Food Chem Toxicol. 2000;38:319-323.
  20. Cosmetic Ingredient Review. Final report on the safety assessment of methylparaben, ethylparaben, propylparaben and butylparaben. J Am Coll Toxicol. 1984;3:147-209.
  21. Cosmetic Ingredient Review. Final report on the safety assessment of isobutylparaben and isopropylparaben. J Am Coll Toxicol. 1995;14:364-372.
  22. Scientific Committee on Consumer Products. Extended Opinion on the Safety Evaluation of Parabens. European Commission website. https://ec.europa.eu/health/ph_risk/committees/04_sccp/docs/sccp_o_019.pdf. Published January 28, 2005. Accessed December 20, 2017.
  23. Scientific Committee on Consumer Products. Opinion on Parabens. European Commission website. http://ec.europa.eu/health/scientific_committees/consumer_safety/docs/sccs_o_041.pdf. Revised March 22, 2011. Accessed December 20, 2017.
  24. European Commission. Commission Regulation (EU) No 258/2014 of 9 April 2014 amending Annexes II and V to Regulation (EC) No 1223/2009 of the European Parliament and of the Council on cosmetic products. EUR-Lex website. http://eur-lex.europa.eu/legal-content/EN/TXT/?uri=uriserv:OJ.L_.2014.107.01.0005.01.ENG. Accessed December 20, 2017.
  25. American Cancer Society. Antiperspirants and breast cancer risk. https://www.cancer.org/cancer/cancer-causes/antiperspirants-and-breast-cancer-risk.html#references. Revised October 14, 2014. Accessed January 2, 2018.
  26. MacMillan A. Cutting back on shampoo? 15 things you should know. Health. February 25, 2014. http://www.health.com/health/gallery/0,,20788089,00.html#should-you-go-no-poo--1. Accessed December 10, 2017.
  27. The ‘no poo’ method. https://www.nopoomethod.com/. Accessed December 10, 2017.
  28. Fong, D, Gaulin C, Le M, et al. Effectiveness of alternative antimicrobial agents for disinfection of hard surfaces. National Collaborating Centre for Environmental Health website. http://www.ncceh.ca/sites/default/files/Alternative_Antimicrobial_Agents_Aug_2014.pdf. Published August 2014. Accessed December 10, 2017.
  29. Is baking soda too harsh for natural hair? Black Girl With Long Hair website. http://blackgirllonghair.com/2012/02/is-baking-soda-too-harsh-for-hair/2/. Published February 5, 2012. Accessed December 12, 2017.
  30. O’Lenick T. Anionic/cationic complexes in hair care. J Cosmet Sci. 2011;62:209-228.
  31. Gavazzoni Dias MF, de Almeida AM, Cecato PM, et al. The shampoo pH can affect the hair: myth or reality? Int J Trichology. 2014;6:95-99.
  32. Goodman H. The acid mantle of the skin surface. Ind Med Surg. 1958;27:105-108.
  33. Korting HC, Kober M, Mueller M, et al. Influence of repeated washings with soap and synthetic detergents on pH and resident flora of the skin of forehead and forearm. results of a cross-over trial in health probationers. Acta Derm Venereol. 1987;67:41-47.
  34. Tarun J, Susan J, Suria J, et al. Evaluation of pH of bathing soaps and shampoos for skin and hair care. Indian J Dermatol. 2014;59:442-444.
  35. Corbett JF. The chemistry of hair-care products. J Soc Dyers Colour. 1976;92:285-303.
  36. McMichael AJ, Hordinsky M. Hair Diseases: Medical, Surgical, and Cosmetic Treatments. New York, NY: Taylor & Francis; 2008:59-72.
  37. Allardice A, Gummo G. Hair conditioning: quaternary ammonium compounds on various hair types. Cosmet Toiletries. 1993;108:107-109.
  38. Larson D, Jacob SE. Tea tree oil. Dermatitis. 2012;23:48-49.
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Practice Points

  • The ingredients in shampoos and other cosmetic products have become scrutinized by the general public and the Internet has contributed to misinformation about certain shampoos.
  • Dermatologists must be prepared to acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making.
  • This article reviews the controversy surrounding the use of sulfates and parabens in shampoos, as well as commonly used shampoo alternatives, often called the “no-poo” method.
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Approach to Treatment of Medical and Cosmetic Facial Concerns in Skin of Color Patients

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Approach to Treatment of Medical and Cosmetic Facial Concerns in Skin of Color Patients
In Collaboration With the Skin of Color Society
Author(s)
Valerie D. Callender, MD
Victoria Barbosa, MD
Cheryl M. Burgess, MD
Candrice Heath, MD
Amy J. McMichael, MD
Temitayo Ogunleye, MD
Susan C. Taylor, MD

The approach to the treatment of common skin disorders and cosmetic concerns in patients with skin of color (SOC) requires the clinician to understand the biological differences, nuances, and special considerations that are unique to patients with darker skin types.1-3 This article addresses 4 common facial concerns in SOC patients—acne, rosacea, facial hyperpigmentation, and cosmetic enhancement—and provides treatment recommendations and management pearls to assist the clinician with optimal outcomes for SOC patients.

Acne in SOC Patients

Acne vulgaris is one of the most common conditions that dermatologists treat and is estimated to affect 40 to 50 million individuals in the United States.1 Many of these acne patients are individuals with SOC.2-4 A study of 2835 females (aged 10–70 years) conducted in 4 different cities—Los Angeles, California; London, United Kingdom; Akita, Japan; and Rome, Italy—demonstrated acne prevalence of 37% in blacks, 32% in Hispanics, 30% in Asians, 24% in whites, and 23% in Continental Indians.5 Blacks, Hispanics, and Continental Indians demonstrated equal prevalence with comedonal and inflammatory acne. Asians displayed more inflammatory acne lesions than comedones. In contrast, whites demonstrated more comedones than inflammatory acne. Dyspigmentation, postinflammatory hyperpigmentation (PIH), and atrophic scars were more common in black and Hispanic females than other ethnicities.5 This study illustrated that acne-induced PIH is a common sequela in SOC patients and is the main reason they seek treatment.6,7

The pathogenesis of acne is the same in all racial and ethnic groups: (1) follicular hyperkeratinization and the formation of a microcomedone caused by abnormal desquamation of the keratinocytes within the sebaceous follicle, (2) production of sebum by circulating androgens, (3) proliferation of Propionibacterium acnes, and (4) inflammation. Subclinical inflammation is present throughout all stages of acne, including normal-appearing skin, inflammatory lesions, comedones, and scarring, and may contribute to PIH in acne patients with SOC (Figure 1).8 A thorough history should be obtained from acne patients, including answers to the following questions7:

  • What skin and hair care products do you use?
  • Do you use sunscreen daily?
  • What cosmetic products or makeup do you use?
  • Do you use any ethnic skin care products, including skin lightening creams?
  • Do you have a history of keloids?

Figure 1. Acne and postinflammatory hyperpigmentation in a patient with skin of color (Fitzpatrick skin type V).

It is important to ask these questions to assess if the SOC patient has developed pomade acne,9 acne cosmetica,10 or a potential risk of skin irritation from the use of skin care practices. It is best to take total control of the patient’s skin care regimen and discontinue use of toners, astringents, witch hazel, exfoliants, and rubbing alcohol, which may lead to skin dryness and irritation, particularly when combined with topical acne medications.

Treatment
Treatment of acne in SOC patients is similar to generally recommended treatments, with special considerations. Consider the following key points when treating acne in SOC patients:

  • Treat acne early and aggressively to prevent or minimize subsequent PIH and acne scarring.
  • Balance aggressive treatment with nonirritating topical skin care.
  • Most importantly, target PIH in addition to acne and choose a regimen that limits skin irritation that might exacerbate existing PIH.7

Develop a maintenance program to control future breakouts. Topical agents can be used as monotherapy or in fixed combinations and may include benzoyl peroxide, antibiotics, dapsone, azelaic acid (AZA), and retinoids. Similar to white patients, topical retinoids remain a first-line treatment for acne in patients with SOC.11,12

Tolerability must be managed in SOC acne patients. Therapeutic maneuvers that can be instituted should include a discussion on using gentle skin care, initiating therapy with a retinoid applied every other night starting with a low concentration and gradually titrating up, and applying a moisturizer before or after applying acne medication. Oral therapies consist of antibiotics (doxycycline, minocycline), retinoids (isotretinoin), and hormonal modulators (oral contraceptives, spironolactone). Isotretinoin, recommended for patients with nodulocystic acne, may play a possible role in treating acne-induced PIH.13

Two common procedural therapies for acne include comedone extraction and intralesional corticosteroid injection. A 6- to 8-week course of a topical retinoid prior to comedonal extraction may facilitate the procedure and is recommended in SOC patients to help reduce cutaneous trauma and PIH.11 Inflammatory acne lesions can be treated with intralesional injection of triamcinolone acetonide 2.5 or 5.0 mg/mL, which usually reduces inflammation within 2 to 5 days.11

Treatment of acne-induced PIH includes sun protection, topical and oral medications, chemical peels, lasers, and energy devices. Treatment of hypertrophic scarring and keloids involves intralesional injection of triamcinolone acetonide 20, 30, or 40 mg/mL every 4 weeks until the lesion is flat.11

Superficial chemical peels can be used to treat acne and PIH in SOC patients,14 such as salicylic acid (20%–30%), glycolic acid (20%–70%), trichloroacetic acid (15%–30%), and Jessner peels.

Acne Scarring
Surgical approaches to acne scarring in patients with SOC include elliptical excision, punch excision, punch elevation, punch autografting, dermal grafting, dermal planning, subcutaneous incision (subcision), dermabrasion, microneedling, fillers, and laser skin resurfacing. The treatment of choice depends on the size, type, and depth of the scar and the clinician’s preference.

Lasers
Fractional photothermolysis has emerged as a treatment option for acne scars in SOC patients. This procedure produces microscopic columns of thermal injury in the epidermis and dermis, sparing the surrounding tissue and minimizing downtime and adverse events. Because fractional photothermolysis does not target melanin and produces limited epidermal injury, darker Fitzpatrick skin types (IV–VI) can be safely and effectively treated with this procedure.15

 

 

Rosacea in SOC Patients

Rosacea is a chronic inflammatory disorder that affects the vasculature and pilosebaceous units of the face. It commonly is seen in Fitzpatrick skin types I and II; however, rosacea can occur in all skin types (Figure 2). Triggers include emotional stress, extreme environmental temperatures, hot and spicy foods, red wine or alcohol, and topical irritants or allergens found in common cosmetic products.16

Figure 2. Rosacea in a patient with skin of color (Fitzpatrick skin type IV).

Data suggest that 4% of rosacea patients in the United States are of African, Latino, or Asian descent.11 National Ambulatory Medical Care Survey data revealed that of 31.5 million rosacea visits, 2% of patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino. In a 5-year longitudinal study of 2587 rosacea patients enrolled in Medicaid in North Carolina who were prescribed at least 1 topical treatment for rosacea, 16.27% were black and 10% were of a race other than white.17

Although the pathogenesis of rosacea is unclear, hypotheses include immune system abnormalities, neurogenic dysregulation, presence of microorganisms (eg, Demodex folliculorum), UV damage, and skin barrier dysfunction.18

The 4 major subtypes of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea.16 Interestingly, rosacea in SOC patients may present with hypopigmentation surrounding the borders of the facial erythema. For phymatous rosacea, isotretinoin may reduce incipient rhinophyma but must be carefully monitored and pregnancy must be excluded. Surgical or laser therapy may be indicated to recontour the nose if severe.

There are several skin conditions that can present with facial erythema in patients with SOC, including seborrheic dermatitis, systemic lupus erythematosus, and contact dermatitis. It is important to note that the detection of facial erythema in darker skin types may be difficult; therefore, laboratory evaluation (antinuclear antibodies), patch testing, and skin biopsy should be considered if the clinical diagnosis is unclear.

Treatment
Treatment of rosacea in SOC patients does not differ from other racial groups. Common strategies include gentle skin care, sun protection (sun protection factor 30+), and barrier repair creams. Topical agents include metronidazole, AZA, sodium sulfacetamide/sulfur, ivermectin, and retinoids.16 Oral treatments include antibiotics in the tetracycline family (eg, subantimicrobial dose doxycycline) and isotretinoin.16 Persistent erythema associated with rosacea can be treated with brimonidine19 and oxymetazoline.20 Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea21; however, the latter is not recommended in Fitzpatrick skin types IV through VI.

Facial Hyperpigmentation in SOC Patients

Hyperpigmentation disorders can be divided into conditions that affect Fitzpatrick skin types I through III and IV though VI. Mottled hyperpigmentation (photodamage) and solar lentigines occur in patients with lighter skin types as compared to melasma, PIH, and age-related (UV-induced) hyperpigmentation, which occur more commonly in patients with darker skin types. Facial hyperpigmentation is a common concern in SOC patients. In a survey of cosmetic concerns of 100 women with SOC, hyperpigmentation or dark spots (86%) and blotchy uneven skin (80%) were the top concerns.22 In addition, facial hyperpigmentation has been shown to negatively impact quality of life.23

Postinflammatory hyperpigmentation occurs from a pathophysiological response to inflammation, cutaneous irritation or injury, and subsequent melanocyte lability. Postinflammatory hyperpigmentation is a common presenting concern in patients with SOC and is seen as a result of many inflammatory skin disorders (eg, acne, eczema) and dermatologic procedures (eg, adverse reaction to electrodesiccation, microdermabrasion, chemical peels, laser surgery).24

Melasma is an acquired idiopathic disorder of hyperpigmentation and often referred to as the mask of pregnancy (Figure 3). It occurs on sun-exposed areas of skin, mainly in women with Fitzpatrick skin types III through V. Associated factors or triggers include pregnancy, hormonal treatments, exposure to UV radiation, and medications.25 Hereditary factors play a role in more than 40% of cases.26

Figure 3. Facial hyperpigmentation consistent with melasma in a patient with skin of color (Fitzpatrick skin type IV).

Other not-so-common facial dyschromias include contact dermatitis, acanthosis nigricans, exogenous ochronosis, lichen planus pigmentosus (associated with frontal fibrosing alopecia),27 drug-induced hyperpigmentation (associated with minocycline or diltiazem),28,29 and UV-induced (age-related) hyperpigmentation.

Treatment
The treatment of hyperpigmentation should provide the following: (1) protection from sun exposure; (2) inhibition of tyrosinase, the enzyme responsible for the conversion of tyrosine to melanin; (3) inhibition of melanosome transfer from the melanocyte to the keratinocyte; (4) removal of melanin from the epidermis through exfoliation; and (5) destruction or disruption of melanin in the dermis.30 Therapies for facial hyperpigmentation are listed in Table 1.

Topical therapies include prescription medications and nonprescription cosmeceuticals. Prescription medications include hydroquinone (HQ), topical retinoids, and AZA. Hydroquinone, a tyrosinase inhibitor, is the gold standard for skin lightening and often is used as a first-line therapy. It is used as a monotherapy (HQ 4%) or as a fixed combination with tretinoin 0.05% and fluocinolone 0.01%.31 Use caution with HQ in high concentrations (6% and higher) and low concentrations (2% [over-the-counter strength]) used long-term due to the potential risk of exogenous ochronosis.

Topical retinoids have been shown to be effective therapeutic agents for melasma and PIH. Tretinoin,32 tazarotene,33 and adapalene34 all have demonstrated efficacy for acne and acne-induced PIH in SOC patients. Patients must be monitored for the development of retinoid dermatitis and worsening of hyperpigmentation.

Azelaic acid is a naturally occurring dicarboxylic acid obtained from cultures of Malassezia furfur. Azelaic acid inhibits tyrosinase activity, DNA synthesis, and mitochondrial enzymes, thus blocking direct cytotoxic effects toward melanocytes. Azelaic acid is approved by the US Food and Drug Administration for acne in a 20% cream formulation and rosacea in 15% gel and foam formulations, and it is used off label for melasma and PIH.35

Oral tranexamic acid is currently used as a hemostatic agent due to its ability to inhibit the plasminogen-plasmin pathway. In melasma, it blocks the interaction between melanocytes and keratinocytes in the epidermis and modulates the vascular component of melasma in the dermis. In an open-label study, 561 Asian melasma patients were treated with oral tranexamic acid 250 mg twice daily for 4 months. Results demonstrated improvement in 90% of patients, and 7.1% reported adverse effects (eg, abdominal bloating and pain, nausea, vomiting, headache, tinnitus, numbness, menstrual irregularities).36 Coagulation screening should be monitored monthly, and any patient with a history of clotting abnormalities should be excluded from off-label treatment with oral tranexamic acid.

Nonprescription cosmeceuticals are available over-the-counter or are office dispensed.37 For optimal results, cosmeceutical agents for skin lightening are used in combination. Most of these combinations are HQ free and have additive benefits such as a multimodal skin lightening agent containing key ingredients that correct and prevent skin pigmentation via several pathways affecting melanogenesis.38 It is an excellent alternative to HQ for mottled and diffuse UV-induced hyperpigmentation and can be used for maintenance therapy in patients with melasma.

Photoprotection is an essential component of therapy for melasma and PIH, but there is a paucity of data on the benefits for SOC patients. Halder et al39 performed a randomized prospective study of 89 black and Hispanic patients who applied sunscreen with a sun protection factor of 30 or 60 daily for 8 weeks. Clinical grading, triplicate L*A*B chromameter, and clinical photography were taken at baseline and weeks 4 and 8. The results demonstrated skin lightening in both black and Hispanic patients and support the use of sunscreen in the prevention and management of dyschromia in SOC patients.39 Visible light also may play a role in melasma development, and thus use of sunscreens or makeup containing iron oxides are recommended.40

Procedural treatments for facial hyperpigmentation include microdermabrasion, chemical peels, lasers, energy-based devices, and microneedling. There are many types and formulations of chemical peeling agents available; however, superficial and medium-depth chemical peels are recommended for SOC patients (Table 2). Deep chemical peels are not recommended for SOC patients due to the potential increased risk for PIH and scarring.

 

 

Cosmetic Enhancement in SOC Patients

Cosmetic procedures are gaining popularity in the SOC population and account for more than 20% of cosmetic procedures in the United States.41 Facial cosmetic concerns in SOC include dyschromia, benign growths (dermatosis papulosa nigra), hyperkinetic facial lines, volume loss, and skin laxity.42 Key principles to consider when treating SOC patients are the impact of ethnicity on aging and facial structure, the patient’s desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient’s expectations for recommended therapies.

Aging in SOC Patients
Skin aging can be classified as intrinsic aging or extrinsic aging. Intrinsic aging is genetic and involves subsurface changes such as volume loss, muscle atrophy, and resorption of bony structure. Extrinsic aging (or photoaging) involves surface changes of the epidermis/dermis and manifests as mottled pigmentation, textural changes, and fine wrinkling. Due to the photoprotection of melanin (black skin=SPF 13.4), skin aging in SOC patients is delayed by 10 to 20 years.43 In addition, SOC patients have more reactive collagen and can benefit from noninvasive cosmetic procedures such as fillers and skin-tightening procedures.42

Cosmetic Treatments and Procedures
Dermatosis papulosa nigra (benign growths of skin that have a genetic predisposition)44 occur mainly on the face but can involve the entire body. Treatment modalities include electrodesiccation, cryotherapy, scissor excision, and laser surgery.45

Treatment of hyperkinetic facial lines with botulinum toxin type A is a safe and effective procedure in patients with SOC. Grimes and Shabazz46 performed a 4-month, randomized, double-blind study that evaluated the treatment of glabellar lines in women with Fitzpatrick skin types V and VI. The results demonstrated that the duration of effects was the same in the patients who received either 20 or 30 U of botulinum toxin type A.46 Dynamic rhytides (furrows and frown/scowl lines arising from laughing, frowning, or smiling) can be treated safely in patients with SOC using botulinum toxin type A off label for relaxation of the upper and lower hyperkinetic muscles that result in these unwanted signs of aging. Botulinum toxin type A often is used for etched-in crow’s-feet, which rarely are evident in SOC patients.47 Facial shaping also can be accomplished by injecting botulinum toxin type A in combination with soft-tissue dermal fillers.47

Although black individuals do not experience perioral rhytides at the frequency of white individuals, they experience a variety of other cosmetic issues related to skin sagging and sinking. Currently available hyaluronic acid (HA) fillers have been shown to be safe in patients with Fitzpatrick skin types IV through VI.48 Two studies evaluated fillers in patients with SOC, specifically HA49 and calcium hydroxylapatite,50 focused on treatment of the nasolabial folds and the potential risk for dyspigmentation and keloidal scarring. Taylor et al49 noted that the risk of hyperpigmentation was 6% to 9% for large- and small-particle HA, respectively, and was associated with the serial or multiple puncture injection technique. No hypertrophic or keloidal scarring occurred in both studies.49,50

Facial contouring applications with fillers include glabellar lines, temples, nasal bridge, tear troughs, malar and submalar areas, nasolabial folds, radial lines, lips, marionette lines, mental crease, and chin. Hyaluronic acid fillers also can be used for lip enhancement.47 Although white women are looking to increase the size of their lips, black women are seeking augmentation to restore their lip size to that of their youth. Black individuals do not experience the same frequency of perioral rhytides as white patients, but they experience a variety of other issues related to skin sagging and sinking. Unlike white women, enhancement of the vermilion border rarely is performed in black women due to development of rhytides, predominantly in the body of the lip below the vermilion border in response to volume loss in the upper lip while the lower lip usually maintains its same appearance.47

Facial enhancement utilizing poly-L-lactic acid can be used safely in SOC patients.51 Poly-L-lactic acid microparticles induce collagen formation, leading to dermal thickening over 3 to 6 months; however, multiple sessions are required to achieve optimal aesthetic results.

Patients with more reactive collagen can benefit from noninvasive cosmetic procedures such as skin-tightening procedures.52 Radiofrequency and microfocused ultrasound are cosmetic procedures used to provide skin tightening and facial lifting. They are safe and effective treatments for patients with Fitzpatrick skin types IV to VI.53 Histologically, there is less thinning of collagen bundles and elastic tissue in ethnic skin. Due to stimulation of collagen by these procedures, most SOC patients will experience a more enhanced response, requiring fewer treatment sessions than white individuals.

Conclusion

Medical and aesthetic facial concerns in SOC patients vary and can be a source of emotional and psychological distress that can negatively impact quality of life. The approach to the treatment of SOC patients should be a balance between tolerability and efficacy, considering the potential risk for PIH.

References
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  44. Grimes PE, Arora S, Minus HR, et al. Dermatosis papulosa nigra. Cutis. 1983;32:385-386.
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  46. Grimes PE, Shabazz D. A four-month randomized, double-blind evaluation of the efficacy of botulinum toxin type A for the treatment of glabellar lines in women with skin types V and VI. Dermatol Surg. 2009;35:429-435.
  47. Burgess CM, Awosika O. Ethnic and gender considerations in the use of facial injectables: African-American patients. Plast Reconstr Surg. 2015;136(5 suppl):28S-31S.
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Author and Disclosure Information

Dr. Callender is from Callender Dermatology and Cosmetic Center, Glenn Dale, Maryland. Dr. Barbosa is from Millennium Park Dermatology, Chicago, Illinois. Dr. Burgess is from the Center for Dermatology and Dermatologic Surgery, Washington, DC. Dr. Heath is from Premier Dermatology and Cosmetic Surgery, Newark, Delaware. Dr. McMichael is from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Drs. Ogunleye and Taylor are from the Department of Dermatology, University of Pennsylvania, Philadelphia.

Dr. Callender is a consultant for Allergan; Galderma Laboratories, LP; and Unilever. She also is a researcher for Aclaris Therapeutics, Inc; Allergan; and Revance Therapeutics Inc. Drs. Barbosa, Heath, and Ogunleye report no conflict of interest. Dr. Burgess is a clinical research investigator and stockholder and has received honorarium from Allergan. She also is a clinical research investigator for Aclaris Therapeutics, Inc; Cutanea Life Sciences; Foamix Pharmaceuticals; and Revance Therapeutics Inc, and is a clinical research investigator and speaker and has received honoraria from Merz Pharma. Dr. McMichael is a consultant for Allergan; Galderma Laboratories, LP; Johnson & Johnson; and Procter & Gamble. She also has received research grants from Allergan and Procter & Gamble. Dr. Taylor is an advisory board member for Allergan; Aclaris Therapeutics Inc; Beiersdorf Inc; Galderma Laboratories, LP; and NeoStrata Company, Inc. She also is an investigator for Aclaris Therapeutics Inc and Croma-Pharma.

Correspondence: Valerie D. Callender, MD, 12200 Annapolis Rd, Ste 315, Glenn Dale, MD 20769 ([email protected]).

Issue
Cutis - 100(6)
Publications
MDedge Dermatology
Cutis
Topics
Pigmentation Disorders
Diversity in Medicine
Page Number
375-380
Sections
Skin of Color
Author(s)
Valerie D. Callender, MD
Victoria Barbosa, MD
Cheryl M. Burgess, MD
Candrice Heath, MD
Amy J. McMichael, MD
Temitayo Ogunleye, MD
Susan C. Taylor, MD
Author(s)
Valerie D. Callender, MD
Victoria Barbosa, MD
Cheryl M. Burgess, MD
Candrice Heath, MD
Amy J. McMichael, MD
Temitayo Ogunleye, MD
Susan C. Taylor, MD
Author and Disclosure Information

Dr. Callender is from Callender Dermatology and Cosmetic Center, Glenn Dale, Maryland. Dr. Barbosa is from Millennium Park Dermatology, Chicago, Illinois. Dr. Burgess is from the Center for Dermatology and Dermatologic Surgery, Washington, DC. Dr. Heath is from Premier Dermatology and Cosmetic Surgery, Newark, Delaware. Dr. McMichael is from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Drs. Ogunleye and Taylor are from the Department of Dermatology, University of Pennsylvania, Philadelphia.

Dr. Callender is a consultant for Allergan; Galderma Laboratories, LP; and Unilever. She also is a researcher for Aclaris Therapeutics, Inc; Allergan; and Revance Therapeutics Inc. Drs. Barbosa, Heath, and Ogunleye report no conflict of interest. Dr. Burgess is a clinical research investigator and stockholder and has received honorarium from Allergan. She also is a clinical research investigator for Aclaris Therapeutics, Inc; Cutanea Life Sciences; Foamix Pharmaceuticals; and Revance Therapeutics Inc, and is a clinical research investigator and speaker and has received honoraria from Merz Pharma. Dr. McMichael is a consultant for Allergan; Galderma Laboratories, LP; Johnson & Johnson; and Procter & Gamble. She also has received research grants from Allergan and Procter & Gamble. Dr. Taylor is an advisory board member for Allergan; Aclaris Therapeutics Inc; Beiersdorf Inc; Galderma Laboratories, LP; and NeoStrata Company, Inc. She also is an investigator for Aclaris Therapeutics Inc and Croma-Pharma.

Correspondence: Valerie D. Callender, MD, 12200 Annapolis Rd, Ste 315, Glenn Dale, MD 20769 ([email protected]).

Author and Disclosure Information

Dr. Callender is from Callender Dermatology and Cosmetic Center, Glenn Dale, Maryland. Dr. Barbosa is from Millennium Park Dermatology, Chicago, Illinois. Dr. Burgess is from the Center for Dermatology and Dermatologic Surgery, Washington, DC. Dr. Heath is from Premier Dermatology and Cosmetic Surgery, Newark, Delaware. Dr. McMichael is from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Drs. Ogunleye and Taylor are from the Department of Dermatology, University of Pennsylvania, Philadelphia.

Dr. Callender is a consultant for Allergan; Galderma Laboratories, LP; and Unilever. She also is a researcher for Aclaris Therapeutics, Inc; Allergan; and Revance Therapeutics Inc. Drs. Barbosa, Heath, and Ogunleye report no conflict of interest. Dr. Burgess is a clinical research investigator and stockholder and has received honorarium from Allergan. She also is a clinical research investigator for Aclaris Therapeutics, Inc; Cutanea Life Sciences; Foamix Pharmaceuticals; and Revance Therapeutics Inc, and is a clinical research investigator and speaker and has received honoraria from Merz Pharma. Dr. McMichael is a consultant for Allergan; Galderma Laboratories, LP; Johnson & Johnson; and Procter & Gamble. She also has received research grants from Allergan and Procter & Gamble. Dr. Taylor is an advisory board member for Allergan; Aclaris Therapeutics Inc; Beiersdorf Inc; Galderma Laboratories, LP; and NeoStrata Company, Inc. She also is an investigator for Aclaris Therapeutics Inc and Croma-Pharma.

Correspondence: Valerie D. Callender, MD, 12200 Annapolis Rd, Ste 315, Glenn Dale, MD 20769 ([email protected]).

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In Collaboration With the Skin of Color Society

The approach to the treatment of common skin disorders and cosmetic concerns in patients with skin of color (SOC) requires the clinician to understand the biological differences, nuances, and special considerations that are unique to patients with darker skin types.1-3 This article addresses 4 common facial concerns in SOC patients—acne, rosacea, facial hyperpigmentation, and cosmetic enhancement—and provides treatment recommendations and management pearls to assist the clinician with optimal outcomes for SOC patients.

Acne in SOC Patients

Acne vulgaris is one of the most common conditions that dermatologists treat and is estimated to affect 40 to 50 million individuals in the United States.1 Many of these acne patients are individuals with SOC.2-4 A study of 2835 females (aged 10–70 years) conducted in 4 different cities—Los Angeles, California; London, United Kingdom; Akita, Japan; and Rome, Italy—demonstrated acne prevalence of 37% in blacks, 32% in Hispanics, 30% in Asians, 24% in whites, and 23% in Continental Indians.5 Blacks, Hispanics, and Continental Indians demonstrated equal prevalence with comedonal and inflammatory acne. Asians displayed more inflammatory acne lesions than comedones. In contrast, whites demonstrated more comedones than inflammatory acne. Dyspigmentation, postinflammatory hyperpigmentation (PIH), and atrophic scars were more common in black and Hispanic females than other ethnicities.5 This study illustrated that acne-induced PIH is a common sequela in SOC patients and is the main reason they seek treatment.6,7

The pathogenesis of acne is the same in all racial and ethnic groups: (1) follicular hyperkeratinization and the formation of a microcomedone caused by abnormal desquamation of the keratinocytes within the sebaceous follicle, (2) production of sebum by circulating androgens, (3) proliferation of Propionibacterium acnes, and (4) inflammation. Subclinical inflammation is present throughout all stages of acne, including normal-appearing skin, inflammatory lesions, comedones, and scarring, and may contribute to PIH in acne patients with SOC (Figure 1).8 A thorough history should be obtained from acne patients, including answers to the following questions7:

  • What skin and hair care products do you use?
  • Do you use sunscreen daily?
  • What cosmetic products or makeup do you use?
  • Do you use any ethnic skin care products, including skin lightening creams?
  • Do you have a history of keloids?

Figure 1. Acne and postinflammatory hyperpigmentation in a patient with skin of color (Fitzpatrick skin type V).

It is important to ask these questions to assess if the SOC patient has developed pomade acne,9 acne cosmetica,10 or a potential risk of skin irritation from the use of skin care practices. It is best to take total control of the patient’s skin care regimen and discontinue use of toners, astringents, witch hazel, exfoliants, and rubbing alcohol, which may lead to skin dryness and irritation, particularly when combined with topical acne medications.

Treatment
Treatment of acne in SOC patients is similar to generally recommended treatments, with special considerations. Consider the following key points when treating acne in SOC patients:

  • Treat acne early and aggressively to prevent or minimize subsequent PIH and acne scarring.
  • Balance aggressive treatment with nonirritating topical skin care.
  • Most importantly, target PIH in addition to acne and choose a regimen that limits skin irritation that might exacerbate existing PIH.7

Develop a maintenance program to control future breakouts. Topical agents can be used as monotherapy or in fixed combinations and may include benzoyl peroxide, antibiotics, dapsone, azelaic acid (AZA), and retinoids. Similar to white patients, topical retinoids remain a first-line treatment for acne in patients with SOC.11,12

Tolerability must be managed in SOC acne patients. Therapeutic maneuvers that can be instituted should include a discussion on using gentle skin care, initiating therapy with a retinoid applied every other night starting with a low concentration and gradually titrating up, and applying a moisturizer before or after applying acne medication. Oral therapies consist of antibiotics (doxycycline, minocycline), retinoids (isotretinoin), and hormonal modulators (oral contraceptives, spironolactone). Isotretinoin, recommended for patients with nodulocystic acne, may play a possible role in treating acne-induced PIH.13

Two common procedural therapies for acne include comedone extraction and intralesional corticosteroid injection. A 6- to 8-week course of a topical retinoid prior to comedonal extraction may facilitate the procedure and is recommended in SOC patients to help reduce cutaneous trauma and PIH.11 Inflammatory acne lesions can be treated with intralesional injection of triamcinolone acetonide 2.5 or 5.0 mg/mL, which usually reduces inflammation within 2 to 5 days.11

Treatment of acne-induced PIH includes sun protection, topical and oral medications, chemical peels, lasers, and energy devices. Treatment of hypertrophic scarring and keloids involves intralesional injection of triamcinolone acetonide 20, 30, or 40 mg/mL every 4 weeks until the lesion is flat.11

Superficial chemical peels can be used to treat acne and PIH in SOC patients,14 such as salicylic acid (20%–30%), glycolic acid (20%–70%), trichloroacetic acid (15%–30%), and Jessner peels.

Acne Scarring
Surgical approaches to acne scarring in patients with SOC include elliptical excision, punch excision, punch elevation, punch autografting, dermal grafting, dermal planning, subcutaneous incision (subcision), dermabrasion, microneedling, fillers, and laser skin resurfacing. The treatment of choice depends on the size, type, and depth of the scar and the clinician’s preference.

Lasers
Fractional photothermolysis has emerged as a treatment option for acne scars in SOC patients. This procedure produces microscopic columns of thermal injury in the epidermis and dermis, sparing the surrounding tissue and minimizing downtime and adverse events. Because fractional photothermolysis does not target melanin and produces limited epidermal injury, darker Fitzpatrick skin types (IV–VI) can be safely and effectively treated with this procedure.15

 

 

Rosacea in SOC Patients

Rosacea is a chronic inflammatory disorder that affects the vasculature and pilosebaceous units of the face. It commonly is seen in Fitzpatrick skin types I and II; however, rosacea can occur in all skin types (Figure 2). Triggers include emotional stress, extreme environmental temperatures, hot and spicy foods, red wine or alcohol, and topical irritants or allergens found in common cosmetic products.16

Figure 2. Rosacea in a patient with skin of color (Fitzpatrick skin type IV).

Data suggest that 4% of rosacea patients in the United States are of African, Latino, or Asian descent.11 National Ambulatory Medical Care Survey data revealed that of 31.5 million rosacea visits, 2% of patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino. In a 5-year longitudinal study of 2587 rosacea patients enrolled in Medicaid in North Carolina who were prescribed at least 1 topical treatment for rosacea, 16.27% were black and 10% were of a race other than white.17

Although the pathogenesis of rosacea is unclear, hypotheses include immune system abnormalities, neurogenic dysregulation, presence of microorganisms (eg, Demodex folliculorum), UV damage, and skin barrier dysfunction.18

The 4 major subtypes of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea.16 Interestingly, rosacea in SOC patients may present with hypopigmentation surrounding the borders of the facial erythema. For phymatous rosacea, isotretinoin may reduce incipient rhinophyma but must be carefully monitored and pregnancy must be excluded. Surgical or laser therapy may be indicated to recontour the nose if severe.

There are several skin conditions that can present with facial erythema in patients with SOC, including seborrheic dermatitis, systemic lupus erythematosus, and contact dermatitis. It is important to note that the detection of facial erythema in darker skin types may be difficult; therefore, laboratory evaluation (antinuclear antibodies), patch testing, and skin biopsy should be considered if the clinical diagnosis is unclear.

Treatment
Treatment of rosacea in SOC patients does not differ from other racial groups. Common strategies include gentle skin care, sun protection (sun protection factor 30+), and barrier repair creams. Topical agents include metronidazole, AZA, sodium sulfacetamide/sulfur, ivermectin, and retinoids.16 Oral treatments include antibiotics in the tetracycline family (eg, subantimicrobial dose doxycycline) and isotretinoin.16 Persistent erythema associated with rosacea can be treated with brimonidine19 and oxymetazoline.20 Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea21; however, the latter is not recommended in Fitzpatrick skin types IV through VI.

Facial Hyperpigmentation in SOC Patients

Hyperpigmentation disorders can be divided into conditions that affect Fitzpatrick skin types I through III and IV though VI. Mottled hyperpigmentation (photodamage) and solar lentigines occur in patients with lighter skin types as compared to melasma, PIH, and age-related (UV-induced) hyperpigmentation, which occur more commonly in patients with darker skin types. Facial hyperpigmentation is a common concern in SOC patients. In a survey of cosmetic concerns of 100 women with SOC, hyperpigmentation or dark spots (86%) and blotchy uneven skin (80%) were the top concerns.22 In addition, facial hyperpigmentation has been shown to negatively impact quality of life.23

Postinflammatory hyperpigmentation occurs from a pathophysiological response to inflammation, cutaneous irritation or injury, and subsequent melanocyte lability. Postinflammatory hyperpigmentation is a common presenting concern in patients with SOC and is seen as a result of many inflammatory skin disorders (eg, acne, eczema) and dermatologic procedures (eg, adverse reaction to electrodesiccation, microdermabrasion, chemical peels, laser surgery).24

Melasma is an acquired idiopathic disorder of hyperpigmentation and often referred to as the mask of pregnancy (Figure 3). It occurs on sun-exposed areas of skin, mainly in women with Fitzpatrick skin types III through V. Associated factors or triggers include pregnancy, hormonal treatments, exposure to UV radiation, and medications.25 Hereditary factors play a role in more than 40% of cases.26

Figure 3. Facial hyperpigmentation consistent with melasma in a patient with skin of color (Fitzpatrick skin type IV).

Other not-so-common facial dyschromias include contact dermatitis, acanthosis nigricans, exogenous ochronosis, lichen planus pigmentosus (associated with frontal fibrosing alopecia),27 drug-induced hyperpigmentation (associated with minocycline or diltiazem),28,29 and UV-induced (age-related) hyperpigmentation.

Treatment
The treatment of hyperpigmentation should provide the following: (1) protection from sun exposure; (2) inhibition of tyrosinase, the enzyme responsible for the conversion of tyrosine to melanin; (3) inhibition of melanosome transfer from the melanocyte to the keratinocyte; (4) removal of melanin from the epidermis through exfoliation; and (5) destruction or disruption of melanin in the dermis.30 Therapies for facial hyperpigmentation are listed in Table 1.

Topical therapies include prescription medications and nonprescription cosmeceuticals. Prescription medications include hydroquinone (HQ), topical retinoids, and AZA. Hydroquinone, a tyrosinase inhibitor, is the gold standard for skin lightening and often is used as a first-line therapy. It is used as a monotherapy (HQ 4%) or as a fixed combination with tretinoin 0.05% and fluocinolone 0.01%.31 Use caution with HQ in high concentrations (6% and higher) and low concentrations (2% [over-the-counter strength]) used long-term due to the potential risk of exogenous ochronosis.

Topical retinoids have been shown to be effective therapeutic agents for melasma and PIH. Tretinoin,32 tazarotene,33 and adapalene34 all have demonstrated efficacy for acne and acne-induced PIH in SOC patients. Patients must be monitored for the development of retinoid dermatitis and worsening of hyperpigmentation.

Azelaic acid is a naturally occurring dicarboxylic acid obtained from cultures of Malassezia furfur. Azelaic acid inhibits tyrosinase activity, DNA synthesis, and mitochondrial enzymes, thus blocking direct cytotoxic effects toward melanocytes. Azelaic acid is approved by the US Food and Drug Administration for acne in a 20% cream formulation and rosacea in 15% gel and foam formulations, and it is used off label for melasma and PIH.35

Oral tranexamic acid is currently used as a hemostatic agent due to its ability to inhibit the plasminogen-plasmin pathway. In melasma, it blocks the interaction between melanocytes and keratinocytes in the epidermis and modulates the vascular component of melasma in the dermis. In an open-label study, 561 Asian melasma patients were treated with oral tranexamic acid 250 mg twice daily for 4 months. Results demonstrated improvement in 90% of patients, and 7.1% reported adverse effects (eg, abdominal bloating and pain, nausea, vomiting, headache, tinnitus, numbness, menstrual irregularities).36 Coagulation screening should be monitored monthly, and any patient with a history of clotting abnormalities should be excluded from off-label treatment with oral tranexamic acid.

Nonprescription cosmeceuticals are available over-the-counter or are office dispensed.37 For optimal results, cosmeceutical agents for skin lightening are used in combination. Most of these combinations are HQ free and have additive benefits such as a multimodal skin lightening agent containing key ingredients that correct and prevent skin pigmentation via several pathways affecting melanogenesis.38 It is an excellent alternative to HQ for mottled and diffuse UV-induced hyperpigmentation and can be used for maintenance therapy in patients with melasma.

Photoprotection is an essential component of therapy for melasma and PIH, but there is a paucity of data on the benefits for SOC patients. Halder et al39 performed a randomized prospective study of 89 black and Hispanic patients who applied sunscreen with a sun protection factor of 30 or 60 daily for 8 weeks. Clinical grading, triplicate L*A*B chromameter, and clinical photography were taken at baseline and weeks 4 and 8. The results demonstrated skin lightening in both black and Hispanic patients and support the use of sunscreen in the prevention and management of dyschromia in SOC patients.39 Visible light also may play a role in melasma development, and thus use of sunscreens or makeup containing iron oxides are recommended.40

Procedural treatments for facial hyperpigmentation include microdermabrasion, chemical peels, lasers, energy-based devices, and microneedling. There are many types and formulations of chemical peeling agents available; however, superficial and medium-depth chemical peels are recommended for SOC patients (Table 2). Deep chemical peels are not recommended for SOC patients due to the potential increased risk for PIH and scarring.

 

 

Cosmetic Enhancement in SOC Patients

Cosmetic procedures are gaining popularity in the SOC population and account for more than 20% of cosmetic procedures in the United States.41 Facial cosmetic concerns in SOC include dyschromia, benign growths (dermatosis papulosa nigra), hyperkinetic facial lines, volume loss, and skin laxity.42 Key principles to consider when treating SOC patients are the impact of ethnicity on aging and facial structure, the patient’s desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient’s expectations for recommended therapies.

Aging in SOC Patients
Skin aging can be classified as intrinsic aging or extrinsic aging. Intrinsic aging is genetic and involves subsurface changes such as volume loss, muscle atrophy, and resorption of bony structure. Extrinsic aging (or photoaging) involves surface changes of the epidermis/dermis and manifests as mottled pigmentation, textural changes, and fine wrinkling. Due to the photoprotection of melanin (black skin=SPF 13.4), skin aging in SOC patients is delayed by 10 to 20 years.43 In addition, SOC patients have more reactive collagen and can benefit from noninvasive cosmetic procedures such as fillers and skin-tightening procedures.42

Cosmetic Treatments and Procedures
Dermatosis papulosa nigra (benign growths of skin that have a genetic predisposition)44 occur mainly on the face but can involve the entire body. Treatment modalities include electrodesiccation, cryotherapy, scissor excision, and laser surgery.45

Treatment of hyperkinetic facial lines with botulinum toxin type A is a safe and effective procedure in patients with SOC. Grimes and Shabazz46 performed a 4-month, randomized, double-blind study that evaluated the treatment of glabellar lines in women with Fitzpatrick skin types V and VI. The results demonstrated that the duration of effects was the same in the patients who received either 20 or 30 U of botulinum toxin type A.46 Dynamic rhytides (furrows and frown/scowl lines arising from laughing, frowning, or smiling) can be treated safely in patients with SOC using botulinum toxin type A off label for relaxation of the upper and lower hyperkinetic muscles that result in these unwanted signs of aging. Botulinum toxin type A often is used for etched-in crow’s-feet, which rarely are evident in SOC patients.47 Facial shaping also can be accomplished by injecting botulinum toxin type A in combination with soft-tissue dermal fillers.47

Although black individuals do not experience perioral rhytides at the frequency of white individuals, they experience a variety of other cosmetic issues related to skin sagging and sinking. Currently available hyaluronic acid (HA) fillers have been shown to be safe in patients with Fitzpatrick skin types IV through VI.48 Two studies evaluated fillers in patients with SOC, specifically HA49 and calcium hydroxylapatite,50 focused on treatment of the nasolabial folds and the potential risk for dyspigmentation and keloidal scarring. Taylor et al49 noted that the risk of hyperpigmentation was 6% to 9% for large- and small-particle HA, respectively, and was associated with the serial or multiple puncture injection technique. No hypertrophic or keloidal scarring occurred in both studies.49,50

Facial contouring applications with fillers include glabellar lines, temples, nasal bridge, tear troughs, malar and submalar areas, nasolabial folds, radial lines, lips, marionette lines, mental crease, and chin. Hyaluronic acid fillers also can be used for lip enhancement.47 Although white women are looking to increase the size of their lips, black women are seeking augmentation to restore their lip size to that of their youth. Black individuals do not experience the same frequency of perioral rhytides as white patients, but they experience a variety of other issues related to skin sagging and sinking. Unlike white women, enhancement of the vermilion border rarely is performed in black women due to development of rhytides, predominantly in the body of the lip below the vermilion border in response to volume loss in the upper lip while the lower lip usually maintains its same appearance.47

Facial enhancement utilizing poly-L-lactic acid can be used safely in SOC patients.51 Poly-L-lactic acid microparticles induce collagen formation, leading to dermal thickening over 3 to 6 months; however, multiple sessions are required to achieve optimal aesthetic results.

Patients with more reactive collagen can benefit from noninvasive cosmetic procedures such as skin-tightening procedures.52 Radiofrequency and microfocused ultrasound are cosmetic procedures used to provide skin tightening and facial lifting. They are safe and effective treatments for patients with Fitzpatrick skin types IV to VI.53 Histologically, there is less thinning of collagen bundles and elastic tissue in ethnic skin. Due to stimulation of collagen by these procedures, most SOC patients will experience a more enhanced response, requiring fewer treatment sessions than white individuals.

Conclusion

Medical and aesthetic facial concerns in SOC patients vary and can be a source of emotional and psychological distress that can negatively impact quality of life. The approach to the treatment of SOC patients should be a balance between tolerability and efficacy, considering the potential risk for PIH.

The approach to the treatment of common skin disorders and cosmetic concerns in patients with skin of color (SOC) requires the clinician to understand the biological differences, nuances, and special considerations that are unique to patients with darker skin types.1-3 This article addresses 4 common facial concerns in SOC patients—acne, rosacea, facial hyperpigmentation, and cosmetic enhancement—and provides treatment recommendations and management pearls to assist the clinician with optimal outcomes for SOC patients.

Acne in SOC Patients

Acne vulgaris is one of the most common conditions that dermatologists treat and is estimated to affect 40 to 50 million individuals in the United States.1 Many of these acne patients are individuals with SOC.2-4 A study of 2835 females (aged 10–70 years) conducted in 4 different cities—Los Angeles, California; London, United Kingdom; Akita, Japan; and Rome, Italy—demonstrated acne prevalence of 37% in blacks, 32% in Hispanics, 30% in Asians, 24% in whites, and 23% in Continental Indians.5 Blacks, Hispanics, and Continental Indians demonstrated equal prevalence with comedonal and inflammatory acne. Asians displayed more inflammatory acne lesions than comedones. In contrast, whites demonstrated more comedones than inflammatory acne. Dyspigmentation, postinflammatory hyperpigmentation (PIH), and atrophic scars were more common in black and Hispanic females than other ethnicities.5 This study illustrated that acne-induced PIH is a common sequela in SOC patients and is the main reason they seek treatment.6,7

The pathogenesis of acne is the same in all racial and ethnic groups: (1) follicular hyperkeratinization and the formation of a microcomedone caused by abnormal desquamation of the keratinocytes within the sebaceous follicle, (2) production of sebum by circulating androgens, (3) proliferation of Propionibacterium acnes, and (4) inflammation. Subclinical inflammation is present throughout all stages of acne, including normal-appearing skin, inflammatory lesions, comedones, and scarring, and may contribute to PIH in acne patients with SOC (Figure 1).8 A thorough history should be obtained from acne patients, including answers to the following questions7:

  • What skin and hair care products do you use?
  • Do you use sunscreen daily?
  • What cosmetic products or makeup do you use?
  • Do you use any ethnic skin care products, including skin lightening creams?
  • Do you have a history of keloids?

Figure 1. Acne and postinflammatory hyperpigmentation in a patient with skin of color (Fitzpatrick skin type V).

It is important to ask these questions to assess if the SOC patient has developed pomade acne,9 acne cosmetica,10 or a potential risk of skin irritation from the use of skin care practices. It is best to take total control of the patient’s skin care regimen and discontinue use of toners, astringents, witch hazel, exfoliants, and rubbing alcohol, which may lead to skin dryness and irritation, particularly when combined with topical acne medications.

Treatment
Treatment of acne in SOC patients is similar to generally recommended treatments, with special considerations. Consider the following key points when treating acne in SOC patients:

  • Treat acne early and aggressively to prevent or minimize subsequent PIH and acne scarring.
  • Balance aggressive treatment with nonirritating topical skin care.
  • Most importantly, target PIH in addition to acne and choose a regimen that limits skin irritation that might exacerbate existing PIH.7

Develop a maintenance program to control future breakouts. Topical agents can be used as monotherapy or in fixed combinations and may include benzoyl peroxide, antibiotics, dapsone, azelaic acid (AZA), and retinoids. Similar to white patients, topical retinoids remain a first-line treatment for acne in patients with SOC.11,12

Tolerability must be managed in SOC acne patients. Therapeutic maneuvers that can be instituted should include a discussion on using gentle skin care, initiating therapy with a retinoid applied every other night starting with a low concentration and gradually titrating up, and applying a moisturizer before or after applying acne medication. Oral therapies consist of antibiotics (doxycycline, minocycline), retinoids (isotretinoin), and hormonal modulators (oral contraceptives, spironolactone). Isotretinoin, recommended for patients with nodulocystic acne, may play a possible role in treating acne-induced PIH.13

Two common procedural therapies for acne include comedone extraction and intralesional corticosteroid injection. A 6- to 8-week course of a topical retinoid prior to comedonal extraction may facilitate the procedure and is recommended in SOC patients to help reduce cutaneous trauma and PIH.11 Inflammatory acne lesions can be treated with intralesional injection of triamcinolone acetonide 2.5 or 5.0 mg/mL, which usually reduces inflammation within 2 to 5 days.11

Treatment of acne-induced PIH includes sun protection, topical and oral medications, chemical peels, lasers, and energy devices. Treatment of hypertrophic scarring and keloids involves intralesional injection of triamcinolone acetonide 20, 30, or 40 mg/mL every 4 weeks until the lesion is flat.11

Superficial chemical peels can be used to treat acne and PIH in SOC patients,14 such as salicylic acid (20%–30%), glycolic acid (20%–70%), trichloroacetic acid (15%–30%), and Jessner peels.

Acne Scarring
Surgical approaches to acne scarring in patients with SOC include elliptical excision, punch excision, punch elevation, punch autografting, dermal grafting, dermal planning, subcutaneous incision (subcision), dermabrasion, microneedling, fillers, and laser skin resurfacing. The treatment of choice depends on the size, type, and depth of the scar and the clinician’s preference.

Lasers
Fractional photothermolysis has emerged as a treatment option for acne scars in SOC patients. This procedure produces microscopic columns of thermal injury in the epidermis and dermis, sparing the surrounding tissue and minimizing downtime and adverse events. Because fractional photothermolysis does not target melanin and produces limited epidermal injury, darker Fitzpatrick skin types (IV–VI) can be safely and effectively treated with this procedure.15

 

 

Rosacea in SOC Patients

Rosacea is a chronic inflammatory disorder that affects the vasculature and pilosebaceous units of the face. It commonly is seen in Fitzpatrick skin types I and II; however, rosacea can occur in all skin types (Figure 2). Triggers include emotional stress, extreme environmental temperatures, hot and spicy foods, red wine or alcohol, and topical irritants or allergens found in common cosmetic products.16

Figure 2. Rosacea in a patient with skin of color (Fitzpatrick skin type IV).

Data suggest that 4% of rosacea patients in the United States are of African, Latino, or Asian descent.11 National Ambulatory Medical Care Survey data revealed that of 31.5 million rosacea visits, 2% of patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino. In a 5-year longitudinal study of 2587 rosacea patients enrolled in Medicaid in North Carolina who were prescribed at least 1 topical treatment for rosacea, 16.27% were black and 10% were of a race other than white.17

Although the pathogenesis of rosacea is unclear, hypotheses include immune system abnormalities, neurogenic dysregulation, presence of microorganisms (eg, Demodex folliculorum), UV damage, and skin barrier dysfunction.18

The 4 major subtypes of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea.16 Interestingly, rosacea in SOC patients may present with hypopigmentation surrounding the borders of the facial erythema. For phymatous rosacea, isotretinoin may reduce incipient rhinophyma but must be carefully monitored and pregnancy must be excluded. Surgical or laser therapy may be indicated to recontour the nose if severe.

There are several skin conditions that can present with facial erythema in patients with SOC, including seborrheic dermatitis, systemic lupus erythematosus, and contact dermatitis. It is important to note that the detection of facial erythema in darker skin types may be difficult; therefore, laboratory evaluation (antinuclear antibodies), patch testing, and skin biopsy should be considered if the clinical diagnosis is unclear.

Treatment
Treatment of rosacea in SOC patients does not differ from other racial groups. Common strategies include gentle skin care, sun protection (sun protection factor 30+), and barrier repair creams. Topical agents include metronidazole, AZA, sodium sulfacetamide/sulfur, ivermectin, and retinoids.16 Oral treatments include antibiotics in the tetracycline family (eg, subantimicrobial dose doxycycline) and isotretinoin.16 Persistent erythema associated with rosacea can be treated with brimonidine19 and oxymetazoline.20 Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea21; however, the latter is not recommended in Fitzpatrick skin types IV through VI.

Facial Hyperpigmentation in SOC Patients

Hyperpigmentation disorders can be divided into conditions that affect Fitzpatrick skin types I through III and IV though VI. Mottled hyperpigmentation (photodamage) and solar lentigines occur in patients with lighter skin types as compared to melasma, PIH, and age-related (UV-induced) hyperpigmentation, which occur more commonly in patients with darker skin types. Facial hyperpigmentation is a common concern in SOC patients. In a survey of cosmetic concerns of 100 women with SOC, hyperpigmentation or dark spots (86%) and blotchy uneven skin (80%) were the top concerns.22 In addition, facial hyperpigmentation has been shown to negatively impact quality of life.23

Postinflammatory hyperpigmentation occurs from a pathophysiological response to inflammation, cutaneous irritation or injury, and subsequent melanocyte lability. Postinflammatory hyperpigmentation is a common presenting concern in patients with SOC and is seen as a result of many inflammatory skin disorders (eg, acne, eczema) and dermatologic procedures (eg, adverse reaction to electrodesiccation, microdermabrasion, chemical peels, laser surgery).24

Melasma is an acquired idiopathic disorder of hyperpigmentation and often referred to as the mask of pregnancy (Figure 3). It occurs on sun-exposed areas of skin, mainly in women with Fitzpatrick skin types III through V. Associated factors or triggers include pregnancy, hormonal treatments, exposure to UV radiation, and medications.25 Hereditary factors play a role in more than 40% of cases.26

Figure 3. Facial hyperpigmentation consistent with melasma in a patient with skin of color (Fitzpatrick skin type IV).

Other not-so-common facial dyschromias include contact dermatitis, acanthosis nigricans, exogenous ochronosis, lichen planus pigmentosus (associated with frontal fibrosing alopecia),27 drug-induced hyperpigmentation (associated with minocycline or diltiazem),28,29 and UV-induced (age-related) hyperpigmentation.

Treatment
The treatment of hyperpigmentation should provide the following: (1) protection from sun exposure; (2) inhibition of tyrosinase, the enzyme responsible for the conversion of tyrosine to melanin; (3) inhibition of melanosome transfer from the melanocyte to the keratinocyte; (4) removal of melanin from the epidermis through exfoliation; and (5) destruction or disruption of melanin in the dermis.30 Therapies for facial hyperpigmentation are listed in Table 1.

Topical therapies include prescription medications and nonprescription cosmeceuticals. Prescription medications include hydroquinone (HQ), topical retinoids, and AZA. Hydroquinone, a tyrosinase inhibitor, is the gold standard for skin lightening and often is used as a first-line therapy. It is used as a monotherapy (HQ 4%) or as a fixed combination with tretinoin 0.05% and fluocinolone 0.01%.31 Use caution with HQ in high concentrations (6% and higher) and low concentrations (2% [over-the-counter strength]) used long-term due to the potential risk of exogenous ochronosis.

Topical retinoids have been shown to be effective therapeutic agents for melasma and PIH. Tretinoin,32 tazarotene,33 and adapalene34 all have demonstrated efficacy for acne and acne-induced PIH in SOC patients. Patients must be monitored for the development of retinoid dermatitis and worsening of hyperpigmentation.

Azelaic acid is a naturally occurring dicarboxylic acid obtained from cultures of Malassezia furfur. Azelaic acid inhibits tyrosinase activity, DNA synthesis, and mitochondrial enzymes, thus blocking direct cytotoxic effects toward melanocytes. Azelaic acid is approved by the US Food and Drug Administration for acne in a 20% cream formulation and rosacea in 15% gel and foam formulations, and it is used off label for melasma and PIH.35

Oral tranexamic acid is currently used as a hemostatic agent due to its ability to inhibit the plasminogen-plasmin pathway. In melasma, it blocks the interaction between melanocytes and keratinocytes in the epidermis and modulates the vascular component of melasma in the dermis. In an open-label study, 561 Asian melasma patients were treated with oral tranexamic acid 250 mg twice daily for 4 months. Results demonstrated improvement in 90% of patients, and 7.1% reported adverse effects (eg, abdominal bloating and pain, nausea, vomiting, headache, tinnitus, numbness, menstrual irregularities).36 Coagulation screening should be monitored monthly, and any patient with a history of clotting abnormalities should be excluded from off-label treatment with oral tranexamic acid.

Nonprescription cosmeceuticals are available over-the-counter or are office dispensed.37 For optimal results, cosmeceutical agents for skin lightening are used in combination. Most of these combinations are HQ free and have additive benefits such as a multimodal skin lightening agent containing key ingredients that correct and prevent skin pigmentation via several pathways affecting melanogenesis.38 It is an excellent alternative to HQ for mottled and diffuse UV-induced hyperpigmentation and can be used for maintenance therapy in patients with melasma.

Photoprotection is an essential component of therapy for melasma and PIH, but there is a paucity of data on the benefits for SOC patients. Halder et al39 performed a randomized prospective study of 89 black and Hispanic patients who applied sunscreen with a sun protection factor of 30 or 60 daily for 8 weeks. Clinical grading, triplicate L*A*B chromameter, and clinical photography were taken at baseline and weeks 4 and 8. The results demonstrated skin lightening in both black and Hispanic patients and support the use of sunscreen in the prevention and management of dyschromia in SOC patients.39 Visible light also may play a role in melasma development, and thus use of sunscreens or makeup containing iron oxides are recommended.40

Procedural treatments for facial hyperpigmentation include microdermabrasion, chemical peels, lasers, energy-based devices, and microneedling. There are many types and formulations of chemical peeling agents available; however, superficial and medium-depth chemical peels are recommended for SOC patients (Table 2). Deep chemical peels are not recommended for SOC patients due to the potential increased risk for PIH and scarring.

 

 

Cosmetic Enhancement in SOC Patients

Cosmetic procedures are gaining popularity in the SOC population and account for more than 20% of cosmetic procedures in the United States.41 Facial cosmetic concerns in SOC include dyschromia, benign growths (dermatosis papulosa nigra), hyperkinetic facial lines, volume loss, and skin laxity.42 Key principles to consider when treating SOC patients are the impact of ethnicity on aging and facial structure, the patient’s desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient’s expectations for recommended therapies.

Aging in SOC Patients
Skin aging can be classified as intrinsic aging or extrinsic aging. Intrinsic aging is genetic and involves subsurface changes such as volume loss, muscle atrophy, and resorption of bony structure. Extrinsic aging (or photoaging) involves surface changes of the epidermis/dermis and manifests as mottled pigmentation, textural changes, and fine wrinkling. Due to the photoprotection of melanin (black skin=SPF 13.4), skin aging in SOC patients is delayed by 10 to 20 years.43 In addition, SOC patients have more reactive collagen and can benefit from noninvasive cosmetic procedures such as fillers and skin-tightening procedures.42

Cosmetic Treatments and Procedures
Dermatosis papulosa nigra (benign growths of skin that have a genetic predisposition)44 occur mainly on the face but can involve the entire body. Treatment modalities include electrodesiccation, cryotherapy, scissor excision, and laser surgery.45

Treatment of hyperkinetic facial lines with botulinum toxin type A is a safe and effective procedure in patients with SOC. Grimes and Shabazz46 performed a 4-month, randomized, double-blind study that evaluated the treatment of glabellar lines in women with Fitzpatrick skin types V and VI. The results demonstrated that the duration of effects was the same in the patients who received either 20 or 30 U of botulinum toxin type A.46 Dynamic rhytides (furrows and frown/scowl lines arising from laughing, frowning, or smiling) can be treated safely in patients with SOC using botulinum toxin type A off label for relaxation of the upper and lower hyperkinetic muscles that result in these unwanted signs of aging. Botulinum toxin type A often is used for etched-in crow’s-feet, which rarely are evident in SOC patients.47 Facial shaping also can be accomplished by injecting botulinum toxin type A in combination with soft-tissue dermal fillers.47

Although black individuals do not experience perioral rhytides at the frequency of white individuals, they experience a variety of other cosmetic issues related to skin sagging and sinking. Currently available hyaluronic acid (HA) fillers have been shown to be safe in patients with Fitzpatrick skin types IV through VI.48 Two studies evaluated fillers in patients with SOC, specifically HA49 and calcium hydroxylapatite,50 focused on treatment of the nasolabial folds and the potential risk for dyspigmentation and keloidal scarring. Taylor et al49 noted that the risk of hyperpigmentation was 6% to 9% for large- and small-particle HA, respectively, and was associated with the serial or multiple puncture injection technique. No hypertrophic or keloidal scarring occurred in both studies.49,50

Facial contouring applications with fillers include glabellar lines, temples, nasal bridge, tear troughs, malar and submalar areas, nasolabial folds, radial lines, lips, marionette lines, mental crease, and chin. Hyaluronic acid fillers also can be used for lip enhancement.47 Although white women are looking to increase the size of their lips, black women are seeking augmentation to restore their lip size to that of their youth. Black individuals do not experience the same frequency of perioral rhytides as white patients, but they experience a variety of other issues related to skin sagging and sinking. Unlike white women, enhancement of the vermilion border rarely is performed in black women due to development of rhytides, predominantly in the body of the lip below the vermilion border in response to volume loss in the upper lip while the lower lip usually maintains its same appearance.47

Facial enhancement utilizing poly-L-lactic acid can be used safely in SOC patients.51 Poly-L-lactic acid microparticles induce collagen formation, leading to dermal thickening over 3 to 6 months; however, multiple sessions are required to achieve optimal aesthetic results.

Patients with more reactive collagen can benefit from noninvasive cosmetic procedures such as skin-tightening procedures.52 Radiofrequency and microfocused ultrasound are cosmetic procedures used to provide skin tightening and facial lifting. They are safe and effective treatments for patients with Fitzpatrick skin types IV to VI.53 Histologically, there is less thinning of collagen bundles and elastic tissue in ethnic skin. Due to stimulation of collagen by these procedures, most SOC patients will experience a more enhanced response, requiring fewer treatment sessions than white individuals.

Conclusion

Medical and aesthetic facial concerns in SOC patients vary and can be a source of emotional and psychological distress that can negatively impact quality of life. The approach to the treatment of SOC patients should be a balance between tolerability and efficacy, considering the potential risk for PIH.

References
  1. White GM. Recent findings in the epidemiologic evidence, classification, and subtypes of acne vulgaris. J Am Acad Dermatol. 1998;39(2 pt 3):S34-S37.
  2. Halder RM, Grimes PE, McLaurin CL, et al. Incidence of common dermatoses in a predominantly black dermatologic practice. Cutis. 1983;32:388, 390.
  3. Alexis AF, Sergay AB, Taylor SC. Common dermatologic disorders in skin of color: a comparative practice survey. Cutis. 2007;80:387-394.
  4. Davis SA, Narahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  5. Perkins AC, Cheng CE, Hillebrand GG, et al. Comparison of the epidemiology of acne vulgaris among Caucasians, Asian, Continental Indian and African American women. J Eur Acad Dermatol Venereol. 2011;25:1054-1060.
  6. Taylor SC, Cook-Bolden F, Rahman Z, et al. Acne vulgaris in skin of color. J Am Acad Dermatol. 2002;46(2 suppl):S98-S106.
  7. Davis EC, Callender VD. A review of acne in ethnic skin: pathogenesis, clinical manifestations, and management strategies. J Clin Aesthet Dermatol. 2010;3:24-38.
  8. Halder RM, Holmes YC, Bridgeman-Shah S, et al. A clinicohistologic study of acne vulgaris in black females (abstract). J Invest Dermatol. 1996;106:888.
  9. Plewig G, Fulton JE, Kligman AM. Pomade acne. Arch Dermatol. 1970;101:580-584.
  10. Kligman AM, Mills OH. Acne cosmetica. Arch Dermatol. 1972;106:893-897.
  11. Halder RM, Brooks HL, Callender VD. Acne in ethnic skin. Dermatol Clin. 2003;21:609-615.
  12. Callender VD. Acne in ethnic skin: special considerations for therapy. Dermatol Ther. 2004;17:184-195.
  13. Winhoven SM. Postinflammatory hyperpigmentation in an Asian patient. a dramatic response to oral isotretinoin (13-cis-retinoic acid). Br J Med. 2005;152:368-403.
  14. Sarkar R, Bansal S, Garg VK. Chemical peels for melasma in dark-skinned patients. J Cutan Aesthet Surg. 2012;5:247-253.
  15. Alexis AF, Coley MK, Nijhawan RI, et al. Nonablative fractional laser resurfacing for acne scarring in patients with Fitzpatrick skin phototypes IV-VI. Dermatol Surg. 2016;42:392-402.
  16. Culp B, Scheinfeld N. Rosacea: a review. P T. 2009;34:38-45.
  17. Al-Dabagh A, Davis SA, McMichael AJ, et al. Rosacea in skin of color: not a rare diagnosis. Dermatol Online J. 2014:20. pii:13030/qt1mv9r0ss.
  18. Del Rosso JQ. Advances in understanding and managing rosacea: part 1: connecting the dots between pathophysiological mechanisms and common clinical features of rosacea with emphasis on vascular changes and facial erythema. J Clin Aesthet Dermatol. 2012;5:16-25.
  19. Jackson JM, Knuckles M, Minni JP, et al. The role of brimonidine tartrate gel in the treatment of rosacea. Clin Cosmet Investig Dermatol. 2015;23:529-538.
  20. Patel NU, Shukla S, Zaki J, et al. Oxymetazoline hydrochloride cream for facial erythema associated with rosacea. Expert Rev Clin Pharmacol. 2017;10:104954.
  21. Weinkle AP, Doktor V, Emer J. Update on the management of rosacea. Clin Cosmet Investig Dermatol. 2015;8:159-177.
  22. Grimes PE. Skin and hair cosmetic issues in women of color. Dermatol Clin. 2000;19:659-665.
  23. Taylor A, Pawaskar M, Taylor SL, et al. Prevalence of pigmentary disorders and their impact on quality of life: a prospective cohort study. J Cosmet Dermatol. 2008;7:164-168.
  24. Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010;3:20-31.
  25. Grimes PE. Melasma: etiologic and therapeutic considerations. Arch Dermatol. 1995;131:1453-1457.
  26. Handel AC, Miot LD, Miot HA. Melasma: a clinical and epidemiological review. An Bras Dermatol. 2014;89:771-782.
  27. Callender VD, Reid SD, Obayan O, et al. Diagnostic clues to frontal fibrosing alopecia in patients of African descent. J Clin Aesthet Dermatol. 2016;9:45-51.
  28. Narang T, Sawatkar GU, Kumaran MS, et al. Minocycline for recurrent and/or chronic erythema nodosum leprosum. JAMA Dermatol. 2015;151:1026-1028.
  29. Boyer M, Katta R, Markus R. Diltiazem-induced photodistributed hyperpigmentation. Dermatol Online J. 2003;9:10.
  30. Pandya AG, Guevara IL. Disorders of hyperpigmentation. Dermatol Clin. 2000;18:91-98.
  31. Taylor SC, Torok H, Jones T, et al. Efficacy and safety of a new triple-combination agent for the treatment of facial melasma. Cutis. 2003;72:67-72.
  32. Bulengo-Ransby SM. Topical tretinoin (retinoic acid) therapy for hyperpigmented lesions caused by inflammation of the skin in black patients. N Engl J Med. 1993;328:1438-1443.
  33. Grimes P, Callender V. Tazarotene cream for postinflammatory hyperpigmentation and acne vulgaris in darker skin: a double-blind, randomized, vehicle-controlled study. Cutis. 2006;77:45-50.
  34. Jacyk WK. Adapalene in the treatment of African patients. J Eur Acad Dermatol Venereol. 2001;15(suppl 3):37-42.
  35. Kircik LH. Efficacy and safety of azelaic acid (AzA) gel 15% in the treatment of postinflammatory hyperpigmentation and acne: a 16-week, baseline-controlled study. J Drugs Dermatol. 2011;10:586-590.
  36. Lee HC, Thng TG, Goh CL. Oral tranexamic acid (TA) in the treatment of melasma. J Am Acad Dermatol. 2016;75:385-392.
  37. Kindred C, Okereke U, Callender VD. Skin-lightening agents: an overview of prescription, office-dispensed, and over-the-counter products. Cosmet Dermatol. 2013;26:18-26.
  38. Makino ET, Kadoya K, Sigler ML, et al. Development and clinical assessment of a comprehensive product for pigmentation control in multiple ethnic populations. J Drugs Dermatol. 2016;15:1562-1570.
  39. Halder R, Rodney I, Munhutu M, et al. Evaluation and effectiveness of a photoprotection composition (sunscreen) on subjects of skin of color. J Am Acad Dermatol. 2015;72(suppl 1):AB215.
  40. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
  41. American Society for Aesthetic Plastic Surgery. 2016 Cosmetic Surgery National Data Bank Statistics. https://www.surgery.org/sites/default/files/ASAPS-Stats2016.pdf. Accessed November 15, 2017.
  42. Burgess CM. Soft tissue augmentation in skin of color: market growth, available fillers and successful techniques. J Drugs Dermatol. 2007;6:51-55.
  43. Davis EC, Callender VD. Aesthetic dermatology for aging ethnic skin. Dermatol Surg. 2011;37:901-917.
  44. Grimes PE, Arora S, Minus HR, et al. Dermatosis papulosa nigra. Cutis. 1983;32:385-386.
  45. Lupo M. Dermatosis papulosa nigra: treatment options. J Drugs Dermatol. 2007;6:29-30.
  46. Grimes PE, Shabazz D. A four-month randomized, double-blind evaluation of the efficacy of botulinum toxin type A for the treatment of glabellar lines in women with skin types V and VI. Dermatol Surg. 2009;35:429-435.
  47. Burgess CM, Awosika O. Ethnic and gender considerations in the use of facial injectables: African-American patients. Plast Reconstr Surg. 2015;136(5 suppl):28S-31S.
  48. Taylor SC, Kelly AP, Lim HW, et al, eds. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. New York, NY: McGraw-Hill Education; 2016.
  49.  Taylor SC, Burgess CM, Callender VD. Safety of nonanimal stabilized hyaluronic acid dermal fillers in patients with skin of color: a randomized, evaluator-blinded comparative trial. Dermatol Surg. 2009;35(suppl 2):1653-1660.
  50. Marmur ES, Taylor SC, Grimes PE, et al. Six-month safety results of calcium hydroxylapatite for treatment of nasolabial folds in Fitzpatrick skin types IV to VI. Dermatol Surg. 2009;35(suppl 2):1641-1645.
  51. Hamilton TK, Burgess CM. Consideration for the use of injectable poly-L-lactic acid in people of color. J Drugs Dermatol. 2010;9:451-456.
  52. Fabi SG, Goldman MP. Retrospective evaluation of micro-focused ultrasound for lifting and tightening of the face and neck. Dermatol Surg. 2014;40:569-575.
  53. Harris MO, Sundaram HA. Safety of microfocused ultrasound with visualization in patients with Fitzpatrick skin phototypes III to VI. JAMA Facial Plast Surg. 2015;17:355-357.
References
  1. White GM. Recent findings in the epidemiologic evidence, classification, and subtypes of acne vulgaris. J Am Acad Dermatol. 1998;39(2 pt 3):S34-S37.
  2. Halder RM, Grimes PE, McLaurin CL, et al. Incidence of common dermatoses in a predominantly black dermatologic practice. Cutis. 1983;32:388, 390.
  3. Alexis AF, Sergay AB, Taylor SC. Common dermatologic disorders in skin of color: a comparative practice survey. Cutis. 2007;80:387-394.
  4. Davis SA, Narahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  5. Perkins AC, Cheng CE, Hillebrand GG, et al. Comparison of the epidemiology of acne vulgaris among Caucasians, Asian, Continental Indian and African American women. J Eur Acad Dermatol Venereol. 2011;25:1054-1060.
  6. Taylor SC, Cook-Bolden F, Rahman Z, et al. Acne vulgaris in skin of color. J Am Acad Dermatol. 2002;46(2 suppl):S98-S106.
  7. Davis EC, Callender VD. A review of acne in ethnic skin: pathogenesis, clinical manifestations, and management strategies. J Clin Aesthet Dermatol. 2010;3:24-38.
  8. Halder RM, Holmes YC, Bridgeman-Shah S, et al. A clinicohistologic study of acne vulgaris in black females (abstract). J Invest Dermatol. 1996;106:888.
  9. Plewig G, Fulton JE, Kligman AM. Pomade acne. Arch Dermatol. 1970;101:580-584.
  10. Kligman AM, Mills OH. Acne cosmetica. Arch Dermatol. 1972;106:893-897.
  11. Halder RM, Brooks HL, Callender VD. Acne in ethnic skin. Dermatol Clin. 2003;21:609-615.
  12. Callender VD. Acne in ethnic skin: special considerations for therapy. Dermatol Ther. 2004;17:184-195.
  13. Winhoven SM. Postinflammatory hyperpigmentation in an Asian patient. a dramatic response to oral isotretinoin (13-cis-retinoic acid). Br J Med. 2005;152:368-403.
  14. Sarkar R, Bansal S, Garg VK. Chemical peels for melasma in dark-skinned patients. J Cutan Aesthet Surg. 2012;5:247-253.
  15. Alexis AF, Coley MK, Nijhawan RI, et al. Nonablative fractional laser resurfacing for acne scarring in patients with Fitzpatrick skin phototypes IV-VI. Dermatol Surg. 2016;42:392-402.
  16. Culp B, Scheinfeld N. Rosacea: a review. P T. 2009;34:38-45.
  17. Al-Dabagh A, Davis SA, McMichael AJ, et al. Rosacea in skin of color: not a rare diagnosis. Dermatol Online J. 2014:20. pii:13030/qt1mv9r0ss.
  18. Del Rosso JQ. Advances in understanding and managing rosacea: part 1: connecting the dots between pathophysiological mechanisms and common clinical features of rosacea with emphasis on vascular changes and facial erythema. J Clin Aesthet Dermatol. 2012;5:16-25.
  19. Jackson JM, Knuckles M, Minni JP, et al. The role of brimonidine tartrate gel in the treatment of rosacea. Clin Cosmet Investig Dermatol. 2015;23:529-538.
  20. Patel NU, Shukla S, Zaki J, et al. Oxymetazoline hydrochloride cream for facial erythema associated with rosacea. Expert Rev Clin Pharmacol. 2017;10:104954.
  21. Weinkle AP, Doktor V, Emer J. Update on the management of rosacea. Clin Cosmet Investig Dermatol. 2015;8:159-177.
  22. Grimes PE. Skin and hair cosmetic issues in women of color. Dermatol Clin. 2000;19:659-665.
  23. Taylor A, Pawaskar M, Taylor SL, et al. Prevalence of pigmentary disorders and their impact on quality of life: a prospective cohort study. J Cosmet Dermatol. 2008;7:164-168.
  24. Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010;3:20-31.
  25. Grimes PE. Melasma: etiologic and therapeutic considerations. Arch Dermatol. 1995;131:1453-1457.
  26. Handel AC, Miot LD, Miot HA. Melasma: a clinical and epidemiological review. An Bras Dermatol. 2014;89:771-782.
  27. Callender VD, Reid SD, Obayan O, et al. Diagnostic clues to frontal fibrosing alopecia in patients of African descent. J Clin Aesthet Dermatol. 2016;9:45-51.
  28. Narang T, Sawatkar GU, Kumaran MS, et al. Minocycline for recurrent and/or chronic erythema nodosum leprosum. JAMA Dermatol. 2015;151:1026-1028.
  29. Boyer M, Katta R, Markus R. Diltiazem-induced photodistributed hyperpigmentation. Dermatol Online J. 2003;9:10.
  30. Pandya AG, Guevara IL. Disorders of hyperpigmentation. Dermatol Clin. 2000;18:91-98.
  31. Taylor SC, Torok H, Jones T, et al. Efficacy and safety of a new triple-combination agent for the treatment of facial melasma. Cutis. 2003;72:67-72.
  32. Bulengo-Ransby SM. Topical tretinoin (retinoic acid) therapy for hyperpigmented lesions caused by inflammation of the skin in black patients. N Engl J Med. 1993;328:1438-1443.
  33. Grimes P, Callender V. Tazarotene cream for postinflammatory hyperpigmentation and acne vulgaris in darker skin: a double-blind, randomized, vehicle-controlled study. Cutis. 2006;77:45-50.
  34. Jacyk WK. Adapalene in the treatment of African patients. J Eur Acad Dermatol Venereol. 2001;15(suppl 3):37-42.
  35. Kircik LH. Efficacy and safety of azelaic acid (AzA) gel 15% in the treatment of postinflammatory hyperpigmentation and acne: a 16-week, baseline-controlled study. J Drugs Dermatol. 2011;10:586-590.
  36. Lee HC, Thng TG, Goh CL. Oral tranexamic acid (TA) in the treatment of melasma. J Am Acad Dermatol. 2016;75:385-392.
  37. Kindred C, Okereke U, Callender VD. Skin-lightening agents: an overview of prescription, office-dispensed, and over-the-counter products. Cosmet Dermatol. 2013;26:18-26.
  38. Makino ET, Kadoya K, Sigler ML, et al. Development and clinical assessment of a comprehensive product for pigmentation control in multiple ethnic populations. J Drugs Dermatol. 2016;15:1562-1570.
  39. Halder R, Rodney I, Munhutu M, et al. Evaluation and effectiveness of a photoprotection composition (sunscreen) on subjects of skin of color. J Am Acad Dermatol. 2015;72(suppl 1):AB215.
  40. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
  41. American Society for Aesthetic Plastic Surgery. 2016 Cosmetic Surgery National Data Bank Statistics. https://www.surgery.org/sites/default/files/ASAPS-Stats2016.pdf. Accessed November 15, 2017.
  42. Burgess CM. Soft tissue augmentation in skin of color: market growth, available fillers and successful techniques. J Drugs Dermatol. 2007;6:51-55.
  43. Davis EC, Callender VD. Aesthetic dermatology for aging ethnic skin. Dermatol Surg. 2011;37:901-917.
  44. Grimes PE, Arora S, Minus HR, et al. Dermatosis papulosa nigra. Cutis. 1983;32:385-386.
  45. Lupo M. Dermatosis papulosa nigra: treatment options. J Drugs Dermatol. 2007;6:29-30.
  46. Grimes PE, Shabazz D. A four-month randomized, double-blind evaluation of the efficacy of botulinum toxin type A for the treatment of glabellar lines in women with skin types V and VI. Dermatol Surg. 2009;35:429-435.
  47. Burgess CM, Awosika O. Ethnic and gender considerations in the use of facial injectables: African-American patients. Plast Reconstr Surg. 2015;136(5 suppl):28S-31S.
  48. Taylor SC, Kelly AP, Lim HW, et al, eds. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. New York, NY: McGraw-Hill Education; 2016.
  49.  Taylor SC, Burgess CM, Callender VD. Safety of nonanimal stabilized hyaluronic acid dermal fillers in patients with skin of color: a randomized, evaluator-blinded comparative trial. Dermatol Surg. 2009;35(suppl 2):1653-1660.
  50. Marmur ES, Taylor SC, Grimes PE, et al. Six-month safety results of calcium hydroxylapatite for treatment of nasolabial folds in Fitzpatrick skin types IV to VI. Dermatol Surg. 2009;35(suppl 2):1641-1645.
  51. Hamilton TK, Burgess CM. Consideration for the use of injectable poly-L-lactic acid in people of color. J Drugs Dermatol. 2010;9:451-456.
  52. Fabi SG, Goldman MP. Retrospective evaluation of micro-focused ultrasound for lifting and tightening of the face and neck. Dermatol Surg. 2014;40:569-575.
  53. Harris MO, Sundaram HA. Safety of microfocused ultrasound with visualization in patients with Fitzpatrick skin phototypes III to VI. JAMA Facial Plast Surg. 2015;17:355-357.
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Approach to Treatment of Medical and Cosmetic Facial Concerns in Skin of Color Patients
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Practice Points

  • Treat acne in skin of color (SOC) patients early and aggressively to prevent or minimize subsequent postinflammatory hyperpigmentation (PIH) and acne scarring.
  • Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea; however, the latter is not recommended in Fitzpatrick skin types IV to VI.
  • Hydroquinone is the gold standard for skin lightening and is often used as a first-line therapy for melasma and PIH.
  • Photoprotection is an essential component of therapy for hyperpigmented skin disorders.  
  • Cosmetic procedures are gaining popularity in the SOC population. When treating SOC patients, consider the impact of ethnicity on aging and facial structure, the patient's desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient's expectations for recommended therapies.
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Hair and Scalp Disorders in Adult and Pediatric Patients With Skin of Color

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Hair and Scalp Disorders in Adult and Pediatric Patients With Skin of Color
In Collaboration with the Skin of Color Society
Author(s)
Susan C. Taylor, MD
Victoria Barbosa, MD
Cheryl Burgess, MD
Candrice Heath, MD
Amy J. McMichael, MD
Temitayo Ogunleye, MD
Valerie Callender, MD

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.1 Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.2 Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.3 Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.6

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).8 Another study by Hall et al9 of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al6 investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al10 examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

 

 

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.11 Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.12 Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.13 Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.14 The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan15 revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.16

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling17 demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

 

 

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard22 shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.22 Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.25 Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.28 Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).8 Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

References
  1. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  2. Hickman JG, Cardin C, Dawson TL, et al. Dandruff, part I: scalp disease prevalence in Caucasians, African Americans, and Chinese and the effects of shampoo frequency on scalp health. Poster presented at: 60th Annual Meeting of the American Academy of Dermatology; February 22-27, 2002; New Orleans, LA.
  3. Swee W, Klontz KC, Lambert LA. A nationwide outbreak of alopecia associated with the use of a hair-relaxing formulation. Arch Dermatol. 2000;136:1104-1108.
  4. Nicholson AG, Harland CC, Bull RH, et al. Chemically induced cosmetic alopecia. Br J Dermatol. 1993;128:537-541.
  5. Detwiler SP, Carson JL, Woosley JT, et al. Bubble hair. case caused by an overheating hair dryer and reproducibility in normal hair with heat. J Am Acad Dermatol. 1994;30:54-60.
  6. Khumalo NP, Dawber RP, Ferguson DJ. Apparent fragility of African hair is unrelated to the cystine-rich protein distribution: a cytochemical electron microscopic study. Exp Dermatol. 2005;14:311-314.
  7. Robbins C. Hair breakage during combing. I. pathways of breakage. J Cosmet Sci. 2006;57:233-243.
  8. Lewallen R, Francis S, Fisher B, et al. Hair care practices and structural evaluation of scalp and hair shaft parameter in African American and Caucasian women. J Cosmet Dermatol. 2015;14:216-223.
  9. Hall RR, Francis S, Whitt-Glover M, et al. Hair care practices as a barrier to physical activity in African American women. JAMA Dermatol. 2013;149:310-314.
  10. Franbourg A, Hallegot P, Baltenneck F, et al. Current research on ethnic hair. J Am Acad Dermatol. 2003;48(6 suppl):S115-S119.
  11. Ogunbiyi A. Acne keloidalis nuchae: prevalence, impact, and management challenges. Clin Cosmet Investig Dermatol. 2016;9:483-489.
  12. Gray J, McMichael AJ. Pseudofolliculitis barbae: understanding the condition and the role of facial grooming. Int J Cosmet Sci. 2016;38(suppl 1):24-27.
  13. Kundu RV, Patterson S. Dermatologic conditions in skin of color: part II. disorders occurring predominately in skin of color. Am Fam Physician. 2013;87:859-865.
  14. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  15. Gathers RC, Mahan MG. African American women, hair care and health barriers. J Clin Aesthet Dermatol. 2014;7:26-29.
  16. Dlova NC, Fabbrocini G, Lauro C, et al. Quality of life in South African black women with alopecia: a pilot study. Int J Dermatol. 2016;55:875-881.
  17. Wohltmann WE, Sperling L. Histopathologic diagnosis of multifactorial alopecia. J Cutan Pathol. 2016;43:483-491.
  18. McDonald KA, Shelley AJ, Colantonio S, et al. Hair pull test: evidence-based update and revision of guidelines. J Am Acad Dermatol. 2017;76:472-477.
  19. Miteva M, Tosti A. Dermatoscopic features of central centrifugal cicatricial alopecia. J Am Acad Dermatol. 2014;71:443-444.
  20. Coley MK, Bhanusali DG, Silverberg JI, et al. Scalp hyperkeratosis and alopecia in children of color. J Drugs Dermatol. 2011;10:511-516.
  21. Silverberg NB. Scalp hyperkeratosis in children with skin of color: diagnostic and therapeutic considerations. Cutis. 2015;95:199-204, 207.
  22. Hubbard TW. The predictive value of symptoms in diagnosing childhood tinea capitis. Arch Pediatr Adolesc Med. 1999;153:1150-1153.
  23. Kakourou T, Uksal U; European Society for Pediatric Dermatology. Guidelines for the management of tinea capitis in children. Pediatr Dermatol. 2010;27:226-228.
  24. Sethi A, Antanya R. Systemic antifungal therapy for cutaneous infections in children. Pediatr Infect Dis J. 2006;25:643-644.
  25. Gupta AK. Drummond-Main C. Meta-analysis of randomized, controlled trials comparing particular doses of griseofulvin and terbinafine for the treatment of tinea capitis. Pediatr Dermatol. 2013;30:1-6.
  26. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol 2000;39:302-304.
  27. Sharma V, Silverberg NB, Howard R, et al. Do hair care practices affect the acquisition of tinea capitis? a case-control study. Arch Pediatr Adolesc Med. 2001;155:818-821.
  28. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol. 2000;39:302-304.
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Author and Disclosure Information

Drs. Taylor and Ogunleye are from the Department of Dermatology, University of Pennsylvania, Philadelphia. Dr. Barbosa is from Millennium Park Dermatology, Chicago, Illinois. Dr. Burgess is from the Center for Dermatology and Dermatologic Surgery, Washington, DC. Dr. Heath is from Premier Dermatology and Cosmetic Surgery, Newark, Delaware. Dr. McMichael is from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Dr. Callender is from Callender Dermatology and Cosmetic Center, Glenn Dale, Maryland.

Dr. Taylor is an advisory board member for Allergan; Aqua Pharmaceuticals; Beiersdorf; and NeoStrata Company, Inc. She also is an investigator for Allergan; Alphaeon; Croma-Pharma; and Evolus, Inc. Drs. Barbosa, Heath, and Ogunleye report no conflict of interest. Dr. Burgess is a clinical research investigator and stockholder and has received honorarium from Allergan; is a clinical research investigator for Aclaris Therapeutics, Cutanea Life Sciences, Foamix, and Revance; and is a clinical research investigator and speaker and has received honoraria from Merz Pharma. Dr. McMichael is a consultant for Allergan; Galderma Laboratories, LP; Johnson & Johnson; and Procter & Gamble. She also has received research grants from Allergan and Procter & Gamble. Dr. Callender is a consultant for Allergan; Galderma Laboratories, LP; and Unilever. She also is a researcher for Allergan.

Presented in part at the 2017 American Academy of Dermatology Annual Meeting; March 3-7, 2017; Orlando, Florida.

Correspondence: Susan C. Taylor, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 1050 BRB II/III, Philadelphia, PA 19104 ([email protected]).

Issue
Cutis - 100(1)
Publications
Cutis
MDedge Dermatology
Topics
Hair & Nails
Page Number
31-35
Sections
Skin of Color
Author(s)
Susan C. Taylor, MD
Victoria Barbosa, MD
Cheryl Burgess, MD
Candrice Heath, MD
Amy J. McMichael, MD
Temitayo Ogunleye, MD
Valerie Callender, MD
Author(s)
Susan C. Taylor, MD
Victoria Barbosa, MD
Cheryl Burgess, MD
Candrice Heath, MD
Amy J. McMichael, MD
Temitayo Ogunleye, MD
Valerie Callender, MD
Author and Disclosure Information

Drs. Taylor and Ogunleye are from the Department of Dermatology, University of Pennsylvania, Philadelphia. Dr. Barbosa is from Millennium Park Dermatology, Chicago, Illinois. Dr. Burgess is from the Center for Dermatology and Dermatologic Surgery, Washington, DC. Dr. Heath is from Premier Dermatology and Cosmetic Surgery, Newark, Delaware. Dr. McMichael is from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Dr. Callender is from Callender Dermatology and Cosmetic Center, Glenn Dale, Maryland.

Dr. Taylor is an advisory board member for Allergan; Aqua Pharmaceuticals; Beiersdorf; and NeoStrata Company, Inc. She also is an investigator for Allergan; Alphaeon; Croma-Pharma; and Evolus, Inc. Drs. Barbosa, Heath, and Ogunleye report no conflict of interest. Dr. Burgess is a clinical research investigator and stockholder and has received honorarium from Allergan; is a clinical research investigator for Aclaris Therapeutics, Cutanea Life Sciences, Foamix, and Revance; and is a clinical research investigator and speaker and has received honoraria from Merz Pharma. Dr. McMichael is a consultant for Allergan; Galderma Laboratories, LP; Johnson & Johnson; and Procter & Gamble. She also has received research grants from Allergan and Procter & Gamble. Dr. Callender is a consultant for Allergan; Galderma Laboratories, LP; and Unilever. She also is a researcher for Allergan.

Presented in part at the 2017 American Academy of Dermatology Annual Meeting; March 3-7, 2017; Orlando, Florida.

Correspondence: Susan C. Taylor, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 1050 BRB II/III, Philadelphia, PA 19104 ([email protected]).

Author and Disclosure Information

Drs. Taylor and Ogunleye are from the Department of Dermatology, University of Pennsylvania, Philadelphia. Dr. Barbosa is from Millennium Park Dermatology, Chicago, Illinois. Dr. Burgess is from the Center for Dermatology and Dermatologic Surgery, Washington, DC. Dr. Heath is from Premier Dermatology and Cosmetic Surgery, Newark, Delaware. Dr. McMichael is from the Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, North Carolina. Dr. Callender is from Callender Dermatology and Cosmetic Center, Glenn Dale, Maryland.

Dr. Taylor is an advisory board member for Allergan; Aqua Pharmaceuticals; Beiersdorf; and NeoStrata Company, Inc. She also is an investigator for Allergan; Alphaeon; Croma-Pharma; and Evolus, Inc. Drs. Barbosa, Heath, and Ogunleye report no conflict of interest. Dr. Burgess is a clinical research investigator and stockholder and has received honorarium from Allergan; is a clinical research investigator for Aclaris Therapeutics, Cutanea Life Sciences, Foamix, and Revance; and is a clinical research investigator and speaker and has received honoraria from Merz Pharma. Dr. McMichael is a consultant for Allergan; Galderma Laboratories, LP; Johnson & Johnson; and Procter & Gamble. She also has received research grants from Allergan and Procter & Gamble. Dr. Callender is a consultant for Allergan; Galderma Laboratories, LP; and Unilever. She also is a researcher for Allergan.

Presented in part at the 2017 American Academy of Dermatology Annual Meeting; March 3-7, 2017; Orlando, Florida.

Correspondence: Susan C. Taylor, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 1050 BRB II/III, Philadelphia, PA 19104 ([email protected]).

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In Collaboration with the Skin of Color Society

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.1 Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.2 Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.3 Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.6

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).8 Another study by Hall et al9 of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al6 investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al10 examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

 

 

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.11 Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.12 Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.13 Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.14 The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan15 revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.16

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling17 demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

 

 

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard22 shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.22 Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.25 Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.28 Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).8 Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.1 Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.2 Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.3 Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.6

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).8 Another study by Hall et al9 of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al6 investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al10 examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

 

 

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.11 Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.12 Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.13 Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.14 The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan15 revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.16

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling17 demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

 

 

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard22 shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.22 Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.25 Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.28 Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).8 Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

References
  1. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  2. Hickman JG, Cardin C, Dawson TL, et al. Dandruff, part I: scalp disease prevalence in Caucasians, African Americans, and Chinese and the effects of shampoo frequency on scalp health. Poster presented at: 60th Annual Meeting of the American Academy of Dermatology; February 22-27, 2002; New Orleans, LA.
  3. Swee W, Klontz KC, Lambert LA. A nationwide outbreak of alopecia associated with the use of a hair-relaxing formulation. Arch Dermatol. 2000;136:1104-1108.
  4. Nicholson AG, Harland CC, Bull RH, et al. Chemically induced cosmetic alopecia. Br J Dermatol. 1993;128:537-541.
  5. Detwiler SP, Carson JL, Woosley JT, et al. Bubble hair. case caused by an overheating hair dryer and reproducibility in normal hair with heat. J Am Acad Dermatol. 1994;30:54-60.
  6. Khumalo NP, Dawber RP, Ferguson DJ. Apparent fragility of African hair is unrelated to the cystine-rich protein distribution: a cytochemical electron microscopic study. Exp Dermatol. 2005;14:311-314.
  7. Robbins C. Hair breakage during combing. I. pathways of breakage. J Cosmet Sci. 2006;57:233-243.
  8. Lewallen R, Francis S, Fisher B, et al. Hair care practices and structural evaluation of scalp and hair shaft parameter in African American and Caucasian women. J Cosmet Dermatol. 2015;14:216-223.
  9. Hall RR, Francis S, Whitt-Glover M, et al. Hair care practices as a barrier to physical activity in African American women. JAMA Dermatol. 2013;149:310-314.
  10. Franbourg A, Hallegot P, Baltenneck F, et al. Current research on ethnic hair. J Am Acad Dermatol. 2003;48(6 suppl):S115-S119.
  11. Ogunbiyi A. Acne keloidalis nuchae: prevalence, impact, and management challenges. Clin Cosmet Investig Dermatol. 2016;9:483-489.
  12. Gray J, McMichael AJ. Pseudofolliculitis barbae: understanding the condition and the role of facial grooming. Int J Cosmet Sci. 2016;38(suppl 1):24-27.
  13. Kundu RV, Patterson S. Dermatologic conditions in skin of color: part II. disorders occurring predominately in skin of color. Am Fam Physician. 2013;87:859-865.
  14. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  15. Gathers RC, Mahan MG. African American women, hair care and health barriers. J Clin Aesthet Dermatol. 2014;7:26-29.
  16. Dlova NC, Fabbrocini G, Lauro C, et al. Quality of life in South African black women with alopecia: a pilot study. Int J Dermatol. 2016;55:875-881.
  17. Wohltmann WE, Sperling L. Histopathologic diagnosis of multifactorial alopecia. J Cutan Pathol. 2016;43:483-491.
  18. McDonald KA, Shelley AJ, Colantonio S, et al. Hair pull test: evidence-based update and revision of guidelines. J Am Acad Dermatol. 2017;76:472-477.
  19. Miteva M, Tosti A. Dermatoscopic features of central centrifugal cicatricial alopecia. J Am Acad Dermatol. 2014;71:443-444.
  20. Coley MK, Bhanusali DG, Silverberg JI, et al. Scalp hyperkeratosis and alopecia in children of color. J Drugs Dermatol. 2011;10:511-516.
  21. Silverberg NB. Scalp hyperkeratosis in children with skin of color: diagnostic and therapeutic considerations. Cutis. 2015;95:199-204, 207.
  22. Hubbard TW. The predictive value of symptoms in diagnosing childhood tinea capitis. Arch Pediatr Adolesc Med. 1999;153:1150-1153.
  23. Kakourou T, Uksal U; European Society for Pediatric Dermatology. Guidelines for the management of tinea capitis in children. Pediatr Dermatol. 2010;27:226-228.
  24. Sethi A, Antanya R. Systemic antifungal therapy for cutaneous infections in children. Pediatr Infect Dis J. 2006;25:643-644.
  25. Gupta AK. Drummond-Main C. Meta-analysis of randomized, controlled trials comparing particular doses of griseofulvin and terbinafine for the treatment of tinea capitis. Pediatr Dermatol. 2013;30:1-6.
  26. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol 2000;39:302-304.
  27. Sharma V, Silverberg NB, Howard R, et al. Do hair care practices affect the acquisition of tinea capitis? a case-control study. Arch Pediatr Adolesc Med. 2001;155:818-821.
  28. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol. 2000;39:302-304.
References
  1. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  2. Hickman JG, Cardin C, Dawson TL, et al. Dandruff, part I: scalp disease prevalence in Caucasians, African Americans, and Chinese and the effects of shampoo frequency on scalp health. Poster presented at: 60th Annual Meeting of the American Academy of Dermatology; February 22-27, 2002; New Orleans, LA.
  3. Swee W, Klontz KC, Lambert LA. A nationwide outbreak of alopecia associated with the use of a hair-relaxing formulation. Arch Dermatol. 2000;136:1104-1108.
  4. Nicholson AG, Harland CC, Bull RH, et al. Chemically induced cosmetic alopecia. Br J Dermatol. 1993;128:537-541.
  5. Detwiler SP, Carson JL, Woosley JT, et al. Bubble hair. case caused by an overheating hair dryer and reproducibility in normal hair with heat. J Am Acad Dermatol. 1994;30:54-60.
  6. Khumalo NP, Dawber RP, Ferguson DJ. Apparent fragility of African hair is unrelated to the cystine-rich protein distribution: a cytochemical electron microscopic study. Exp Dermatol. 2005;14:311-314.
  7. Robbins C. Hair breakage during combing. I. pathways of breakage. J Cosmet Sci. 2006;57:233-243.
  8. Lewallen R, Francis S, Fisher B, et al. Hair care practices and structural evaluation of scalp and hair shaft parameter in African American and Caucasian women. J Cosmet Dermatol. 2015;14:216-223.
  9. Hall RR, Francis S, Whitt-Glover M, et al. Hair care practices as a barrier to physical activity in African American women. JAMA Dermatol. 2013;149:310-314.
  10. Franbourg A, Hallegot P, Baltenneck F, et al. Current research on ethnic hair. J Am Acad Dermatol. 2003;48(6 suppl):S115-S119.
  11. Ogunbiyi A. Acne keloidalis nuchae: prevalence, impact, and management challenges. Clin Cosmet Investig Dermatol. 2016;9:483-489.
  12. Gray J, McMichael AJ. Pseudofolliculitis barbae: understanding the condition and the role of facial grooming. Int J Cosmet Sci. 2016;38(suppl 1):24-27.
  13. Kundu RV, Patterson S. Dermatologic conditions in skin of color: part II. disorders occurring predominately in skin of color. Am Fam Physician. 2013;87:859-865.
  14. Davis SA, Naarahari S, Feldman SR, et al. Top dermatologic conditions in patients of color: an analysis of nationally representative data. J Drugs Dermatol. 2012;11:466-473.
  15. Gathers RC, Mahan MG. African American women, hair care and health barriers. J Clin Aesthet Dermatol. 2014;7:26-29.
  16. Dlova NC, Fabbrocini G, Lauro C, et al. Quality of life in South African black women with alopecia: a pilot study. Int J Dermatol. 2016;55:875-881.
  17. Wohltmann WE, Sperling L. Histopathologic diagnosis of multifactorial alopecia. J Cutan Pathol. 2016;43:483-491.
  18. McDonald KA, Shelley AJ, Colantonio S, et al. Hair pull test: evidence-based update and revision of guidelines. J Am Acad Dermatol. 2017;76:472-477.
  19. Miteva M, Tosti A. Dermatoscopic features of central centrifugal cicatricial alopecia. J Am Acad Dermatol. 2014;71:443-444.
  20. Coley MK, Bhanusali DG, Silverberg JI, et al. Scalp hyperkeratosis and alopecia in children of color. J Drugs Dermatol. 2011;10:511-516.
  21. Silverberg NB. Scalp hyperkeratosis in children with skin of color: diagnostic and therapeutic considerations. Cutis. 2015;95:199-204, 207.
  22. Hubbard TW. The predictive value of symptoms in diagnosing childhood tinea capitis. Arch Pediatr Adolesc Med. 1999;153:1150-1153.
  23. Kakourou T, Uksal U; European Society for Pediatric Dermatology. Guidelines for the management of tinea capitis in children. Pediatr Dermatol. 2010;27:226-228.
  24. Sethi A, Antanya R. Systemic antifungal therapy for cutaneous infections in children. Pediatr Infect Dis J. 2006;25:643-644.
  25. Gupta AK. Drummond-Main C. Meta-analysis of randomized, controlled trials comparing particular doses of griseofulvin and terbinafine for the treatment of tinea capitis. Pediatr Dermatol. 2013;30:1-6.
  26. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol 2000;39:302-304.
  27. Sharma V, Silverberg NB, Howard R, et al. Do hair care practices affect the acquisition of tinea capitis? a case-control study. Arch Pediatr Adolesc Med. 2001;155:818-821.
  28. Greer DL. Successful treatment of tinea capitis with 2% ketoconazole shampoo. Int J Dermatol. 2000;39:302-304.
Issue
Cutis - 100(1)
Issue
Cutis - 100(1)
Page Number
31-35
Page Number
31-35
Publications
Cutis
MDedge Dermatology
Publications
Cutis
MDedge Dermatology
Topics
Hair & Nails
Article Type
Article
Display Headline
Hair and Scalp Disorders in Adult and Pediatric Patients With Skin of Color
Display Headline
Hair and Scalp Disorders in Adult and Pediatric Patients With Skin of Color
Sections
Skin of Color
Inside the Article

Practice Points

  • Instruct patients with acquired trichorrhexis nodosa to discontinue use of heat, colorants, and chemical relaxers on their hair.
  • Create a contract with your seborrheic dermatitis patients to have them shampoo at least weekly or every 2 weeks.
  • For children with treated tinea capitis that has not completely resolved, increase or extend the griseofulvin dosage, encourage ingestion of fatty foods to enhance absorption, and divide dosage of griseofulvin from once to twice daily.
  • Selection of a biopsy site at the periphery of an alopecic area that includes hair and hair follicles and evaluation by a dermatopathologist familiar with the features of central centrifugal cicatricial, traction, and traumatic alopecias will ensure an accurate diagnosis of alopecia.
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