Hair & Nails

THE DIAGNOSIS: Nail Lichen Planus

The biopsy results showed features of hypergranulosis of the matricial epithelium, irregular acanthosis, apoptotic keratinocytes along the basal layer, and a lichenoid infiltrate consistent with nail lichen planus. The patient was started on topical clobetasol propionate 0.05% applied once daily under overnight occlusion. Additionally, intramatricial triamcinolone acetonide (2.5 mg/mL; 0.1 mL per injection) was administered into the affected nail matrix at 4-week intervals for a total of 2 sessions. At the 2-month follow-up visit, the patient reported improvement in longitudinal ridging; however, he subsequently was lost to follow-up.

Nail lichen planus is a chronic inflammatory disorder that occurs in 10% to 15% of patients with lichen planus worldwide and is more common in adults than children.¹ It can manifest independently or concurrently with cutaneous and/or oral mucosal involvement. The fingernails are more commonly affected than the toenails.² The clinical features of nail lichen planus can be classified based on involvement of the nail matrix (longitudinal ridging, red lunula, thinning of the nail plate, koilonychia, trachyonychia, pterygium, and anonychia) or nail bed (onycholysis, subungual hyperkeratosis, and splinter hemorrhages).¹

In our patient, who presented with chronic progressive nail dystrophy affecting all 20 nails, onychomycosis, nail psoriasis, onychotillomania, and idiopathic trachyonychia were included in the differential.¹

Onychomycosis manifests as white or yellow-brown discoloration of the nail, onycholysis, subungual hyperkeratosis, and thickening of the nail plate. Diagnosis is confirmed by the presence of septate hyphae (dermatophytes) or budding yeast cells (Candida species) on a potassium hydroxide mount. Other diagnostic modalities include dermoscopy, fungal culture, and histopathology of nail clippings, with demonstration of fungal elements identified on periodic acid-Schiff staining (eFigure 1).³

Nail psoriasis characteristically manifests as deep irregular pitting of the nails. Other features favoring psoriasis include involvement of the nail matrix manifesting as leukonychia, red lunula, and crumbling, as well as involvement of the nail bed manifesting as onycholysis, subungual hyperkeratosis, salmon patches/oil spots, and splinter hemorrhages (eFigure 2).⁴ Diagnosis primarily is clinical, supported by histopathology when uncertainty exists.

Onychotillomania is a behavioral disorder characterized by an irresistible urge or impulse in patients to either pick or pull at their fingernails and/or toenails. Clinicopathologic features of the involved nails are nonspecific and atypical, with possible involvement of periungual and digital skin. Diagnosis of onychotillomania is challenging.⁵ Dermoscopic features including anonychia with multiple obliquely arranged nail bed hemorrhages, gray pigmentation of the nail bed, and wavy lines, has been proposed to aid the diagnosis of onychotillomania.⁶

Idiopathic trachyonychia is isolated nail involvement characterized by rough, ridged, and thin nails affecting multiple or all of the fingernails and toenails without an underlying systemic or dermatologic condition (eFigure 3). The terms trachyonychia and 20-nail dystrophy have been used interchangeably in the literature; however, trachyonychia does not always involve all 20 nails. Other conditions causing widespread dystrophy of all 20 nails cannot be diagnosed as 20-nail dystrophy or trachyonychia without the distinct morphologic features of thin brittle nails with pronounced longitudinal ridging.⁷

Prompt diagnosis and early intervention in nail lichen planus is crucial due to the potential for irreversible scarring. First-line treatment options include intramatricial and intramuscular triamcinolone acetonide for 3 to 6 months.⁴ Second-line therapies include oral retinoids such as acitretin and alitretinoin and immunosuppressive agents such as azathioprine, mycophenolate mofetil, and cyclosporine. Other reported treatment options include clobetasol propionate, tacrolimus, dapsone, griseofulvin, etanercept, hydroxychloroquine, methotrexate, and UV therapy.⁴

THE DIAGNOSIS: Nail Lichen Planus

The biopsy results showed features of hypergranulosis of the matricial epithelium, irregular acanthosis, apoptotic keratinocytes along the basal layer, and a lichenoid infiltrate consistent with nail lichen planus. The patient was started on topical clobetasol propionate 0.05% applied once daily under overnight occlusion. Additionally, intramatricial triamcinolone acetonide (2.5 mg/mL; 0.1 mL per injection) was administered into the affected nail matrix at 4-week intervals for a total of 2 sessions. At the 2-month follow-up visit, the patient reported improvement in longitudinal ridging; however, he subsequently was lost to follow-up.

Nail lichen planus is a chronic inflammatory disorder that occurs in 10% to 15% of patients with lichen planus worldwide and is more common in adults than children.¹ It can manifest independently or concurrently with cutaneous and/or oral mucosal involvement. The fingernails are more commonly affected than the toenails.² The clinical features of nail lichen planus can be classified based on involvement of the nail matrix (longitudinal ridging, red lunula, thinning of the nail plate, koilonychia, trachyonychia, pterygium, and anonychia) or nail bed (onycholysis, subungual hyperkeratosis, and splinter hemorrhages).¹

In our patient, who presented with chronic progressive nail dystrophy affecting all 20 nails, onychomycosis, nail psoriasis, onychotillomania, and idiopathic trachyonychia were included in the differential.¹

Onychomycosis manifests as white or yellow-brown discoloration of the nail, onycholysis, subungual hyperkeratosis, and thickening of the nail plate. Diagnosis is confirmed by the presence of septate hyphae (dermatophytes) or budding yeast cells (Candida species) on a potassium hydroxide mount. Other diagnostic modalities include dermoscopy, fungal culture, and histopathology of nail clippings, with demonstration of fungal elements identified on periodic acid-Schiff staining (eFigure 1).³

Nail psoriasis characteristically manifests as deep irregular pitting of the nails. Other features favoring psoriasis include involvement of the nail matrix manifesting as leukonychia, red lunula, and crumbling, as well as involvement of the nail bed manifesting as onycholysis, subungual hyperkeratosis, salmon patches/oil spots, and splinter hemorrhages (eFigure 2).⁴ Diagnosis primarily is clinical, supported by histopathology when uncertainty exists.

Onychotillomania is a behavioral disorder characterized by an irresistible urge or impulse in patients to either pick or pull at their fingernails and/or toenails. Clinicopathologic features of the involved nails are nonspecific and atypical, with possible involvement of periungual and digital skin. Diagnosis of onychotillomania is challenging.⁵ Dermoscopic features including anonychia with multiple obliquely arranged nail bed hemorrhages, gray pigmentation of the nail bed, and wavy lines, has been proposed to aid the diagnosis of onychotillomania.⁶

Idiopathic trachyonychia is isolated nail involvement characterized by rough, ridged, and thin nails affecting multiple or all of the fingernails and toenails without an underlying systemic or dermatologic condition (eFigure 3). The terms trachyonychia and 20-nail dystrophy have been used interchangeably in the literature; however, trachyonychia does not always involve all 20 nails. Other conditions causing widespread dystrophy of all 20 nails cannot be diagnosed as 20-nail dystrophy or trachyonychia without the distinct morphologic features of thin brittle nails with pronounced longitudinal ridging.⁷

Prompt diagnosis and early intervention in nail lichen planus is crucial due to the potential for irreversible scarring. First-line treatment options include intramatricial and intramuscular triamcinolone acetonide for 3 to 6 months.⁴ Second-line therapies include oral retinoids such as acitretin and alitretinoin and immunosuppressive agents such as azathioprine, mycophenolate mofetil, and cyclosporine. Other reported treatment options include clobetasol propionate, tacrolimus, dapsone, griseofulvin, etanercept, hydroxychloroquine, methotrexate, and UV therapy.⁴

THE DIAGNOSIS: Nail Lichen Planus

The biopsy results showed features of hypergranulosis of the matricial epithelium, irregular acanthosis, apoptotic keratinocytes along the basal layer, and a lichenoid infiltrate consistent with nail lichen planus. The patient was started on topical clobetasol propionate 0.05% applied once daily under overnight occlusion. Additionally, intramatricial triamcinolone acetonide (2.5 mg/mL; 0.1 mL per injection) was administered into the affected nail matrix at 4-week intervals for a total of 2 sessions. At the 2-month follow-up visit, the patient reported improvement in longitudinal ridging; however, he subsequently was lost to follow-up.

Nail lichen planus is a chronic inflammatory disorder that occurs in 10% to 15% of patients with lichen planus worldwide and is more common in adults than children.¹ It can manifest independently or concurrently with cutaneous and/or oral mucosal involvement. The fingernails are more commonly affected than the toenails.² The clinical features of nail lichen planus can be classified based on involvement of the nail matrix (longitudinal ridging, red lunula, thinning of the nail plate, koilonychia, trachyonychia, pterygium, and anonychia) or nail bed (onycholysis, subungual hyperkeratosis, and splinter hemorrhages).¹

In our patient, who presented with chronic progressive nail dystrophy affecting all 20 nails, onychomycosis, nail psoriasis, onychotillomania, and idiopathic trachyonychia were included in the differential.¹

Onychomycosis manifests as white or yellow-brown discoloration of the nail, onycholysis, subungual hyperkeratosis, and thickening of the nail plate. Diagnosis is confirmed by the presence of septate hyphae (dermatophytes) or budding yeast cells (Candida species) on a potassium hydroxide mount. Other diagnostic modalities include dermoscopy, fungal culture, and histopathology of nail clippings, with demonstration of fungal elements identified on periodic acid-Schiff staining (eFigure 1).³

Nail psoriasis characteristically manifests as deep irregular pitting of the nails. Other features favoring psoriasis include involvement of the nail matrix manifesting as leukonychia, red lunula, and crumbling, as well as involvement of the nail bed manifesting as onycholysis, subungual hyperkeratosis, salmon patches/oil spots, and splinter hemorrhages (eFigure 2).⁴ Diagnosis primarily is clinical, supported by histopathology when uncertainty exists.

Onychotillomania is a behavioral disorder characterized by an irresistible urge or impulse in patients to either pick or pull at their fingernails and/or toenails. Clinicopathologic features of the involved nails are nonspecific and atypical, with possible involvement of periungual and digital skin. Diagnosis of onychotillomania is challenging.⁵ Dermoscopic features including anonychia with multiple obliquely arranged nail bed hemorrhages, gray pigmentation of the nail bed, and wavy lines, has been proposed to aid the diagnosis of onychotillomania.⁶

Idiopathic trachyonychia is isolated nail involvement characterized by rough, ridged, and thin nails affecting multiple or all of the fingernails and toenails without an underlying systemic or dermatologic condition (eFigure 3). The terms trachyonychia and 20-nail dystrophy have been used interchangeably in the literature; however, trachyonychia does not always involve all 20 nails. Other conditions causing widespread dystrophy of all 20 nails cannot be diagnosed as 20-nail dystrophy or trachyonychia without the distinct morphologic features of thin brittle nails with pronounced longitudinal ridging.⁷

Prompt diagnosis and early intervention in nail lichen planus is crucial due to the potential for irreversible scarring. First-line treatment options include intramatricial and intramuscular triamcinolone acetonide for 3 to 6 months.⁴ Second-line therapies include oral retinoids such as acitretin and alitretinoin and immunosuppressive agents such as azathioprine, mycophenolate mofetil, and cyclosporine. Other reported treatment options include clobetasol propionate, tacrolimus, dapsone, griseofulvin, etanercept, hydroxychloroquine, methotrexate, and UV therapy.⁴

THE DIAGNOSIS: Folliculitis Decalvans

Biopsy results revealed a brisk perifollicular and intrafollicular mixed inflammatory infiltrate comprising lymphocytes, neutrophils, and plasma cells filling the upper dermis and encircling dilated hair follicles. Elastic stain (Verhoeff-van Gieson) demonstrated loss of elastic fibers in areas of scarring. Periodic acid–Schiff with diastase staining was negative for fungal elements, while Gram staining revealed colonies of bacterial cocci in the stratum corneum and within the hair follicles. Immunofluorescence was unremarkable, and culture revealed methicillin-sensitive Staphylococcus aureus, leading to a diagnosis of folliculitis decalvans (FD). The patient was treated with doxycycline 100 mg twice daily and received intralesional triamcinolone 2.5 mg/mL (total volume, 2 mL) every 6 weeks with considerable improvement in pustules, erythema, and scaling (Figure). While not yet in complete remission, our patient demonstrated short regrowing hairs in areas of incomplete scarring and focal remaining perifollicular erythema and scale along the midline frontal scalp 5 months after initial presentation.

Folliculitis decalvans is an uncommon subtype of cicatricial alopecia that may mimic other forms of alopecia. Cicatricial alopecia often is difficult to diagnose due to its overlapping clinical characteristics, but early diagnosis is essential for appropriate management and prevention of further permanent hair loss. Traditionally classified as a primary neutrophilic cicatricial alopecia, lymphocyte-predominant variants of FD now are recognized.¹

Patients with FD typically present with patchy scarring alopecia at the vertex scalp that gradually expands and may demonstrate secondary features of follicular tufting and pustules.^1-3 While the epidemiology of FD is poorly characterized, Vañó-Galván et al⁴ reported that FD accounted for 2.8% of all alopecia cases and 10.5% of cicatricial alopecia cases in a multicenter study of 2835 patients. The pathophysiology of FD still is under investigation but is thought to result from a dysregulated immune response to a chronic bacterial infection (eg, S aureus), with resulting neutrophilpredominant inflammation in early stages.^1-3 Vañó-Galván et al⁴ reported that, among 35 patients with FD cultured for bacteria, 74% (26/35) returned positive results, 96% (25/26) of which grew S aureus.⁵

A systematic review of 20 studies that included 263 patients found rifampin and clindamycin to be the most common treatments for FD; however, there is insufficient evidence to determine if this treatment is the most effective.⁶ In our patient, clindamycin was avoided due to its propensity to negatively alter the gut microbiome long term.⁷ Other therapies such as oral tetracyclines, high-potency topical steroids, and intralesional triamcinolone also can be used to achieve disease remission.^5,6 Other treatments such as isotretinoin, red-light photodynamic therapy, tacrolimus, and external beam radiation have been reported in the literature but vary in efficacy.⁶ Our patient improved on a regimen of topical benzoyl peroxide wash, oral doxycycline, and intralesional triamcinolone.

Notably, FD may share clinical features with other causes of cicatricial alopecia. In our patient, FD mimicked other entities including discoid lupus erythematosus, frontal fibrosing alopecia, dissecting cellulitis, and erosive pustular dermatosis (Table).^1-14 Discoid lupus erythematosus manifests as round hypopigmented and hyperpigmented plaques with associated atrophy, perifollicular erythema, and follicular plugging. Frontal fibrosing alopecia is a primary lymphocytic scarring alopecia that manifests in a bandlike linear distribution over the frontal scalp and may involve the temporal scalp, posterior hairline, and/or eyebrows. Isolated hairs (known as lonely hairs) often are seen. Dissecting cellulitis is characterized by boggy nodules associated with alopecia on the scalp without notable epidermal change, although pustules and sinus tracts may develop.⁹ Erosive pustular dermatosis is a diagnosis of exclusion but often is seen in older adults with chronic sun damage and clinically manifests with eroded plaques with adherent crusts.¹⁰

While our patient presented with several overlapping clinical features, including progressive hair loss along the frontal scalp in a bandlike pattern suspicious for frontal fibrosing alopecia as well as atrophic depigmented plaques with adherent peripheral scaling suspicious for discoid lupus erythematosus, the presence of pustules was an important clue. The biopsy demonstrating a mixed infiltrate inclusive of neutrophils confirmed the diagnosis of FD.

THE DIAGNOSIS: Folliculitis Decalvans

Biopsy results revealed a brisk perifollicular and intrafollicular mixed inflammatory infiltrate comprising lymphocytes, neutrophils, and plasma cells filling the upper dermis and encircling dilated hair follicles. Elastic stain (Verhoeff-van Gieson) demonstrated loss of elastic fibers in areas of scarring. Periodic acid–Schiff with diastase staining was negative for fungal elements, while Gram staining revealed colonies of bacterial cocci in the stratum corneum and within the hair follicles. Immunofluorescence was unremarkable, and culture revealed methicillin-sensitive Staphylococcus aureus, leading to a diagnosis of folliculitis decalvans (FD). The patient was treated with doxycycline 100 mg twice daily and received intralesional triamcinolone 2.5 mg/mL (total volume, 2 mL) every 6 weeks with considerable improvement in pustules, erythema, and scaling (Figure). While not yet in complete remission, our patient demonstrated short regrowing hairs in areas of incomplete scarring and focal remaining perifollicular erythema and scale along the midline frontal scalp 5 months after initial presentation.

Folliculitis decalvans is an uncommon subtype of cicatricial alopecia that may mimic other forms of alopecia. Cicatricial alopecia often is difficult to diagnose due to its overlapping clinical characteristics, but early diagnosis is essential for appropriate management and prevention of further permanent hair loss. Traditionally classified as a primary neutrophilic cicatricial alopecia, lymphocyte-predominant variants of FD now are recognized.¹

Patients with FD typically present with patchy scarring alopecia at the vertex scalp that gradually expands and may demonstrate secondary features of follicular tufting and pustules.^1-3 While the epidemiology of FD is poorly characterized, Vañó-Galván et al⁴ reported that FD accounted for 2.8% of all alopecia cases and 10.5% of cicatricial alopecia cases in a multicenter study of 2835 patients. The pathophysiology of FD still is under investigation but is thought to result from a dysregulated immune response to a chronic bacterial infection (eg, S aureus), with resulting neutrophilpredominant inflammation in early stages.^1-3 Vañó-Galván et al⁴ reported that, among 35 patients with FD cultured for bacteria, 74% (26/35) returned positive results, 96% (25/26) of which grew S aureus.⁵

A systematic review of 20 studies that included 263 patients found rifampin and clindamycin to be the most common treatments for FD; however, there is insufficient evidence to determine if this treatment is the most effective.⁶ In our patient, clindamycin was avoided due to its propensity to negatively alter the gut microbiome long term.⁷ Other therapies such as oral tetracyclines, high-potency topical steroids, and intralesional triamcinolone also can be used to achieve disease remission.^5,6 Other treatments such as isotretinoin, red-light photodynamic therapy, tacrolimus, and external beam radiation have been reported in the literature but vary in efficacy.⁶ Our patient improved on a regimen of topical benzoyl peroxide wash, oral doxycycline, and intralesional triamcinolone.

Notably, FD may share clinical features with other causes of cicatricial alopecia. In our patient, FD mimicked other entities including discoid lupus erythematosus, frontal fibrosing alopecia, dissecting cellulitis, and erosive pustular dermatosis (Table).^1-14 Discoid lupus erythematosus manifests as round hypopigmented and hyperpigmented plaques with associated atrophy, perifollicular erythema, and follicular plugging. Frontal fibrosing alopecia is a primary lymphocytic scarring alopecia that manifests in a bandlike linear distribution over the frontal scalp and may involve the temporal scalp, posterior hairline, and/or eyebrows. Isolated hairs (known as lonely hairs) often are seen. Dissecting cellulitis is characterized by boggy nodules associated with alopecia on the scalp without notable epidermal change, although pustules and sinus tracts may develop.⁹ Erosive pustular dermatosis is a diagnosis of exclusion but often is seen in older adults with chronic sun damage and clinically manifests with eroded plaques with adherent crusts.¹⁰

While our patient presented with several overlapping clinical features, including progressive hair loss along the frontal scalp in a bandlike pattern suspicious for frontal fibrosing alopecia as well as atrophic depigmented plaques with adherent peripheral scaling suspicious for discoid lupus erythematosus, the presence of pustules was an important clue. The biopsy demonstrating a mixed infiltrate inclusive of neutrophils confirmed the diagnosis of FD.

THE DIAGNOSIS: Folliculitis Decalvans

Biopsy results revealed a brisk perifollicular and intrafollicular mixed inflammatory infiltrate comprising lymphocytes, neutrophils, and plasma cells filling the upper dermis and encircling dilated hair follicles. Elastic stain (Verhoeff-van Gieson) demonstrated loss of elastic fibers in areas of scarring. Periodic acid–Schiff with diastase staining was negative for fungal elements, while Gram staining revealed colonies of bacterial cocci in the stratum corneum and within the hair follicles. Immunofluorescence was unremarkable, and culture revealed methicillin-sensitive Staphylococcus aureus, leading to a diagnosis of folliculitis decalvans (FD). The patient was treated with doxycycline 100 mg twice daily and received intralesional triamcinolone 2.5 mg/mL (total volume, 2 mL) every 6 weeks with considerable improvement in pustules, erythema, and scaling (Figure). While not yet in complete remission, our patient demonstrated short regrowing hairs in areas of incomplete scarring and focal remaining perifollicular erythema and scale along the midline frontal scalp 5 months after initial presentation.

Folliculitis decalvans is an uncommon subtype of cicatricial alopecia that may mimic other forms of alopecia. Cicatricial alopecia often is difficult to diagnose due to its overlapping clinical characteristics, but early diagnosis is essential for appropriate management and prevention of further permanent hair loss. Traditionally classified as a primary neutrophilic cicatricial alopecia, lymphocyte-predominant variants of FD now are recognized.¹

Patients with FD typically present with patchy scarring alopecia at the vertex scalp that gradually expands and may demonstrate secondary features of follicular tufting and pustules.^1-3 While the epidemiology of FD is poorly characterized, Vañó-Galván et al⁴ reported that FD accounted for 2.8% of all alopecia cases and 10.5% of cicatricial alopecia cases in a multicenter study of 2835 patients. The pathophysiology of FD still is under investigation but is thought to result from a dysregulated immune response to a chronic bacterial infection (eg, S aureus), with resulting neutrophilpredominant inflammation in early stages.^1-3 Vañó-Galván et al⁴ reported that, among 35 patients with FD cultured for bacteria, 74% (26/35) returned positive results, 96% (25/26) of which grew S aureus.⁵

A systematic review of 20 studies that included 263 patients found rifampin and clindamycin to be the most common treatments for FD; however, there is insufficient evidence to determine if this treatment is the most effective.⁶ In our patient, clindamycin was avoided due to its propensity to negatively alter the gut microbiome long term.⁷ Other therapies such as oral tetracyclines, high-potency topical steroids, and intralesional triamcinolone also can be used to achieve disease remission.^5,6 Other treatments such as isotretinoin, red-light photodynamic therapy, tacrolimus, and external beam radiation have been reported in the literature but vary in efficacy.⁶ Our patient improved on a regimen of topical benzoyl peroxide wash, oral doxycycline, and intralesional triamcinolone.

Notably, FD may share clinical features with other causes of cicatricial alopecia. In our patient, FD mimicked other entities including discoid lupus erythematosus, frontal fibrosing alopecia, dissecting cellulitis, and erosive pustular dermatosis (Table).^1-14 Discoid lupus erythematosus manifests as round hypopigmented and hyperpigmented plaques with associated atrophy, perifollicular erythema, and follicular plugging. Frontal fibrosing alopecia is a primary lymphocytic scarring alopecia that manifests in a bandlike linear distribution over the frontal scalp and may involve the temporal scalp, posterior hairline, and/or eyebrows. Isolated hairs (known as lonely hairs) often are seen. Dissecting cellulitis is characterized by boggy nodules associated with alopecia on the scalp without notable epidermal change, although pustules and sinus tracts may develop.⁹ Erosive pustular dermatosis is a diagnosis of exclusion but often is seen in older adults with chronic sun damage and clinically manifests with eroded plaques with adherent crusts.¹⁰

While our patient presented with several overlapping clinical features, including progressive hair loss along the frontal scalp in a bandlike pattern suspicious for frontal fibrosing alopecia as well as atrophic depigmented plaques with adherent peripheral scaling suspicious for discoid lupus erythematosus, the presence of pustules was an important clue. The biopsy demonstrating a mixed infiltrate inclusive of neutrophils confirmed the diagnosis of FD.

Facial hair growth in women is complex and multifaceted. It is not a disease but rather a part of normal anatomy or a symptom influenced by an underlying condition such as hypertrichosis, a hormonal imbalance (eg, hirsutism due to polycystic ovary syndrome [PCOS]), mechanical factors such as pseudofolliculitis barbae (PFB) from shaving, and perimenopausal and postmenopausal hormonal shifts. Additionally, normal facial hair patterns can vary substantially based on genetics, ethnicity, and cultural background. Some populations may naturally have more visible vellus or terminal hairs on the face, which are entirely physiologic rather than indicative of an underlying disorder. Despite this, societal expectations and beauty standards across many cultures dictate that facial hair in women is undesirable, often associating hair-free skin with femininity and attractiveness. This perception drives many women to seek treatment—not necessarily for medical reasons, but due to social pressure and aesthetic preferences.

Hypertrichosis, whether congenital or acquired, refers to excessive hair growth that is not androgen dependent and can appear on any site of the body. Causes include genetic predisposition, porphyria, thyroid disorders, internal malignancies, malnutrition, anorexia nervosa, or use of medications such as cyclosporine, prednisolone, and phenytoin.¹ Hirsutism, by contrast, is characterized by the growth of terminal hairs in women at androgen-dependent sites such as the face, neck, and upper chest, where coarse hair typically grows in men.² This condition often is associated with excess androgens produced by the ovaries or adrenal glands, most commonly due to PCOS although genetic factors may contribute. 

Before initiating treatment, a thorough history and physical examination are essential to determine the underlying cause of conditions associated with facial hair growth in women. Clinicians should assess for signs of hyperandrogenism, menstrual irregularities, virilization, medication use, and family history. In cases of a suspected endocrine disorder, further laboratory evaluation may be warranted to guide appropriate management. While each cause of facial hair growth in women has unique management considerations, the shared impact on psychosocial well-being and adherence to grooming standards in the US military warrants an all-encompassing yet targeted approach. This comprehensive review discusses management options for women with facial hair in the military based on a review of PubMed articles indexed for MEDLINE conducted in November 2024 using combinations of the following search terms: hirsutism, facial hair, pseudofolliculitis barbae, women, female, military, grooming standards, hyperandrogenism, and hair removal.

Treatment Modalities

The available treatment modalities, including their mechanisms, potential risks, and considerations are summarized in the eTable.

Mechanical—Shaving remains one of the most widely utilized methods of hair removal in women due to its accessibility and ease of use. It does not disrupt the anagen phase of the hair growth cycle, making it a temporary method that requires frequent repetition (often daily), particularly for individuals with rapid hair growth. The belief that shaving causes hair to grow back thicker or faster is a common misconception. Shaving does not alter the thickness or growth rate of hair; instead, it leaves a blunt tip, making the hair feel coarser or appear thicker than uncut hair.³ Despite its relative convenience, shaving can lead to skin irritation due to mechanical trauma. Potential complications include PFB, superficial abrasions known more broadly as shaving irritation, and an increased risk for infections such as bacterial or fungal folliculitis.⁴

Chemical depilation, which uses thioglycolates mixed with alkali compounds, disrupts disulfide bonds in the hair, effectively breaking down the shaft without affecting the bulb. The depilatory requires application to the skin for approximately 3 to 15 minutes depending on the specific formulation and the thickness or texture of the hair. While it is a cost-effective option that easily can be done at home, the chemicals involved may trigger irritant contact dermatitis or folliculitis and produce an unpleasant odor from hydrogen disulfide gas.⁵ They also can lead to PFB.

Epilation removes the entire hair shaft and bulb, with results lasting approximately 6 weeks.⁶ Methods range from using tweezers to pluck single hairs and devices that simultaneously remove multiple hairs to hot or cold waxing, which use resin to grip and remove hair. Threading is a technique that uses twisted thread to remove the hair at the follicle level; this method may not alter hair growth unless performed during the anagen phase, during which repeated plucking can damage the matrix and potentially lead to permanent hair reduction.⁵ Common adverse effects include pain during removal, burns from waxing, folliculitis, PFB, postinflammatory hyperpigmentation, and scarring, particularly when multiple hairs are removed at once.

Pharmacologic—Pharmacologic therapy commonly is used to manage hirsutism and typically begins with a trial of combined oral contraceptives (COCs) containing estrogen and progestin, which are considered the first-line option unless contraindicated.⁷ If response to COC monotherapy is inadequate, an antiandrogen such as spironolactone may be added. Combination therapy with a COC and an antiandrogen generally is reserved for severe cases or patients who previously have shown suboptimal response to COCs alone.⁷ Patients should be counseled to discontinue antiandrogen therapy if they become pregnant due to the risk for fetal undervirilization observed in animal studies.^8,9 Typical dosing of spironolactone, a competitive inhibitor of 5-α-reductase and androgen receptors, ranges from 100 mg to 200 mg daily.¹⁰ Reported adverse effects include polyuria, postural hypotension, menstrual irregularities, hyperkalemia, and potential liver dysfunction. Although spironolactone has demonstrated tumorigenic effects in animal studies, no such effects have been observed in humans.¹¹

Eflornithine hydrochloride cream 13.9% is the first topical prescription medication approved by the US Food and Drug Administration for reduction of unwanted facial hair in women.¹² It works by irreversibly blocking the activity of ornithine decarboxylase, an enzyme involved in the rate-limiting step of polyamine synthesis, which is essential for hair growth. In a randomized, double-blind clinical trial evaluating its effectiveness and safety, twice-daily application for 24 weeks resulted in a clinically meaningful reduction in hair length and density (measured as surface area) compared with the control group.¹³ When eflornithine hydrochloride cream 13.9% is discontinued, hair growth gradually returns to baseline. Studies have shown that hair regrowth typically begins within 8 weeks after treatment is stopped; within several months, hair returns to pretreatment levels.¹⁴ Adverse effects of eflornithine hydrochloride cream generally are mild and may include local irritation and acneform eruptions. In a randomized bilateral vehicle-controlled trial of 31 women, both eflornithine and vehicle creams were well tolerated, with 1 patient reporting mild tingling with eflornithine that resolved with continued use for 7 days.¹⁵

Procedural—Photoepilation therapies widely are considered by dermatologists to be among the most effective methods for reducing unwanted hair.¹⁶ Laser hair removal employs selective photothermolysis, a principle by which specific wavelengths of light target melanin in hair follicles. This method results in localized thermal damage, destroying hair follicles and reducing regrowth. Wavelengths between 600 and 1100 nm are most effective for hair removal; widely used devices include the ruby (694 nm), alexandrite (755 nm), diode (800-810 nm), and long-pulsed Nd:YAG lasers (1064 nm). Cooling mechanisms such as cryogen spray or contact cooling often are employed to minimize epidermal damage and lessen patient discomfort.

The hair matrix is most responsive to laser treatment during the anagen phase, necessitating multiple sessions to ensure all hairs are treated during this optimal growth stage. Generally, 4 to 6 sessions spaced at intervals of 4 to 6 weeks are required to achieve satisfactory results.¹⁷ Matching the laser wavelength to the absorption properties of melanin—the target chromophore—enables selective destruction of melanin-rich hair follicles while minimizing damage to surrounding skin.

The ideal laser wavelength primarily affects melanin concentrated in the hair bulb, leading to follicular destruction while reducing the risk for unintended depigmentation of the epidermis; however, competing structures in the skin (eg, epidermal pigment) also can absorb laser energy, diminishing treatment efficacy and increasing the risk for adverse effects. Shorter wavelengths are effective for lighter skin types, while longer wavelengths such as the Nd:YAG laser are safer for individuals with darker skin types as they bypass melanin in the epidermis.

It is important to note that laser hair removal is ineffective for white and gray hairs due to the lack of melanin. As a result, alternative methods such as electrolysis, which does not rely on pigment, may be more appropriate for permanent hair removal in individuals with nonpigmented hairs. Research indicates that combining topical eflornithine with alexandrite or Nd:YAG lasers improves outcomes for reducing unwanted facial hair.¹⁸

In military settings, laser hair removal is utilized for specific conditions such as PFB in male service members to assist with the reduction of hair and mitigation of symptoms.¹⁹ The majority of military dermatology clinics have devices for laser hair removal; however, dermatology services are not available at many military treatment facilities, and dermatologic care may be provided by the local civilian dermatologists. That said, laser therapy is covered in the civilian sector for active-duty service members with PFB of the face and neck under certain criteria. These include a documented safety risk in environments requiring respiratory protection, failure of conservative treatments, and evaluation by a military dermatologist who confirms the necessity of civilian-provided laser therapy when it is unavailable at a military facility.²⁰ While such policies demonstrate the military’s recognition of laser therapy as a viable solution for certain grooming-related conditions, many are unaware that the existing laser hair removal policy also applies to women. Increasing awareness of this coverage could help female service members access treatment options that align with both medical and professional grooming needs.

Intense pulsed light (IPL) systems are nonlaser devices that emit broad-spectrum light in the 590- to 1200-nm range. They utilize a flash lamp to achieve thermal damage. Filters are used to narrow the wavelength range based on the specific target. Intense pulsed light devices are less precise than lasers but remain effective for hair reduction. In addition to hair removal, IPL devices are employed in the treatment of pigmented and vascular lesions. Common adverse effects of both laser and IPL hair removal include transient erythema, perifollicular edema, and pigmentary changes, especially in patients with darker skin types. Rare complications include blistering, scarring, and paradoxical hair stimulation in which untreated areas develop increased hair growth.

Electrolysis is recognized as the only method of truly permanent hair removal and is effective for all hair colors.²¹ However, the variability in technique among practitioners often leads to inconsistent results, with some patients experiencing hair regrowth. Galvanic electrolysis involves inserting a fine needle into the hair follicle and applying an electrical current to destroy the it and the rapidly dividing cells of the matrix.²² The introduction of thermolytic electrolysis, which uses a high-frequency alternating current (commonly 13.56 MHz or 27.12 MHz), has enhanced efficiency by creating heat at the needle tip to destroy the follicle. This approach is faster and now is commonly combined with galvanic electrolysis.²³ While no controlled clinical trials directly compare these methods, many patients experience permanent hair removal, with approximately 15% to 25% regrowth within 6 months.^22,24

Alternative Options—Home-use laser and light-based devices have become increasingly popular for managing unwanted hair due to their affordability and convenience, with most devices priced less than $1000.²⁵ These devices utilize various technologies, including lasers (808 nm), IPL, or combinations of IPL and radiofrequency.²⁶ Despite their accessibility, peer-reviewed research on their safety profile and effectiveness is limited, as existing data primarily come from industry-funded, uncontrolled studies with short follow-up durations—making it difficult to assess long-term outcomes.²⁵

Psychosocial Impact

A 2023 study of active-duty female service members with PCOS highlighted the unique challenges they face while managing symptoms such as facial hair within the constraints of military service.²⁷ Although the study focused on PCOS, the findings shed light on how facial hair specifically impacts the psychological well-being of servicewomen. Participants described facial hair as one of the most visible and stigmatizing symptoms, often leading to feelings of embarrassment and diminished confidence. Participants also highlighted the professional implications of facial hair, with some describing feelings of scrutiny and judgment from peers and leadership in public. These challenges can be more pronounced in deployments or field exercises where hygiene resources are limited. The lack of access not only affects self-perception but also can hinder the ability of servicewomen to meet implicit expectations for grooming and appearance.²⁷ There is a notable gap in research examining the impact of facial hair on military servicewomen. Given the unique environmental challenges and professional expectations, further investigation is warranted to better understand how facial hair affects women and to optimize treatment approaches in this population.

Final Thoughts

Limited awareness and understanding of facial hair in woman contribute to stigma, often leaving affected individuals to navigate challenges in isolation. Given the impact on confidence, professional appearance, and adherence to military grooming standards, it is essential for health care practitioners to recognize and address facial hair in women. Importantly, laser hair removal is covered by TRICARE for active-duty female service members with PFB, yet many remain unaware of this benefit. Increased awareness of available mechanical, pharmacologic, and procedural treatment options allows for tailored management, ensuring that women receive appropriate medical care.

Facial hair growth in women is complex and multifaceted. It is not a disease but rather a part of normal anatomy or a symptom influenced by an underlying condition such as hypertrichosis, a hormonal imbalance (eg, hirsutism due to polycystic ovary syndrome [PCOS]), mechanical factors such as pseudofolliculitis barbae (PFB) from shaving, and perimenopausal and postmenopausal hormonal shifts. Additionally, normal facial hair patterns can vary substantially based on genetics, ethnicity, and cultural background. Some populations may naturally have more visible vellus or terminal hairs on the face, which are entirely physiologic rather than indicative of an underlying disorder. Despite this, societal expectations and beauty standards across many cultures dictate that facial hair in women is undesirable, often associating hair-free skin with femininity and attractiveness. This perception drives many women to seek treatment—not necessarily for medical reasons, but due to social pressure and aesthetic preferences.

Hypertrichosis, whether congenital or acquired, refers to excessive hair growth that is not androgen dependent and can appear on any site of the body. Causes include genetic predisposition, porphyria, thyroid disorders, internal malignancies, malnutrition, anorexia nervosa, or use of medications such as cyclosporine, prednisolone, and phenytoin.¹ Hirsutism, by contrast, is characterized by the growth of terminal hairs in women at androgen-dependent sites such as the face, neck, and upper chest, where coarse hair typically grows in men.² This condition often is associated with excess androgens produced by the ovaries or adrenal glands, most commonly due to PCOS although genetic factors may contribute. 

Before initiating treatment, a thorough history and physical examination are essential to determine the underlying cause of conditions associated with facial hair growth in women. Clinicians should assess for signs of hyperandrogenism, menstrual irregularities, virilization, medication use, and family history. In cases of a suspected endocrine disorder, further laboratory evaluation may be warranted to guide appropriate management. While each cause of facial hair growth in women has unique management considerations, the shared impact on psychosocial well-being and adherence to grooming standards in the US military warrants an all-encompassing yet targeted approach. This comprehensive review discusses management options for women with facial hair in the military based on a review of PubMed articles indexed for MEDLINE conducted in November 2024 using combinations of the following search terms: hirsutism, facial hair, pseudofolliculitis barbae, women, female, military, grooming standards, hyperandrogenism, and hair removal.

Treatment Modalities

The available treatment modalities, including their mechanisms, potential risks, and considerations are summarized in the eTable.

Mechanical—Shaving remains one of the most widely utilized methods of hair removal in women due to its accessibility and ease of use. It does not disrupt the anagen phase of the hair growth cycle, making it a temporary method that requires frequent repetition (often daily), particularly for individuals with rapid hair growth. The belief that shaving causes hair to grow back thicker or faster is a common misconception. Shaving does not alter the thickness or growth rate of hair; instead, it leaves a blunt tip, making the hair feel coarser or appear thicker than uncut hair.³ Despite its relative convenience, shaving can lead to skin irritation due to mechanical trauma. Potential complications include PFB, superficial abrasions known more broadly as shaving irritation, and an increased risk for infections such as bacterial or fungal folliculitis.⁴

Chemical depilation, which uses thioglycolates mixed with alkali compounds, disrupts disulfide bonds in the hair, effectively breaking down the shaft without affecting the bulb. The depilatory requires application to the skin for approximately 3 to 15 minutes depending on the specific formulation and the thickness or texture of the hair. While it is a cost-effective option that easily can be done at home, the chemicals involved may trigger irritant contact dermatitis or folliculitis and produce an unpleasant odor from hydrogen disulfide gas.⁵ They also can lead to PFB.

Epilation removes the entire hair shaft and bulb, with results lasting approximately 6 weeks.⁶ Methods range from using tweezers to pluck single hairs and devices that simultaneously remove multiple hairs to hot or cold waxing, which use resin to grip and remove hair. Threading is a technique that uses twisted thread to remove the hair at the follicle level; this method may not alter hair growth unless performed during the anagen phase, during which repeated plucking can damage the matrix and potentially lead to permanent hair reduction.⁵ Common adverse effects include pain during removal, burns from waxing, folliculitis, PFB, postinflammatory hyperpigmentation, and scarring, particularly when multiple hairs are removed at once.

Pharmacologic—Pharmacologic therapy commonly is used to manage hirsutism and typically begins with a trial of combined oral contraceptives (COCs) containing estrogen and progestin, which are considered the first-line option unless contraindicated.⁷ If response to COC monotherapy is inadequate, an antiandrogen such as spironolactone may be added. Combination therapy with a COC and an antiandrogen generally is reserved for severe cases or patients who previously have shown suboptimal response to COCs alone.⁷ Patients should be counseled to discontinue antiandrogen therapy if they become pregnant due to the risk for fetal undervirilization observed in animal studies.^8,9 Typical dosing of spironolactone, a competitive inhibitor of 5-α-reductase and androgen receptors, ranges from 100 mg to 200 mg daily.¹⁰ Reported adverse effects include polyuria, postural hypotension, menstrual irregularities, hyperkalemia, and potential liver dysfunction. Although spironolactone has demonstrated tumorigenic effects in animal studies, no such effects have been observed in humans.¹¹

Eflornithine hydrochloride cream 13.9% is the first topical prescription medication approved by the US Food and Drug Administration for reduction of unwanted facial hair in women.¹² It works by irreversibly blocking the activity of ornithine decarboxylase, an enzyme involved in the rate-limiting step of polyamine synthesis, which is essential for hair growth. In a randomized, double-blind clinical trial evaluating its effectiveness and safety, twice-daily application for 24 weeks resulted in a clinically meaningful reduction in hair length and density (measured as surface area) compared with the control group.¹³ When eflornithine hydrochloride cream 13.9% is discontinued, hair growth gradually returns to baseline. Studies have shown that hair regrowth typically begins within 8 weeks after treatment is stopped; within several months, hair returns to pretreatment levels.¹⁴ Adverse effects of eflornithine hydrochloride cream generally are mild and may include local irritation and acneform eruptions. In a randomized bilateral vehicle-controlled trial of 31 women, both eflornithine and vehicle creams were well tolerated, with 1 patient reporting mild tingling with eflornithine that resolved with continued use for 7 days.¹⁵

Procedural—Photoepilation therapies widely are considered by dermatologists to be among the most effective methods for reducing unwanted hair.¹⁶ Laser hair removal employs selective photothermolysis, a principle by which specific wavelengths of light target melanin in hair follicles. This method results in localized thermal damage, destroying hair follicles and reducing regrowth. Wavelengths between 600 and 1100 nm are most effective for hair removal; widely used devices include the ruby (694 nm), alexandrite (755 nm), diode (800-810 nm), and long-pulsed Nd:YAG lasers (1064 nm). Cooling mechanisms such as cryogen spray or contact cooling often are employed to minimize epidermal damage and lessen patient discomfort.

The hair matrix is most responsive to laser treatment during the anagen phase, necessitating multiple sessions to ensure all hairs are treated during this optimal growth stage. Generally, 4 to 6 sessions spaced at intervals of 4 to 6 weeks are required to achieve satisfactory results.¹⁷ Matching the laser wavelength to the absorption properties of melanin—the target chromophore—enables selective destruction of melanin-rich hair follicles while minimizing damage to surrounding skin.

The ideal laser wavelength primarily affects melanin concentrated in the hair bulb, leading to follicular destruction while reducing the risk for unintended depigmentation of the epidermis; however, competing structures in the skin (eg, epidermal pigment) also can absorb laser energy, diminishing treatment efficacy and increasing the risk for adverse effects. Shorter wavelengths are effective for lighter skin types, while longer wavelengths such as the Nd:YAG laser are safer for individuals with darker skin types as they bypass melanin in the epidermis.

It is important to note that laser hair removal is ineffective for white and gray hairs due to the lack of melanin. As a result, alternative methods such as electrolysis, which does not rely on pigment, may be more appropriate for permanent hair removal in individuals with nonpigmented hairs. Research indicates that combining topical eflornithine with alexandrite or Nd:YAG lasers improves outcomes for reducing unwanted facial hair.¹⁸

In military settings, laser hair removal is utilized for specific conditions such as PFB in male service members to assist with the reduction of hair and mitigation of symptoms.¹⁹ The majority of military dermatology clinics have devices for laser hair removal; however, dermatology services are not available at many military treatment facilities, and dermatologic care may be provided by the local civilian dermatologists. That said, laser therapy is covered in the civilian sector for active-duty service members with PFB of the face and neck under certain criteria. These include a documented safety risk in environments requiring respiratory protection, failure of conservative treatments, and evaluation by a military dermatologist who confirms the necessity of civilian-provided laser therapy when it is unavailable at a military facility.²⁰ While such policies demonstrate the military’s recognition of laser therapy as a viable solution for certain grooming-related conditions, many are unaware that the existing laser hair removal policy also applies to women. Increasing awareness of this coverage could help female service members access treatment options that align with both medical and professional grooming needs.

Intense pulsed light (IPL) systems are nonlaser devices that emit broad-spectrum light in the 590- to 1200-nm range. They utilize a flash lamp to achieve thermal damage. Filters are used to narrow the wavelength range based on the specific target. Intense pulsed light devices are less precise than lasers but remain effective for hair reduction. In addition to hair removal, IPL devices are employed in the treatment of pigmented and vascular lesions. Common adverse effects of both laser and IPL hair removal include transient erythema, perifollicular edema, and pigmentary changes, especially in patients with darker skin types. Rare complications include blistering, scarring, and paradoxical hair stimulation in which untreated areas develop increased hair growth.

Electrolysis is recognized as the only method of truly permanent hair removal and is effective for all hair colors.²¹ However, the variability in technique among practitioners often leads to inconsistent results, with some patients experiencing hair regrowth. Galvanic electrolysis involves inserting a fine needle into the hair follicle and applying an electrical current to destroy the it and the rapidly dividing cells of the matrix.²² The introduction of thermolytic electrolysis, which uses a high-frequency alternating current (commonly 13.56 MHz or 27.12 MHz), has enhanced efficiency by creating heat at the needle tip to destroy the follicle. This approach is faster and now is commonly combined with galvanic electrolysis.²³ While no controlled clinical trials directly compare these methods, many patients experience permanent hair removal, with approximately 15% to 25% regrowth within 6 months.^22,24

Alternative Options—Home-use laser and light-based devices have become increasingly popular for managing unwanted hair due to their affordability and convenience, with most devices priced less than $1000.²⁵ These devices utilize various technologies, including lasers (808 nm), IPL, or combinations of IPL and radiofrequency.²⁶ Despite their accessibility, peer-reviewed research on their safety profile and effectiveness is limited, as existing data primarily come from industry-funded, uncontrolled studies with short follow-up durations—making it difficult to assess long-term outcomes.²⁵

Psychosocial Impact

A 2023 study of active-duty female service members with PCOS highlighted the unique challenges they face while managing symptoms such as facial hair within the constraints of military service.²⁷ Although the study focused on PCOS, the findings shed light on how facial hair specifically impacts the psychological well-being of servicewomen. Participants described facial hair as one of the most visible and stigmatizing symptoms, often leading to feelings of embarrassment and diminished confidence. Participants also highlighted the professional implications of facial hair, with some describing feelings of scrutiny and judgment from peers and leadership in public. These challenges can be more pronounced in deployments or field exercises where hygiene resources are limited. The lack of access not only affects self-perception but also can hinder the ability of servicewomen to meet implicit expectations for grooming and appearance.²⁷ There is a notable gap in research examining the impact of facial hair on military servicewomen. Given the unique environmental challenges and professional expectations, further investigation is warranted to better understand how facial hair affects women and to optimize treatment approaches in this population.

Final Thoughts

Limited awareness and understanding of facial hair in woman contribute to stigma, often leaving affected individuals to navigate challenges in isolation. Given the impact on confidence, professional appearance, and adherence to military grooming standards, it is essential for health care practitioners to recognize and address facial hair in women. Importantly, laser hair removal is covered by TRICARE for active-duty female service members with PFB, yet many remain unaware of this benefit. Increased awareness of available mechanical, pharmacologic, and procedural treatment options allows for tailored management, ensuring that women receive appropriate medical care.

Facial hair growth in women is complex and multifaceted. It is not a disease but rather a part of normal anatomy or a symptom influenced by an underlying condition such as hypertrichosis, a hormonal imbalance (eg, hirsutism due to polycystic ovary syndrome [PCOS]), mechanical factors such as pseudofolliculitis barbae (PFB) from shaving, and perimenopausal and postmenopausal hormonal shifts. Additionally, normal facial hair patterns can vary substantially based on genetics, ethnicity, and cultural background. Some populations may naturally have more visible vellus or terminal hairs on the face, which are entirely physiologic rather than indicative of an underlying disorder. Despite this, societal expectations and beauty standards across many cultures dictate that facial hair in women is undesirable, often associating hair-free skin with femininity and attractiveness. This perception drives many women to seek treatment—not necessarily for medical reasons, but due to social pressure and aesthetic preferences.

Hypertrichosis, whether congenital or acquired, refers to excessive hair growth that is not androgen dependent and can appear on any site of the body. Causes include genetic predisposition, porphyria, thyroid disorders, internal malignancies, malnutrition, anorexia nervosa, or use of medications such as cyclosporine, prednisolone, and phenytoin.¹ Hirsutism, by contrast, is characterized by the growth of terminal hairs in women at androgen-dependent sites such as the face, neck, and upper chest, where coarse hair typically grows in men.² This condition often is associated with excess androgens produced by the ovaries or adrenal glands, most commonly due to PCOS although genetic factors may contribute. 

Before initiating treatment, a thorough history and physical examination are essential to determine the underlying cause of conditions associated with facial hair growth in women. Clinicians should assess for signs of hyperandrogenism, menstrual irregularities, virilization, medication use, and family history. In cases of a suspected endocrine disorder, further laboratory evaluation may be warranted to guide appropriate management. While each cause of facial hair growth in women has unique management considerations, the shared impact on psychosocial well-being and adherence to grooming standards in the US military warrants an all-encompassing yet targeted approach. This comprehensive review discusses management options for women with facial hair in the military based on a review of PubMed articles indexed for MEDLINE conducted in November 2024 using combinations of the following search terms: hirsutism, facial hair, pseudofolliculitis barbae, women, female, military, grooming standards, hyperandrogenism, and hair removal.

Treatment Modalities

The available treatment modalities, including their mechanisms, potential risks, and considerations are summarized in the eTable.

Mechanical—Shaving remains one of the most widely utilized methods of hair removal in women due to its accessibility and ease of use. It does not disrupt the anagen phase of the hair growth cycle, making it a temporary method that requires frequent repetition (often daily), particularly for individuals with rapid hair growth. The belief that shaving causes hair to grow back thicker or faster is a common misconception. Shaving does not alter the thickness or growth rate of hair; instead, it leaves a blunt tip, making the hair feel coarser or appear thicker than uncut hair.³ Despite its relative convenience, shaving can lead to skin irritation due to mechanical trauma. Potential complications include PFB, superficial abrasions known more broadly as shaving irritation, and an increased risk for infections such as bacterial or fungal folliculitis.⁴

Chemical depilation, which uses thioglycolates mixed with alkali compounds, disrupts disulfide bonds in the hair, effectively breaking down the shaft without affecting the bulb. The depilatory requires application to the skin for approximately 3 to 15 minutes depending on the specific formulation and the thickness or texture of the hair. While it is a cost-effective option that easily can be done at home, the chemicals involved may trigger irritant contact dermatitis or folliculitis and produce an unpleasant odor from hydrogen disulfide gas.⁵ They also can lead to PFB.

Epilation removes the entire hair shaft and bulb, with results lasting approximately 6 weeks.⁶ Methods range from using tweezers to pluck single hairs and devices that simultaneously remove multiple hairs to hot or cold waxing, which use resin to grip and remove hair. Threading is a technique that uses twisted thread to remove the hair at the follicle level; this method may not alter hair growth unless performed during the anagen phase, during which repeated plucking can damage the matrix and potentially lead to permanent hair reduction.⁵ Common adverse effects include pain during removal, burns from waxing, folliculitis, PFB, postinflammatory hyperpigmentation, and scarring, particularly when multiple hairs are removed at once.

Pharmacologic—Pharmacologic therapy commonly is used to manage hirsutism and typically begins with a trial of combined oral contraceptives (COCs) containing estrogen and progestin, which are considered the first-line option unless contraindicated.⁷ If response to COC monotherapy is inadequate, an antiandrogen such as spironolactone may be added. Combination therapy with a COC and an antiandrogen generally is reserved for severe cases or patients who previously have shown suboptimal response to COCs alone.⁷ Patients should be counseled to discontinue antiandrogen therapy if they become pregnant due to the risk for fetal undervirilization observed in animal studies.^8,9 Typical dosing of spironolactone, a competitive inhibitor of 5-α-reductase and androgen receptors, ranges from 100 mg to 200 mg daily.¹⁰ Reported adverse effects include polyuria, postural hypotension, menstrual irregularities, hyperkalemia, and potential liver dysfunction. Although spironolactone has demonstrated tumorigenic effects in animal studies, no such effects have been observed in humans.¹¹

Eflornithine hydrochloride cream 13.9% is the first topical prescription medication approved by the US Food and Drug Administration for reduction of unwanted facial hair in women.¹² It works by irreversibly blocking the activity of ornithine decarboxylase, an enzyme involved in the rate-limiting step of polyamine synthesis, which is essential for hair growth. In a randomized, double-blind clinical trial evaluating its effectiveness and safety, twice-daily application for 24 weeks resulted in a clinically meaningful reduction in hair length and density (measured as surface area) compared with the control group.¹³ When eflornithine hydrochloride cream 13.9% is discontinued, hair growth gradually returns to baseline. Studies have shown that hair regrowth typically begins within 8 weeks after treatment is stopped; within several months, hair returns to pretreatment levels.¹⁴ Adverse effects of eflornithine hydrochloride cream generally are mild and may include local irritation and acneform eruptions. In a randomized bilateral vehicle-controlled trial of 31 women, both eflornithine and vehicle creams were well tolerated, with 1 patient reporting mild tingling with eflornithine that resolved with continued use for 7 days.¹⁵

Procedural—Photoepilation therapies widely are considered by dermatologists to be among the most effective methods for reducing unwanted hair.¹⁶ Laser hair removal employs selective photothermolysis, a principle by which specific wavelengths of light target melanin in hair follicles. This method results in localized thermal damage, destroying hair follicles and reducing regrowth. Wavelengths between 600 and 1100 nm are most effective for hair removal; widely used devices include the ruby (694 nm), alexandrite (755 nm), diode (800-810 nm), and long-pulsed Nd:YAG lasers (1064 nm). Cooling mechanisms such as cryogen spray or contact cooling often are employed to minimize epidermal damage and lessen patient discomfort.

The hair matrix is most responsive to laser treatment during the anagen phase, necessitating multiple sessions to ensure all hairs are treated during this optimal growth stage. Generally, 4 to 6 sessions spaced at intervals of 4 to 6 weeks are required to achieve satisfactory results.¹⁷ Matching the laser wavelength to the absorption properties of melanin—the target chromophore—enables selective destruction of melanin-rich hair follicles while minimizing damage to surrounding skin.

The ideal laser wavelength primarily affects melanin concentrated in the hair bulb, leading to follicular destruction while reducing the risk for unintended depigmentation of the epidermis; however, competing structures in the skin (eg, epidermal pigment) also can absorb laser energy, diminishing treatment efficacy and increasing the risk for adverse effects. Shorter wavelengths are effective for lighter skin types, while longer wavelengths such as the Nd:YAG laser are safer for individuals with darker skin types as they bypass melanin in the epidermis.

It is important to note that laser hair removal is ineffective for white and gray hairs due to the lack of melanin. As a result, alternative methods such as electrolysis, which does not rely on pigment, may be more appropriate for permanent hair removal in individuals with nonpigmented hairs. Research indicates that combining topical eflornithine with alexandrite or Nd:YAG lasers improves outcomes for reducing unwanted facial hair.¹⁸

In military settings, laser hair removal is utilized for specific conditions such as PFB in male service members to assist with the reduction of hair and mitigation of symptoms.¹⁹ The majority of military dermatology clinics have devices for laser hair removal; however, dermatology services are not available at many military treatment facilities, and dermatologic care may be provided by the local civilian dermatologists. That said, laser therapy is covered in the civilian sector for active-duty service members with PFB of the face and neck under certain criteria. These include a documented safety risk in environments requiring respiratory protection, failure of conservative treatments, and evaluation by a military dermatologist who confirms the necessity of civilian-provided laser therapy when it is unavailable at a military facility.²⁰ While such policies demonstrate the military’s recognition of laser therapy as a viable solution for certain grooming-related conditions, many are unaware that the existing laser hair removal policy also applies to women. Increasing awareness of this coverage could help female service members access treatment options that align with both medical and professional grooming needs.

Intense pulsed light (IPL) systems are nonlaser devices that emit broad-spectrum light in the 590- to 1200-nm range. They utilize a flash lamp to achieve thermal damage. Filters are used to narrow the wavelength range based on the specific target. Intense pulsed light devices are less precise than lasers but remain effective for hair reduction. In addition to hair removal, IPL devices are employed in the treatment of pigmented and vascular lesions. Common adverse effects of both laser and IPL hair removal include transient erythema, perifollicular edema, and pigmentary changes, especially in patients with darker skin types. Rare complications include blistering, scarring, and paradoxical hair stimulation in which untreated areas develop increased hair growth.

Electrolysis is recognized as the only method of truly permanent hair removal and is effective for all hair colors.²¹ However, the variability in technique among practitioners often leads to inconsistent results, with some patients experiencing hair regrowth. Galvanic electrolysis involves inserting a fine needle into the hair follicle and applying an electrical current to destroy the it and the rapidly dividing cells of the matrix.²² The introduction of thermolytic electrolysis, which uses a high-frequency alternating current (commonly 13.56 MHz or 27.12 MHz), has enhanced efficiency by creating heat at the needle tip to destroy the follicle. This approach is faster and now is commonly combined with galvanic electrolysis.²³ While no controlled clinical trials directly compare these methods, many patients experience permanent hair removal, with approximately 15% to 25% regrowth within 6 months.^22,24

Alternative Options—Home-use laser and light-based devices have become increasingly popular for managing unwanted hair due to their affordability and convenience, with most devices priced less than $1000.²⁵ These devices utilize various technologies, including lasers (808 nm), IPL, or combinations of IPL and radiofrequency.²⁶ Despite their accessibility, peer-reviewed research on their safety profile and effectiveness is limited, as existing data primarily come from industry-funded, uncontrolled studies with short follow-up durations—making it difficult to assess long-term outcomes.²⁵

Psychosocial Impact

A 2023 study of active-duty female service members with PCOS highlighted the unique challenges they face while managing symptoms such as facial hair within the constraints of military service.²⁷ Although the study focused on PCOS, the findings shed light on how facial hair specifically impacts the psychological well-being of servicewomen. Participants described facial hair as one of the most visible and stigmatizing symptoms, often leading to feelings of embarrassment and diminished confidence. Participants also highlighted the professional implications of facial hair, with some describing feelings of scrutiny and judgment from peers and leadership in public. These challenges can be more pronounced in deployments or field exercises where hygiene resources are limited. The lack of access not only affects self-perception but also can hinder the ability of servicewomen to meet implicit expectations for grooming and appearance.²⁷ There is a notable gap in research examining the impact of facial hair on military servicewomen. Given the unique environmental challenges and professional expectations, further investigation is warranted to better understand how facial hair affects women and to optimize treatment approaches in this population.

Final Thoughts

Limited awareness and understanding of facial hair in woman contribute to stigma, often leaving affected individuals to navigate challenges in isolation. Given the impact on confidence, professional appearance, and adherence to military grooming standards, it is essential for health care practitioners to recognize and address facial hair in women. Importantly, laser hair removal is covered by TRICARE for active-duty female service members with PFB, yet many remain unaware of this benefit. Increased awareness of available mechanical, pharmacologic, and procedural treatment options allows for tailored management, ensuring that women receive appropriate medical care.

Pediatric alopecia areata (AA) is a chronic autoimmune disease of the hair follicles characterized by nonscarring hair loss. Its incidence in children in the United States ranges from 13.6 to 33.5 per 100,000 person-years, with a prevalence of 0.04% to 0.11%.¹ Alopecia areata has important effects on quality of life, particularly in children. Hair loss at an early age can decrease participation in school, sports, and extracurricular activities² and is associated with increased rates of comorbid anxiety and depression.³ Families also experience psychosocial stress, often comparable to other chronic pediatric illnesses.⁴ Thus, management requires not only medical therapy but also psychosocial support and school-based accommodations.

Systemic therapies for treatment of AA in adolescents and adults are increasingly available, including US Food and Drug Administration (FDA)–approved Janus kinase (JAK) inhibitors such as baricitinib, deuruxolitinib (for adults), and ritlecitinib (for adolescents and adults); however, no systemic therapies have been approved by the FDA for children younger than 12 years. The therapeutic gap is most acute for those aged 6 to 11 years, for whom the psychosocial burden is high but treatment options are limited.³

This article highlights options and strategies for managing AA in children aged 6 to 11 years, emphasizing supportive and psychosocial care (including camouflage techniques), topical therapies, and off-label systemic approaches.

Supportive and Psychosocial Care

Treatment of AA in children extends beyond the affected child to include parents, caregivers, and even school staff (eg, teachers, principals, nurses).⁴ Disease-specific organizations such as the National Alopecia Areata Foundation ­(naaf.org) and the Children’s Alopecia Project (childrensalopeciaproject.org) provide ­education, support groups, and advocacy resources. These organizations assist families in navigating school accommodations, including Section 504 plans that may allow children with AA to wear hats in school to mitigate stigma. Additional resources include handouts for teachers and school nurses developed by the Society for Pediatric Dermatology.⁵

Psychological support for these patients is critical. Many children benefit from seeing a psychologist, particularly if anxiety, depression, and/or bullying is present.³ In clinics without embedded psychology services, dermatologists should maintain referral lists or encourage families to seek guidance from their pediatrician.

Camouflage techniques can help children cope with visible hair loss. Wigs and hairpieces are available free of charge through charitable organizations for patients younger than 17; however, young children often find adhesives uncomfortable, and they will not wear nonadherent wigs for long periods of time. Alternatives include soft hats, bonnets, scarves, and beanies. For partial hair loss, root concealers, scalp powders, or hair mascara can be useful. Temporary eyebrow tattoos are a good cosmetic approach, whereas microblading generally is not advised in children younger than 12 due to procedural risks including pain.

Topical Therapies

Topical agents remain the mainstay of treatment for AA in children aged 6 to 11 years. Potent class 1 or class 2 topical corticosteroids commonly are used, sometimes in combination with calcineurin inhibitors or topical minoxidil. Off-label compounded topical JAK inhibitors also have been tried in this population and may be helpful for eyebrow hair loss,⁶ though data on their efficacy for scalp AA are mixed.⁷ Intralesional corticosteroid injections, effective in adolescents and adults, generally are poorly tolerated by younger children and may cause considerable distress. Contact immunotherapy with squaric acid dibutyl ester or anthralin can be considered, but these agents are designed to elicit irritation, which may be intolerable for young children.⁸ Shared decision-making with families is essential to balance efficacy, tolerability, and treatment burden.

Systemic Therapies

Systemic therapy generally is reserved for children with extensive or refractory AA. Low-dose oral minoxidil is emerging as an off-label option. One systematic review reported that low-dose oral minoxidil was well tolerated in pediatric patients with minimal adverse effects.⁹ Doses of 0.01 to 0.02 mg/kg/d are reasonable starting points, achieved by cutting tablets or compounding oral solutions.¹⁰

In children with AA and concurrent atopic dermatitis, dupilumab may offer dual benefit. A real-world observational study demonstrated hair regrowth in pediatric patients with AA treated with dupilumab.¹¹ Immunosuppressive options such as low-dose methotrexate or pulse corticosteroids (dexamethasone or prednisolone) also may be considered, although use of these agents requires careful monitoring due to increased risk for infection, clinically significant blood count and liver enzyme changes, and metabolic adverse effects related to long-term use of corticosteroids.

Clinical trials of JAK inhibitors in children aged 6 to 11 years are anticipated to begin in late 2025. Until then, off-label use of ritlecitinib, baricitinib, tofacitinib, or other JAK inhibitors may be considered in select cases with considerable disease burden and quality-of-life impairment following thorough discussion with the patient and their caregivers. Currently available pediatric data show few serious adverse events in children—the most common included upper respiratory infections (nasopharyngitis), acne, and headaches—but long-term risks remain unknown. Dosing challenges also exist for children who cannot swallow pills; currently ritlecitinib is available only as a capsule that cannot be opened while other JAK inhibitors are available in more accessible forms (baricitinib can be crushed and dissolved, and tofacitinib is available in liquid formulation for other pediatric indications). Insurance coverage is a major barrier, as these therapies are not FDA approved for AA in this age group.

Final Thoughts

Alopecia areata in children aged 6 to 11 years presents unique therapeutic challenges. While highly effective systemic therapies exist for older patients, younger children have limited options. For the 6-to-11 age group, management strategies should prioritize psychosocial support, topical therapy, and low-burden systemic alternatives such as low-dose oral minoxidil. Family education, school-based accommodations, and access to camouflage techniques are integral to holistic care. The commencement of pediatric clinical trials for JAK inhibitors offers hope for more robust treatment strategies in the near future. In the meantime, clinicians must engage in shared decision-making, tailoring therapy to the child’s disease severity, emotional well-being, and family priorities.

Pediatric alopecia areata (AA) is a chronic autoimmune disease of the hair follicles characterized by nonscarring hair loss. Its incidence in children in the United States ranges from 13.6 to 33.5 per 100,000 person-years, with a prevalence of 0.04% to 0.11%.¹ Alopecia areata has important effects on quality of life, particularly in children. Hair loss at an early age can decrease participation in school, sports, and extracurricular activities² and is associated with increased rates of comorbid anxiety and depression.³ Families also experience psychosocial stress, often comparable to other chronic pediatric illnesses.⁴ Thus, management requires not only medical therapy but also psychosocial support and school-based accommodations.

Systemic therapies for treatment of AA in adolescents and adults are increasingly available, including US Food and Drug Administration (FDA)–approved Janus kinase (JAK) inhibitors such as baricitinib, deuruxolitinib (for adults), and ritlecitinib (for adolescents and adults); however, no systemic therapies have been approved by the FDA for children younger than 12 years. The therapeutic gap is most acute for those aged 6 to 11 years, for whom the psychosocial burden is high but treatment options are limited.³

This article highlights options and strategies for managing AA in children aged 6 to 11 years, emphasizing supportive and psychosocial care (including camouflage techniques), topical therapies, and off-label systemic approaches.

Supportive and Psychosocial Care

Treatment of AA in children extends beyond the affected child to include parents, caregivers, and even school staff (eg, teachers, principals, nurses).⁴ Disease-specific organizations such as the National Alopecia Areata Foundation ­(naaf.org) and the Children’s Alopecia Project (childrensalopeciaproject.org) provide ­education, support groups, and advocacy resources. These organizations assist families in navigating school accommodations, including Section 504 plans that may allow children with AA to wear hats in school to mitigate stigma. Additional resources include handouts for teachers and school nurses developed by the Society for Pediatric Dermatology.⁵

Psychological support for these patients is critical. Many children benefit from seeing a psychologist, particularly if anxiety, depression, and/or bullying is present.³ In clinics without embedded psychology services, dermatologists should maintain referral lists or encourage families to seek guidance from their pediatrician.

Camouflage techniques can help children cope with visible hair loss. Wigs and hairpieces are available free of charge through charitable organizations for patients younger than 17; however, young children often find adhesives uncomfortable, and they will not wear nonadherent wigs for long periods of time. Alternatives include soft hats, bonnets, scarves, and beanies. For partial hair loss, root concealers, scalp powders, or hair mascara can be useful. Temporary eyebrow tattoos are a good cosmetic approach, whereas microblading generally is not advised in children younger than 12 due to procedural risks including pain.

Topical Therapies

Topical agents remain the mainstay of treatment for AA in children aged 6 to 11 years. Potent class 1 or class 2 topical corticosteroids commonly are used, sometimes in combination with calcineurin inhibitors or topical minoxidil. Off-label compounded topical JAK inhibitors also have been tried in this population and may be helpful for eyebrow hair loss,⁶ though data on their efficacy for scalp AA are mixed.⁷ Intralesional corticosteroid injections, effective in adolescents and adults, generally are poorly tolerated by younger children and may cause considerable distress. Contact immunotherapy with squaric acid dibutyl ester or anthralin can be considered, but these agents are designed to elicit irritation, which may be intolerable for young children.⁸ Shared decision-making with families is essential to balance efficacy, tolerability, and treatment burden.

Systemic Therapies

Systemic therapy generally is reserved for children with extensive or refractory AA. Low-dose oral minoxidil is emerging as an off-label option. One systematic review reported that low-dose oral minoxidil was well tolerated in pediatric patients with minimal adverse effects.⁹ Doses of 0.01 to 0.02 mg/kg/d are reasonable starting points, achieved by cutting tablets or compounding oral solutions.¹⁰

In children with AA and concurrent atopic dermatitis, dupilumab may offer dual benefit. A real-world observational study demonstrated hair regrowth in pediatric patients with AA treated with dupilumab.¹¹ Immunosuppressive options such as low-dose methotrexate or pulse corticosteroids (dexamethasone or prednisolone) also may be considered, although use of these agents requires careful monitoring due to increased risk for infection, clinically significant blood count and liver enzyme changes, and metabolic adverse effects related to long-term use of corticosteroids.

Clinical trials of JAK inhibitors in children aged 6 to 11 years are anticipated to begin in late 2025. Until then, off-label use of ritlecitinib, baricitinib, tofacitinib, or other JAK inhibitors may be considered in select cases with considerable disease burden and quality-of-life impairment following thorough discussion with the patient and their caregivers. Currently available pediatric data show few serious adverse events in children—the most common included upper respiratory infections (nasopharyngitis), acne, and headaches—but long-term risks remain unknown. Dosing challenges also exist for children who cannot swallow pills; currently ritlecitinib is available only as a capsule that cannot be opened while other JAK inhibitors are available in more accessible forms (baricitinib can be crushed and dissolved, and tofacitinib is available in liquid formulation for other pediatric indications). Insurance coverage is a major barrier, as these therapies are not FDA approved for AA in this age group.

Final Thoughts

Alopecia areata in children aged 6 to 11 years presents unique therapeutic challenges. While highly effective systemic therapies exist for older patients, younger children have limited options. For the 6-to-11 age group, management strategies should prioritize psychosocial support, topical therapy, and low-burden systemic alternatives such as low-dose oral minoxidil. Family education, school-based accommodations, and access to camouflage techniques are integral to holistic care. The commencement of pediatric clinical trials for JAK inhibitors offers hope for more robust treatment strategies in the near future. In the meantime, clinicians must engage in shared decision-making, tailoring therapy to the child’s disease severity, emotional well-being, and family priorities.

Pediatric alopecia areata (AA) is a chronic autoimmune disease of the hair follicles characterized by nonscarring hair loss. Its incidence in children in the United States ranges from 13.6 to 33.5 per 100,000 person-years, with a prevalence of 0.04% to 0.11%.¹ Alopecia areata has important effects on quality of life, particularly in children. Hair loss at an early age can decrease participation in school, sports, and extracurricular activities² and is associated with increased rates of comorbid anxiety and depression.³ Families also experience psychosocial stress, often comparable to other chronic pediatric illnesses.⁴ Thus, management requires not only medical therapy but also psychosocial support and school-based accommodations.

Systemic therapies for treatment of AA in adolescents and adults are increasingly available, including US Food and Drug Administration (FDA)–approved Janus kinase (JAK) inhibitors such as baricitinib, deuruxolitinib (for adults), and ritlecitinib (for adolescents and adults); however, no systemic therapies have been approved by the FDA for children younger than 12 years. The therapeutic gap is most acute for those aged 6 to 11 years, for whom the psychosocial burden is high but treatment options are limited.³

This article highlights options and strategies for managing AA in children aged 6 to 11 years, emphasizing supportive and psychosocial care (including camouflage techniques), topical therapies, and off-label systemic approaches.

Supportive and Psychosocial Care

Treatment of AA in children extends beyond the affected child to include parents, caregivers, and even school staff (eg, teachers, principals, nurses).⁴ Disease-specific organizations such as the National Alopecia Areata Foundation ­(naaf.org) and the Children’s Alopecia Project (childrensalopeciaproject.org) provide ­education, support groups, and advocacy resources. These organizations assist families in navigating school accommodations, including Section 504 plans that may allow children with AA to wear hats in school to mitigate stigma. Additional resources include handouts for teachers and school nurses developed by the Society for Pediatric Dermatology.⁵

Psychological support for these patients is critical. Many children benefit from seeing a psychologist, particularly if anxiety, depression, and/or bullying is present.³ In clinics without embedded psychology services, dermatologists should maintain referral lists or encourage families to seek guidance from their pediatrician.

Camouflage techniques can help children cope with visible hair loss. Wigs and hairpieces are available free of charge through charitable organizations for patients younger than 17; however, young children often find adhesives uncomfortable, and they will not wear nonadherent wigs for long periods of time. Alternatives include soft hats, bonnets, scarves, and beanies. For partial hair loss, root concealers, scalp powders, or hair mascara can be useful. Temporary eyebrow tattoos are a good cosmetic approach, whereas microblading generally is not advised in children younger than 12 due to procedural risks including pain.

Topical Therapies

Topical agents remain the mainstay of treatment for AA in children aged 6 to 11 years. Potent class 1 or class 2 topical corticosteroids commonly are used, sometimes in combination with calcineurin inhibitors or topical minoxidil. Off-label compounded topical JAK inhibitors also have been tried in this population and may be helpful for eyebrow hair loss,⁶ though data on their efficacy for scalp AA are mixed.⁷ Intralesional corticosteroid injections, effective in adolescents and adults, generally are poorly tolerated by younger children and may cause considerable distress. Contact immunotherapy with squaric acid dibutyl ester or anthralin can be considered, but these agents are designed to elicit irritation, which may be intolerable for young children.⁸ Shared decision-making with families is essential to balance efficacy, tolerability, and treatment burden.

Systemic Therapies

Systemic therapy generally is reserved for children with extensive or refractory AA. Low-dose oral minoxidil is emerging as an off-label option. One systematic review reported that low-dose oral minoxidil was well tolerated in pediatric patients with minimal adverse effects.⁹ Doses of 0.01 to 0.02 mg/kg/d are reasonable starting points, achieved by cutting tablets or compounding oral solutions.¹⁰

In children with AA and concurrent atopic dermatitis, dupilumab may offer dual benefit. A real-world observational study demonstrated hair regrowth in pediatric patients with AA treated with dupilumab.¹¹ Immunosuppressive options such as low-dose methotrexate or pulse corticosteroids (dexamethasone or prednisolone) also may be considered, although use of these agents requires careful monitoring due to increased risk for infection, clinically significant blood count and liver enzyme changes, and metabolic adverse effects related to long-term use of corticosteroids.

Clinical trials of JAK inhibitors in children aged 6 to 11 years are anticipated to begin in late 2025. Until then, off-label use of ritlecitinib, baricitinib, tofacitinib, or other JAK inhibitors may be considered in select cases with considerable disease burden and quality-of-life impairment following thorough discussion with the patient and their caregivers. Currently available pediatric data show few serious adverse events in children—the most common included upper respiratory infections (nasopharyngitis), acne, and headaches—but long-term risks remain unknown. Dosing challenges also exist for children who cannot swallow pills; currently ritlecitinib is available only as a capsule that cannot be opened while other JAK inhibitors are available in more accessible forms (baricitinib can be crushed and dissolved, and tofacitinib is available in liquid formulation for other pediatric indications). Insurance coverage is a major barrier, as these therapies are not FDA approved for AA in this age group.

Final Thoughts

Alopecia areata in children aged 6 to 11 years presents unique therapeutic challenges. While highly effective systemic therapies exist for older patients, younger children have limited options. For the 6-to-11 age group, management strategies should prioritize psychosocial support, topical therapy, and low-burden systemic alternatives such as low-dose oral minoxidil. Family education, school-based accommodations, and access to camouflage techniques are integral to holistic care. The commencement of pediatric clinical trials for JAK inhibitors offers hope for more robust treatment strategies in the near future. In the meantime, clinicians must engage in shared decision-making, tailoring therapy to the child’s disease severity, emotional well-being, and family priorities.

Synthetic hair extensions are made from various plastic polymers (eg, modacrylic, vinyl chloride, and acrylonitrile) shaped into thin strands that mimic human hair and are used to add fullness, length, and manageability in individuals with textured hair.^1-3 The plastic polymers used to make synthetic hair, most notably acrylonitrile and vinyl chloride, are known to be toxic to humans.^1-4 The US Environmental Protection Agency classifies acrylonitrile as a probable carcinogen, and vinyl chloride is associated with the development of lymphoma; leukemia; and rare malignancies of the brain, liver, and lungs.^1,4 According to the Occupational Safety and Health Administration, the maximum exposure limits of vinyl chloride and acrylonitrile vapor or gas over an 8-hour period are 1 ppm (0.001 g/L) and 2 ppm (0.002 g/L), respectively.⁵ Exposure levels from wearing synthetic hair extensions easily exceed these maximums; for example, a full head of braids requires application of multiple packets of synthetic hair, resulting in continuous exposure to carcinogenic materials that can last for weeks to months at a time.¹ Furthermore, individuals as young as 3 years old can begin to style their hair with synthetic extensions, which not only leads to potentially harmful carcinogenic exposure in young children but also yields notably high levels of lifetime exposure in individuals who regularly style their hair with these products.

There currently are no regulations barring the use of potentially harmful materials from the manufacturing process for synthetic hair extensions.¹ As a result, rinsing with apple cider vinegar (ACV) is a popular remedy that many users claim can effectively remove harmful chemicals from synthetic hair.^6,7 As this is the only known remedy that aims to address this issue, we conducted a literature review of studies investigating the effects of the ACV rinse on the carcinogenicity of synthetic hair extensions.

Methods

We conducted a search of Google Scholar, JSTOR, Science Direct, the Public Library of Science, and PubMed articles indexed for MEDLINE using the terms ACV, apple cider vinegar rinse, ACV rinse, synthetic hair carcinogens, synthetic fiber carcinogens, synthetic hair extension carcinogens, modacrylic fibers, Kanekalon (a flame-retardant modacrylic fiber), acrylonitrile, and vinyl chloride fibers to identify primary research articles investigating the effects of the ACV rinse on the carcinogenicity of synthetic hair extensions for inclusion in our review. To broaden our search, we did not establish a time frame for publication of the articles included in the study. Articles investigating the ACV rinse that were unrelated to carcinogenicity and synthetic hair extensions were excluded from this study.

Results

Our initial literature search identified 270 articles, which decreased to 180 after removal of duplicates. These 180 articles were screened for relevance based on title and abstract, which yielded 6 articles. None of the 6 articles identified through our literature search discussed synthetic hair and carcinogenicity in the context of the ACV rinse and were subsequently excluded from our review (eFigure 1).

Comment

Potentially harmful chemicals and ingredients in hair care products marketed for textured hair are now established topics in public discourse among those familiar with textured hair care and maintenance^1,8; however, the discourse remains limited. Our search for scientific articles investigating the effects of the ACV rinse on the carcinogenicity of synthetic hair extensions revealed a notable deficit in the literature regarding scientific studies assessing this practice. While the likelihood that the ACV rinse effectively alters the carcinogenicity of plastic polymers found in synthetic hair extensions and improves their safety seems improbable, the deficit of empirical data evaluating this practice is concerning given both the prevalence of this remedy and the sizable demographic of patients who practice styling with synthetic hair.¹ Of the potential adverse outcomes (eg, contact dermatitis, traction alopecia) that are possible from styling with synthetic hair that have been reported in the literature, carcinogenic exposure from synthetic hair extensions is relatively absent, with the exception of a few publications,^2,3,9 despite its potential to cause serious long-term consequences for hair stylists and those who regularly use these products.

Interestingly, individuals who style their hair with synthetic hair extensions frequently tout the efficacy of the ACV rinse for removal of mostly unidentified irritants, although the effects are unverified.^6,7 While the ACV rinse may be an effective means of removing toxic chemicals from synthetic hair extensions, without verifiable data this method remains an unproven remedy whose perceived benefits could result from factors unrelated to the rinse itself. Theoretically, simply rinsing synthetic hair extensions with plain water prior to use may demonstrate similar efficacy to that of the ACV rinse. 

An additional factor worth mentioning is the lack of government regulations concerning the manufacturing practices of synthetic hair extensions. Flame-retardant materials such as trichloroethylene, polyvinyl chloride, and hexabromocyclododecane frequently are used in synthetic hair extensions despite their known adverse effects, which include reproductive organ toxicity and links to various cancers, leading to them being banned in 5 states.^1,10-12 With no federal ban on these materials, individuals using synthetic hair remain at risk.  

It is unclear what chemicals, irritants, or toxic substances the ACV rinse method could potentially remove from synthetic hair. In general, manufacturers of synthetic hair extensions are not forthcoming with information regarding materials used in the processing of their products despite public inquiries into their manufacturing practices.⁶ Although Whitehurst’s³ curriculum details the process of making synthetic polymer fibers, the overall processes by which these plastics are made to resemble human hair have not been reviewed in academic publications. Should this information be made available to the public, consumers could potentially avoid specific irritants when purchasing synthetic hair extensions.   

The most common management strategy observed in the literature for adverse outcomes attributable to synthetic hair is discontinuation of use²; however, the prevalence and cultural significance of styling with synthetic hair extensions, along with the convenience these styles offer, make this option suboptimal. The scarcity of publications concerning the management of adverse outcomes related to the use of synthetic hair extensions may explain the absence of alternative management recommendations in the literature. Notably, new synthetic hair extensions from manufacturers that exclude plastic polymers and other harmful additives are now available to the public¹³; however, these hair extensions are cost prohibitive and are less accessible compared to synthetic extensions made from modacrylic fibers (eFigures 2 and 3).^1,13-16 

Final Thoughts

The ACV rinse method is an anecdotal remedy for reducing the harm and risk of adverse outcomes and complications associated with synthetic hair extensions. Discontinued use of these components is the only remedy provided within academic literature to address the harmful ingredients found in synthetic hair extensions.² Presently, there are no known data that support or disprove the efficacy of the ACV rinse. Furthermore, no academic guidance specifically supports remedies for mitigating carcinogen exposure risks in patients who style their hair with synthetic extensions. Given the early onset of exposure to synthetic hair in pediatric populations and the substantial demographic utilizing hairstyles that incorporate synthetic hair extensions, concerns regarding potential exposure risks cannot be overstated. Dermatologists should inform their patients of the potential risks associated with styling with synthetic hair extensions, helping them make informed decisions about future styling habits and hair care choices. Lastly, future studies should investigate how, if at all, ACV rinses alter what are arguably the most harmful components of synthetic hair extensions.

Synthetic hair extensions are made from various plastic polymers (eg, modacrylic, vinyl chloride, and acrylonitrile) shaped into thin strands that mimic human hair and are used to add fullness, length, and manageability in individuals with textured hair.^1-3 The plastic polymers used to make synthetic hair, most notably acrylonitrile and vinyl chloride, are known to be toxic to humans.^1-4 The US Environmental Protection Agency classifies acrylonitrile as a probable carcinogen, and vinyl chloride is associated with the development of lymphoma; leukemia; and rare malignancies of the brain, liver, and lungs.^1,4 According to the Occupational Safety and Health Administration, the maximum exposure limits of vinyl chloride and acrylonitrile vapor or gas over an 8-hour period are 1 ppm (0.001 g/L) and 2 ppm (0.002 g/L), respectively.⁵ Exposure levels from wearing synthetic hair extensions easily exceed these maximums; for example, a full head of braids requires application of multiple packets of synthetic hair, resulting in continuous exposure to carcinogenic materials that can last for weeks to months at a time.¹ Furthermore, individuals as young as 3 years old can begin to style their hair with synthetic extensions, which not only leads to potentially harmful carcinogenic exposure in young children but also yields notably high levels of lifetime exposure in individuals who regularly style their hair with these products.

There currently are no regulations barring the use of potentially harmful materials from the manufacturing process for synthetic hair extensions.¹ As a result, rinsing with apple cider vinegar (ACV) is a popular remedy that many users claim can effectively remove harmful chemicals from synthetic hair.^6,7 As this is the only known remedy that aims to address this issue, we conducted a literature review of studies investigating the effects of the ACV rinse on the carcinogenicity of synthetic hair extensions.

Methods

We conducted a search of Google Scholar, JSTOR, Science Direct, the Public Library of Science, and PubMed articles indexed for MEDLINE using the terms ACV, apple cider vinegar rinse, ACV rinse, synthetic hair carcinogens, synthetic fiber carcinogens, synthetic hair extension carcinogens, modacrylic fibers, Kanekalon (a flame-retardant modacrylic fiber), acrylonitrile, and vinyl chloride fibers to identify primary research articles investigating the effects of the ACV rinse on the carcinogenicity of synthetic hair extensions for inclusion in our review. To broaden our search, we did not establish a time frame for publication of the articles included in the study. Articles investigating the ACV rinse that were unrelated to carcinogenicity and synthetic hair extensions were excluded from this study.

Results

Our initial literature search identified 270 articles, which decreased to 180 after removal of duplicates. These 180 articles were screened for relevance based on title and abstract, which yielded 6 articles. None of the 6 articles identified through our literature search discussed synthetic hair and carcinogenicity in the context of the ACV rinse and were subsequently excluded from our review (eFigure 1).

Comment

Potentially harmful chemicals and ingredients in hair care products marketed for textured hair are now established topics in public discourse among those familiar with textured hair care and maintenance^1,8; however, the discourse remains limited. Our search for scientific articles investigating the effects of the ACV rinse on the carcinogenicity of synthetic hair extensions revealed a notable deficit in the literature regarding scientific studies assessing this practice. While the likelihood that the ACV rinse effectively alters the carcinogenicity of plastic polymers found in synthetic hair extensions and improves their safety seems improbable, the deficit of empirical data evaluating this practice is concerning given both the prevalence of this remedy and the sizable demographic of patients who practice styling with synthetic hair.¹ Of the potential adverse outcomes (eg, contact dermatitis, traction alopecia) that are possible from styling with synthetic hair that have been reported in the literature, carcinogenic exposure from synthetic hair extensions is relatively absent, with the exception of a few publications,^2,3,9 despite its potential to cause serious long-term consequences for hair stylists and those who regularly use these products.

Interestingly, individuals who style their hair with synthetic hair extensions frequently tout the efficacy of the ACV rinse for removal of mostly unidentified irritants, although the effects are unverified.^6,7 While the ACV rinse may be an effective means of removing toxic chemicals from synthetic hair extensions, without verifiable data this method remains an unproven remedy whose perceived benefits could result from factors unrelated to the rinse itself. Theoretically, simply rinsing synthetic hair extensions with plain water prior to use may demonstrate similar efficacy to that of the ACV rinse. 

An additional factor worth mentioning is the lack of government regulations concerning the manufacturing practices of synthetic hair extensions. Flame-retardant materials such as trichloroethylene, polyvinyl chloride, and hexabromocyclododecane frequently are used in synthetic hair extensions despite their known adverse effects, which include reproductive organ toxicity and links to various cancers, leading to them being banned in 5 states.^1,10-12 With no federal ban on these materials, individuals using synthetic hair remain at risk.  

It is unclear what chemicals, irritants, or toxic substances the ACV rinse method could potentially remove from synthetic hair. In general, manufacturers of synthetic hair extensions are not forthcoming with information regarding materials used in the processing of their products despite public inquiries into their manufacturing practices.⁶ Although Whitehurst’s³ curriculum details the process of making synthetic polymer fibers, the overall processes by which these plastics are made to resemble human hair have not been reviewed in academic publications. Should this information be made available to the public, consumers could potentially avoid specific irritants when purchasing synthetic hair extensions.   

The most common management strategy observed in the literature for adverse outcomes attributable to synthetic hair is discontinuation of use²; however, the prevalence and cultural significance of styling with synthetic hair extensions, along with the convenience these styles offer, make this option suboptimal. The scarcity of publications concerning the management of adverse outcomes related to the use of synthetic hair extensions may explain the absence of alternative management recommendations in the literature. Notably, new synthetic hair extensions from manufacturers that exclude plastic polymers and other harmful additives are now available to the public¹³; however, these hair extensions are cost prohibitive and are less accessible compared to synthetic extensions made from modacrylic fibers (eFigures 2 and 3).^1,13-16 

Final Thoughts

The ACV rinse method is an anecdotal remedy for reducing the harm and risk of adverse outcomes and complications associated with synthetic hair extensions. Discontinued use of these components is the only remedy provided within academic literature to address the harmful ingredients found in synthetic hair extensions.² Presently, there are no known data that support or disprove the efficacy of the ACV rinse. Furthermore, no academic guidance specifically supports remedies for mitigating carcinogen exposure risks in patients who style their hair with synthetic extensions. Given the early onset of exposure to synthetic hair in pediatric populations and the substantial demographic utilizing hairstyles that incorporate synthetic hair extensions, concerns regarding potential exposure risks cannot be overstated. Dermatologists should inform their patients of the potential risks associated with styling with synthetic hair extensions, helping them make informed decisions about future styling habits and hair care choices. Lastly, future studies should investigate how, if at all, ACV rinses alter what are arguably the most harmful components of synthetic hair extensions.

Synthetic hair extensions are made from various plastic polymers (eg, modacrylic, vinyl chloride, and acrylonitrile) shaped into thin strands that mimic human hair and are used to add fullness, length, and manageability in individuals with textured hair.^1-3 The plastic polymers used to make synthetic hair, most notably acrylonitrile and vinyl chloride, are known to be toxic to humans.^1-4 The US Environmental Protection Agency classifies acrylonitrile as a probable carcinogen, and vinyl chloride is associated with the development of lymphoma; leukemia; and rare malignancies of the brain, liver, and lungs.^1,4 According to the Occupational Safety and Health Administration, the maximum exposure limits of vinyl chloride and acrylonitrile vapor or gas over an 8-hour period are 1 ppm (0.001 g/L) and 2 ppm (0.002 g/L), respectively.⁵ Exposure levels from wearing synthetic hair extensions easily exceed these maximums; for example, a full head of braids requires application of multiple packets of synthetic hair, resulting in continuous exposure to carcinogenic materials that can last for weeks to months at a time.¹ Furthermore, individuals as young as 3 years old can begin to style their hair with synthetic extensions, which not only leads to potentially harmful carcinogenic exposure in young children but also yields notably high levels of lifetime exposure in individuals who regularly style their hair with these products.

There currently are no regulations barring the use of potentially harmful materials from the manufacturing process for synthetic hair extensions.¹ As a result, rinsing with apple cider vinegar (ACV) is a popular remedy that many users claim can effectively remove harmful chemicals from synthetic hair.^6,7 As this is the only known remedy that aims to address this issue, we conducted a literature review of studies investigating the effects of the ACV rinse on the carcinogenicity of synthetic hair extensions.

Methods

We conducted a search of Google Scholar, JSTOR, Science Direct, the Public Library of Science, and PubMed articles indexed for MEDLINE using the terms ACV, apple cider vinegar rinse, ACV rinse, synthetic hair carcinogens, synthetic fiber carcinogens, synthetic hair extension carcinogens, modacrylic fibers, Kanekalon (a flame-retardant modacrylic fiber), acrylonitrile, and vinyl chloride fibers to identify primary research articles investigating the effects of the ACV rinse on the carcinogenicity of synthetic hair extensions for inclusion in our review. To broaden our search, we did not establish a time frame for publication of the articles included in the study. Articles investigating the ACV rinse that were unrelated to carcinogenicity and synthetic hair extensions were excluded from this study.

Results

Our initial literature search identified 270 articles, which decreased to 180 after removal of duplicates. These 180 articles were screened for relevance based on title and abstract, which yielded 6 articles. None of the 6 articles identified through our literature search discussed synthetic hair and carcinogenicity in the context of the ACV rinse and were subsequently excluded from our review (eFigure 1).

Comment

Potentially harmful chemicals and ingredients in hair care products marketed for textured hair are now established topics in public discourse among those familiar with textured hair care and maintenance^1,8; however, the discourse remains limited. Our search for scientific articles investigating the effects of the ACV rinse on the carcinogenicity of synthetic hair extensions revealed a notable deficit in the literature regarding scientific studies assessing this practice. While the likelihood that the ACV rinse effectively alters the carcinogenicity of plastic polymers found in synthetic hair extensions and improves their safety seems improbable, the deficit of empirical data evaluating this practice is concerning given both the prevalence of this remedy and the sizable demographic of patients who practice styling with synthetic hair.¹ Of the potential adverse outcomes (eg, contact dermatitis, traction alopecia) that are possible from styling with synthetic hair that have been reported in the literature, carcinogenic exposure from synthetic hair extensions is relatively absent, with the exception of a few publications,^2,3,9 despite its potential to cause serious long-term consequences for hair stylists and those who regularly use these products.

Interestingly, individuals who style their hair with synthetic hair extensions frequently tout the efficacy of the ACV rinse for removal of mostly unidentified irritants, although the effects are unverified.^6,7 While the ACV rinse may be an effective means of removing toxic chemicals from synthetic hair extensions, without verifiable data this method remains an unproven remedy whose perceived benefits could result from factors unrelated to the rinse itself. Theoretically, simply rinsing synthetic hair extensions with plain water prior to use may demonstrate similar efficacy to that of the ACV rinse. 

An additional factor worth mentioning is the lack of government regulations concerning the manufacturing practices of synthetic hair extensions. Flame-retardant materials such as trichloroethylene, polyvinyl chloride, and hexabromocyclododecane frequently are used in synthetic hair extensions despite their known adverse effects, which include reproductive organ toxicity and links to various cancers, leading to them being banned in 5 states.^1,10-12 With no federal ban on these materials, individuals using synthetic hair remain at risk.  

It is unclear what chemicals, irritants, or toxic substances the ACV rinse method could potentially remove from synthetic hair. In general, manufacturers of synthetic hair extensions are not forthcoming with information regarding materials used in the processing of their products despite public inquiries into their manufacturing practices.⁶ Although Whitehurst’s³ curriculum details the process of making synthetic polymer fibers, the overall processes by which these plastics are made to resemble human hair have not been reviewed in academic publications. Should this information be made available to the public, consumers could potentially avoid specific irritants when purchasing synthetic hair extensions.   

The most common management strategy observed in the literature for adverse outcomes attributable to synthetic hair is discontinuation of use²; however, the prevalence and cultural significance of styling with synthetic hair extensions, along with the convenience these styles offer, make this option suboptimal. The scarcity of publications concerning the management of adverse outcomes related to the use of synthetic hair extensions may explain the absence of alternative management recommendations in the literature. Notably, new synthetic hair extensions from manufacturers that exclude plastic polymers and other harmful additives are now available to the public¹³; however, these hair extensions are cost prohibitive and are less accessible compared to synthetic extensions made from modacrylic fibers (eFigures 2 and 3).^1,13-16 

Final Thoughts

The ACV rinse method is an anecdotal remedy for reducing the harm and risk of adverse outcomes and complications associated with synthetic hair extensions. Discontinued use of these components is the only remedy provided within academic literature to address the harmful ingredients found in synthetic hair extensions.² Presently, there are no known data that support or disprove the efficacy of the ACV rinse. Furthermore, no academic guidance specifically supports remedies for mitigating carcinogen exposure risks in patients who style their hair with synthetic extensions. Given the early onset of exposure to synthetic hair in pediatric populations and the substantial demographic utilizing hairstyles that incorporate synthetic hair extensions, concerns regarding potential exposure risks cannot be overstated. Dermatologists should inform their patients of the potential risks associated with styling with synthetic hair extensions, helping them make informed decisions about future styling habits and hair care choices. Lastly, future studies should investigate how, if at all, ACV rinses alter what are arguably the most harmful components of synthetic hair extensions.

The Diagnosis: Glomangiomyoma

The nail unit excision specimen showed collections of cuboidal cells and spindled cells within the corium that were consistent with a diagnosis of a glomangiomyoma, a rare glomus tumor variant (Figure). Glomus tumors are benign neoplasms comprising glomus bodies, which are arteriovenous anastomoses involved in thermoregulation.¹ They develop in areas densely populated by glomus bodies, including the fingers, toes, and subungual areas. Glomus tumors most commonly develop in middle-aged women.² Clinically, they manifest with a characteristic triad of intense pain, point tenderness, and cold sensitivity and may appear as reddish-pink or blue macules under the nail plate and/or longitudinal erythronychia.^2-6 The presence of multiple glomus tumors is associated with neurofibromatosis type 1.⁷ 

Advanced imaging including ultrasonography and magnetic resonance imaging (MRI) may help confirm the diagnosis but may not be cost effective, as excision with histopathology is needed to relieve symptoms and render a definitive diagnosis. Radiography is highly insensitive in identifying bone erosions associated with glomus tumors.⁸ With ultrasonography, glomus tumors appear hypoechoic; with Doppler ultrasonography, they appear hypervascular. With MRI, glomus tumors appear as well-defined nodular lesions with hypointense signal intensity on T1-weighted sequence and hyperintense signal intensity on T2-weighted sequence, with strong enhancement using gadolinium-based contrast.^9,10 On histopathology, a glomus tumor appears as a nodular tumor with sheets of oval-nucleated cells arranged in multicellular layers surrounding blood vessels and are immunoreactive for α-smooth muscle actin, muscle-specific actin, and type IV collagen.^11,12 

There are several glomus tumor variants. The most common is a solid glomus tumor, which predominantly is composed of glomus cells, followed by glomangioma, which mainly is composed of blood vessels. Glomangiomyoma, which mostly is composed of smooth muscle cells, is the rarest variant.¹³ 

While glomus tumors are common in the subungual areas, it is an uncommon location for glomangiomyomas, which have been reported in the nail unit in only 7 prior case reports identified through searches of PubMed and Google Scholar using the terms glomangiomyoma, glomangiomyoma nail, and subungual glomangiomyoma (Table).^13-19 Glomangiomyomas more commonly are described in solid organs, including the stomach, kidney, pancreas, and bladder.¹⁶ The mean age of patients with subungual glomangiomyomas, including our patient, was 40.4 years (range, 3-61 years), with the majority being female (75.0% [6/8]). Most patients presented with fingernail involvement (75.0% [6/8]), nail dystrophy (eg, nail plate thinning, longitudinal grooves, splinter hemorrhages, longitudinal erythronychia)(62.5% [5/8]), and intermittent pain and/or point tenderness in the affected nail (75.0% [6/8]).^13-19 Notably, only our patient had longitudinal erythronychia as a clinical feature, and only one other case described MRI findings, which included a lobulated mass with intense contrast and distal phalanx destruction.¹⁸ One patient was a 3-year-old girl with a family history of generalized multiple glomangiomyomas. Although subungual glomangiomyoma was not confirmed on histopathology, the diagnosis in this patient was presumed based on her family history.¹³ On histopathology, glomangiomyomas are composed of oval-nucleated cells surrounding blood vessels. These oval-nucleated cells then gradually transition to smooth muscle cells.²⁰ 

A myxoid cyst is composed of a pseudocyst, which lacks a cyst lining, and is a result of synovial fluid from the distal interphalangeal joint entering the pseudocyst space.² It typically manifests with a longitudinal groove in the nail plate. A flesh-colored nodule may be appreciated between the cuticle and the distal interphalangeal joint.² The depth of the longitudinal groove may vary depending on the volume of synovial fluid within the myxoid cyst.²¹ In a series of 35 cases of subungual myxoid cysts, none manifested with longitudinal erythronychia. Due to their composition, myxoid cysts can be distinguished easily from solid tumors of the nail unit via transillumination.²² Pain is a much less common with myxoid cysts vs glomus tumors, as the filling of the pseudocyst space with synovial fluid typically is gradual, allowing the surrounding tissue to accommodate and adapt over time.²¹ In equivocal cases, MRI or high-resolution ultrasonography may be used to distinguish myxoid cysts and glomus tumors.⁸ Histopathology shows accumulation of mucin in the dermis with surrounding fibrous stroma.²³

Subungual neuromas are painful benign tumors that develop due to disorganized neural proliferation following disruption to peripheral nerves secondary to trauma or surgery. In 3 case reports, subungual neuromas manifested as painful subungual nodules, with proximal nail plate ridging, or onycholysis.^24-26 Since neuromas have only rarely been described in the subungual region, reports of MRI and ultrasonography findings are unknown. Histopathology is needed to distinguish neuromas from glomus tumors. Histopathology shows an acapsular structure consisting of disorganized spindle-cell proliferation and nerve fibers arranged in a tangle of fascicles within fibrotic tissue.²⁵ On immunochemistry, spindle cells typically are positive for cellular antigen protein S100.²⁶ 

Leiomyomas are benign neoplasms derived from smooth muscle, typically localized to the uterus or gastrointestinal tract, and have been described rarely in the nail unit.^27,28 It is hypothesized that subungual leiomyomas originate from the vascular smooth muscle in the subcutaneous layer of the nail unit.²⁸ Like glomus tumors, leiomyomas of the subungual region often manifest with pain and longitudinal erythronychia.^27-30 Subungual leiomyomas may be distinguished from glomus tumors via advanced imaging techniques, including ultrasonography and MRI. Cutaneous leiomyomas have been described with mild to moderate internal low flow vascularity on Doppler ultrasonography, while glomus tumors typically reveal high internal vascularity.²⁸ Biopsy with histopathology is needed for definitive diagnosis. On histopathology, leiomyomas demonstrate bland-appearing spindle-shaped cells with elongated nuclei arranged in fascicles.²⁷ They typically are positive for α-smooth muscle actin and caldesmon on immunostaining. 

Eccrine spiradenomas are benign adnexal tumors likely of apocrine origin with limited case reports in the literature.^31,32 Clinically, eccrine spiradenomas involving the nail unit may manifest with longitudinal nail splitting of the nail or as a papule on the proximal nail fold, with associated tenderness.^31,32 In a report of a 50-year-old woman with a histopathologically confirmed eccrine spiradenoma manifesting with longitudinal splitting of the nail and pain in the proximal nail fold, the mass appeared hypoechoic on ultrasonography with increased intramass vascularity on Doppler, while MRI showed an intensely enhancing lesion.³¹ These imaging features, combined with a classically manifesting feature of pain, make eccrine spiradenomas difficult to distinguish from glomus tumors; therefore, histopathologic examination can provide a definitive diagnosis, and surgical excision is used for treatment.³¹ On histopathology, these tumors are well circumscribed and composed of both small dark basaloid cells with peripheral compact nuclei and larger cells with central pale nuclei, which may be arranged in tubules.^31,32

The Diagnosis: Glomangiomyoma

The nail unit excision specimen showed collections of cuboidal cells and spindled cells within the corium that were consistent with a diagnosis of a glomangiomyoma, a rare glomus tumor variant (Figure). Glomus tumors are benign neoplasms comprising glomus bodies, which are arteriovenous anastomoses involved in thermoregulation.¹ They develop in areas densely populated by glomus bodies, including the fingers, toes, and subungual areas. Glomus tumors most commonly develop in middle-aged women.² Clinically, they manifest with a characteristic triad of intense pain, point tenderness, and cold sensitivity and may appear as reddish-pink or blue macules under the nail plate and/or longitudinal erythronychia.^2-6 The presence of multiple glomus tumors is associated with neurofibromatosis type 1.⁷ 

Advanced imaging including ultrasonography and magnetic resonance imaging (MRI) may help confirm the diagnosis but may not be cost effective, as excision with histopathology is needed to relieve symptoms and render a definitive diagnosis. Radiography is highly insensitive in identifying bone erosions associated with glomus tumors.⁸ With ultrasonography, glomus tumors appear hypoechoic; with Doppler ultrasonography, they appear hypervascular. With MRI, glomus tumors appear as well-defined nodular lesions with hypointense signal intensity on T1-weighted sequence and hyperintense signal intensity on T2-weighted sequence, with strong enhancement using gadolinium-based contrast.^9,10 On histopathology, a glomus tumor appears as a nodular tumor with sheets of oval-nucleated cells arranged in multicellular layers surrounding blood vessels and are immunoreactive for α-smooth muscle actin, muscle-specific actin, and type IV collagen.^11,12 

There are several glomus tumor variants. The most common is a solid glomus tumor, which predominantly is composed of glomus cells, followed by glomangioma, which mainly is composed of blood vessels. Glomangiomyoma, which mostly is composed of smooth muscle cells, is the rarest variant.¹³ 

While glomus tumors are common in the subungual areas, it is an uncommon location for glomangiomyomas, which have been reported in the nail unit in only 7 prior case reports identified through searches of PubMed and Google Scholar using the terms glomangiomyoma, glomangiomyoma nail, and subungual glomangiomyoma (Table).^13-19 Glomangiomyomas more commonly are described in solid organs, including the stomach, kidney, pancreas, and bladder.¹⁶ The mean age of patients with subungual glomangiomyomas, including our patient, was 40.4 years (range, 3-61 years), with the majority being female (75.0% [6/8]). Most patients presented with fingernail involvement (75.0% [6/8]), nail dystrophy (eg, nail plate thinning, longitudinal grooves, splinter hemorrhages, longitudinal erythronychia)(62.5% [5/8]), and intermittent pain and/or point tenderness in the affected nail (75.0% [6/8]).^13-19 Notably, only our patient had longitudinal erythronychia as a clinical feature, and only one other case described MRI findings, which included a lobulated mass with intense contrast and distal phalanx destruction.¹⁸ One patient was a 3-year-old girl with a family history of generalized multiple glomangiomyomas. Although subungual glomangiomyoma was not confirmed on histopathology, the diagnosis in this patient was presumed based on her family history.¹³ On histopathology, glomangiomyomas are composed of oval-nucleated cells surrounding blood vessels. These oval-nucleated cells then gradually transition to smooth muscle cells.²⁰ 

A myxoid cyst is composed of a pseudocyst, which lacks a cyst lining, and is a result of synovial fluid from the distal interphalangeal joint entering the pseudocyst space.² It typically manifests with a longitudinal groove in the nail plate. A flesh-colored nodule may be appreciated between the cuticle and the distal interphalangeal joint.² The depth of the longitudinal groove may vary depending on the volume of synovial fluid within the myxoid cyst.²¹ In a series of 35 cases of subungual myxoid cysts, none manifested with longitudinal erythronychia. Due to their composition, myxoid cysts can be distinguished easily from solid tumors of the nail unit via transillumination.²² Pain is a much less common with myxoid cysts vs glomus tumors, as the filling of the pseudocyst space with synovial fluid typically is gradual, allowing the surrounding tissue to accommodate and adapt over time.²¹ In equivocal cases, MRI or high-resolution ultrasonography may be used to distinguish myxoid cysts and glomus tumors.⁸ Histopathology shows accumulation of mucin in the dermis with surrounding fibrous stroma.²³

Subungual neuromas are painful benign tumors that develop due to disorganized neural proliferation following disruption to peripheral nerves secondary to trauma or surgery. In 3 case reports, subungual neuromas manifested as painful subungual nodules, with proximal nail plate ridging, or onycholysis.^24-26 Since neuromas have only rarely been described in the subungual region, reports of MRI and ultrasonography findings are unknown. Histopathology is needed to distinguish neuromas from glomus tumors. Histopathology shows an acapsular structure consisting of disorganized spindle-cell proliferation and nerve fibers arranged in a tangle of fascicles within fibrotic tissue.²⁵ On immunochemistry, spindle cells typically are positive for cellular antigen protein S100.²⁶ 

Leiomyomas are benign neoplasms derived from smooth muscle, typically localized to the uterus or gastrointestinal tract, and have been described rarely in the nail unit.^27,28 It is hypothesized that subungual leiomyomas originate from the vascular smooth muscle in the subcutaneous layer of the nail unit.²⁸ Like glomus tumors, leiomyomas of the subungual region often manifest with pain and longitudinal erythronychia.^27-30 Subungual leiomyomas may be distinguished from glomus tumors via advanced imaging techniques, including ultrasonography and MRI. Cutaneous leiomyomas have been described with mild to moderate internal low flow vascularity on Doppler ultrasonography, while glomus tumors typically reveal high internal vascularity.²⁸ Biopsy with histopathology is needed for definitive diagnosis. On histopathology, leiomyomas demonstrate bland-appearing spindle-shaped cells with elongated nuclei arranged in fascicles.²⁷ They typically are positive for α-smooth muscle actin and caldesmon on immunostaining. 

Eccrine spiradenomas are benign adnexal tumors likely of apocrine origin with limited case reports in the literature.^31,32 Clinically, eccrine spiradenomas involving the nail unit may manifest with longitudinal nail splitting of the nail or as a papule on the proximal nail fold, with associated tenderness.^31,32 In a report of a 50-year-old woman with a histopathologically confirmed eccrine spiradenoma manifesting with longitudinal splitting of the nail and pain in the proximal nail fold, the mass appeared hypoechoic on ultrasonography with increased intramass vascularity on Doppler, while MRI showed an intensely enhancing lesion.³¹ These imaging features, combined with a classically manifesting feature of pain, make eccrine spiradenomas difficult to distinguish from glomus tumors; therefore, histopathologic examination can provide a definitive diagnosis, and surgical excision is used for treatment.³¹ On histopathology, these tumors are well circumscribed and composed of both small dark basaloid cells with peripheral compact nuclei and larger cells with central pale nuclei, which may be arranged in tubules.^31,32

The Diagnosis: Glomangiomyoma

The nail unit excision specimen showed collections of cuboidal cells and spindled cells within the corium that were consistent with a diagnosis of a glomangiomyoma, a rare glomus tumor variant (Figure). Glomus tumors are benign neoplasms comprising glomus bodies, which are arteriovenous anastomoses involved in thermoregulation.¹ They develop in areas densely populated by glomus bodies, including the fingers, toes, and subungual areas. Glomus tumors most commonly develop in middle-aged women.² Clinically, they manifest with a characteristic triad of intense pain, point tenderness, and cold sensitivity and may appear as reddish-pink or blue macules under the nail plate and/or longitudinal erythronychia.^2-6 The presence of multiple glomus tumors is associated with neurofibromatosis type 1.⁷ 

Advanced imaging including ultrasonography and magnetic resonance imaging (MRI) may help confirm the diagnosis but may not be cost effective, as excision with histopathology is needed to relieve symptoms and render a definitive diagnosis. Radiography is highly insensitive in identifying bone erosions associated with glomus tumors.⁸ With ultrasonography, glomus tumors appear hypoechoic; with Doppler ultrasonography, they appear hypervascular. With MRI, glomus tumors appear as well-defined nodular lesions with hypointense signal intensity on T1-weighted sequence and hyperintense signal intensity on T2-weighted sequence, with strong enhancement using gadolinium-based contrast.^9,10 On histopathology, a glomus tumor appears as a nodular tumor with sheets of oval-nucleated cells arranged in multicellular layers surrounding blood vessels and are immunoreactive for α-smooth muscle actin, muscle-specific actin, and type IV collagen.^11,12 

There are several glomus tumor variants. The most common is a solid glomus tumor, which predominantly is composed of glomus cells, followed by glomangioma, which mainly is composed of blood vessels. Glomangiomyoma, which mostly is composed of smooth muscle cells, is the rarest variant.¹³ 

While glomus tumors are common in the subungual areas, it is an uncommon location for glomangiomyomas, which have been reported in the nail unit in only 7 prior case reports identified through searches of PubMed and Google Scholar using the terms glomangiomyoma, glomangiomyoma nail, and subungual glomangiomyoma (Table).^13-19 Glomangiomyomas more commonly are described in solid organs, including the stomach, kidney, pancreas, and bladder.¹⁶ The mean age of patients with subungual glomangiomyomas, including our patient, was 40.4 years (range, 3-61 years), with the majority being female (75.0% [6/8]). Most patients presented with fingernail involvement (75.0% [6/8]), nail dystrophy (eg, nail plate thinning, longitudinal grooves, splinter hemorrhages, longitudinal erythronychia)(62.5% [5/8]), and intermittent pain and/or point tenderness in the affected nail (75.0% [6/8]).^13-19 Notably, only our patient had longitudinal erythronychia as a clinical feature, and only one other case described MRI findings, which included a lobulated mass with intense contrast and distal phalanx destruction.¹⁸ One patient was a 3-year-old girl with a family history of generalized multiple glomangiomyomas. Although subungual glomangiomyoma was not confirmed on histopathology, the diagnosis in this patient was presumed based on her family history.¹³ On histopathology, glomangiomyomas are composed of oval-nucleated cells surrounding blood vessels. These oval-nucleated cells then gradually transition to smooth muscle cells.²⁰ 

A myxoid cyst is composed of a pseudocyst, which lacks a cyst lining, and is a result of synovial fluid from the distal interphalangeal joint entering the pseudocyst space.² It typically manifests with a longitudinal groove in the nail plate. A flesh-colored nodule may be appreciated between the cuticle and the distal interphalangeal joint.² The depth of the longitudinal groove may vary depending on the volume of synovial fluid within the myxoid cyst.²¹ In a series of 35 cases of subungual myxoid cysts, none manifested with longitudinal erythronychia. Due to their composition, myxoid cysts can be distinguished easily from solid tumors of the nail unit via transillumination.²² Pain is a much less common with myxoid cysts vs glomus tumors, as the filling of the pseudocyst space with synovial fluid typically is gradual, allowing the surrounding tissue to accommodate and adapt over time.²¹ In equivocal cases, MRI or high-resolution ultrasonography may be used to distinguish myxoid cysts and glomus tumors.⁸ Histopathology shows accumulation of mucin in the dermis with surrounding fibrous stroma.²³

Subungual neuromas are painful benign tumors that develop due to disorganized neural proliferation following disruption to peripheral nerves secondary to trauma or surgery. In 3 case reports, subungual neuromas manifested as painful subungual nodules, with proximal nail plate ridging, or onycholysis.^24-26 Since neuromas have only rarely been described in the subungual region, reports of MRI and ultrasonography findings are unknown. Histopathology is needed to distinguish neuromas from glomus tumors. Histopathology shows an acapsular structure consisting of disorganized spindle-cell proliferation and nerve fibers arranged in a tangle of fascicles within fibrotic tissue.²⁵ On immunochemistry, spindle cells typically are positive for cellular antigen protein S100.²⁶ 

Leiomyomas are benign neoplasms derived from smooth muscle, typically localized to the uterus or gastrointestinal tract, and have been described rarely in the nail unit.^27,28 It is hypothesized that subungual leiomyomas originate from the vascular smooth muscle in the subcutaneous layer of the nail unit.²⁸ Like glomus tumors, leiomyomas of the subungual region often manifest with pain and longitudinal erythronychia.^27-30 Subungual leiomyomas may be distinguished from glomus tumors via advanced imaging techniques, including ultrasonography and MRI. Cutaneous leiomyomas have been described with mild to moderate internal low flow vascularity on Doppler ultrasonography, while glomus tumors typically reveal high internal vascularity.²⁸ Biopsy with histopathology is needed for definitive diagnosis. On histopathology, leiomyomas demonstrate bland-appearing spindle-shaped cells with elongated nuclei arranged in fascicles.²⁷ They typically are positive for α-smooth muscle actin and caldesmon on immunostaining. 

Eccrine spiradenomas are benign adnexal tumors likely of apocrine origin with limited case reports in the literature.^31,32 Clinically, eccrine spiradenomas involving the nail unit may manifest with longitudinal nail splitting of the nail or as a papule on the proximal nail fold, with associated tenderness.^31,32 In a report of a 50-year-old woman with a histopathologically confirmed eccrine spiradenoma manifesting with longitudinal splitting of the nail and pain in the proximal nail fold, the mass appeared hypoechoic on ultrasonography with increased intramass vascularity on Doppler, while MRI showed an intensely enhancing lesion.³¹ These imaging features, combined with a classically manifesting feature of pain, make eccrine spiradenomas difficult to distinguish from glomus tumors; therefore, histopathologic examination can provide a definitive diagnosis, and surgical excision is used for treatment.³¹ On histopathology, these tumors are well circumscribed and composed of both small dark basaloid cells with peripheral compact nuclei and larger cells with central pale nuclei, which may be arranged in tubules.^31,32

The Comparison

A. Alopecia areata in a young girl with a lighter skin tone. The fine white vellus hairs are signs of regrowth. 

B. Alopecia areata in a 49-year-old man with tightly coiled hair and darker skin tone. Coiled white hairs are noted in the alopecia patches.

Alopecia areata (AA) is a common autoimmune condition characterized by hair loss resulting from a T cell–mediated attack on the hair follicles. It manifests as nonscarring patches of hair loss on the scalp, eyebrows, eyelashes, and beard area as well as more extensive complete loss of scalp and body hair. While AA may affect individuals of any age, most patients develop their first patch(es) of hair loss during childhood.¹ The treatment landscape for AA has evolved considerably in recent years, but barriers to access to newer treatments persist. 

Epidemiology 

AA is most prevalent among pediatric and adult individuals of African, Asian, or Hispanic/Latino descent.^2-4 In some studies, Black individuals had higher odds and Asian individuals had lower odds of developing AA, while other studies have reported the highest standardized prevalence among Asian individuals.⁵ In the United States, AA affects about 1.47% of adults and as many as 0.11% of children.^6-8 In Black patients, AA often manifests early with a female predominance.⁵ 

AA frequently is associated with autoimmune comorbidities, the most common being thyroid disease.^3,5 In Black patients, AA is associated with more atopic comorbidities, including asthma, atopic dermatitis, and allergic rhinitis.⁵ 

Key Clinical Features 

AA clinically manifests similarly across different skin tones; however, in patients with more tightly coiled or curly hair, the extent of scalp hair loss may be underestimated without a full examination. Culturally sensitive approaches to hair and scalp evaluation are essential, especially for Black women, whose hair care practices and scalp conditions may be overlooked or misunderstood during visits to evaluate hair loss. A thoughtful history and gentle examination of the hair and scalp that considers hair texture, cultural practices such as head coverings (eg, headwraps, turbans, hijabs), use of hair adornments (eg, clips, beads, bows), traditional braiding, and use of natural oils or herbal treatments, as well as styling methods including tight hairstyles, use of heat styling tools (eg, flat irons, curling irons), chemical application (eg, straighteners, hair color), and washing or styling frequency can improve diagnostic accuracy and help build trust in the patient-provider relationship. 

Classic signs of AA visualized with dermoscopy include yellow and/or black dots on the scalp and exclamation point hairs. The appearance of fine white vellus hairs within the alopecic patches also may indicate early regrowth. On scalp trichoscopy, black dots are more prominent, and yellow dots are less prominent, in individuals with darker skin tones vs lighter skin tones.⁹ 

Worth Noting 

In addition to a full examination of the scalp, documenting the extent of hair loss using validated severity scales, including the severity of alopecia tool (SALT), AA severity index (AASI), clinician-reported outcome assessment, and patient-reported outcome measures, can standardize disease severity assessment, facilitate timely insurance or medication approvals, and support objective tracking of treatment response, which may ultimately enhance access to care.¹⁰ 

Prompt treatment of AA is essential. Not surprisingly, patients given a diagnosis of AA may experience considerable emotional and psychological distress—regardless of the extent of the loss.¹¹ Treatment options include mid- to high-potency topical or intralesional corticosteroids and newer and more targeted systemic options, including 3 Janus kinase (JAK) inhibitors—baricitinib, ritlecitinib, and deuruxolitinib—for more extensive disease.¹² Treatment with intralesional corticosteroids may cause transient hypopigmentation, which may be more noticeable in patients with darker skin tones. Delays in treatment with JAK inhibitors can lead to a less-than-optimal response. Of the 3 JAK inhibitors that are approved by the US Food and Drug Administration for AA, only ritlecitinib is approved for children 12 years and older, leaving a therapeutic gap for younger patients that often leads to uncomfortable scalp injections, delayed or no treatment, off-label use of JAK inhibitors as well as the pairing of off-label dupilumab with oral minoxidil.¹² 

Based on adult data, patients with severe disease and a shorter duration of hair loss (ie, < 4 years) tend to respond better to JAK inhibitors than those experiencing hair loss for longer periods. Also, those with more severe AA tend to have poorer outcomes than those with less severe disease.¹³ If treatment proves less than optimal, wigs and hair pieces may need to be considered. It is worth noting that some insurance companies will cover the cost of wigs for patients when prescribed as cranial prostheses. 

Health Disparity Highlight 

Health disparities in AA can be influenced by socioeconomic status and access to care. Patients from lower-income backgrounds often face barriers to accessing dermatologic care and treatments such as JAK inhibitors, which may remain inaccessible due to high costs and insurance limitations.¹⁴ These barriers can intersect with other factors such as age, sex, and race, potentially exacerbating disparities. Women with skin of color in underserved communities may experience delayed diagnosis, limited treatment options, and greater psychosocial distress from hair loss.¹⁴ Addressing these inequities requires advocacy, education for both patients and clinicians, and improved access to treatment to ensure comprehensive care for all patients. 

The Comparison

A. Alopecia areata in a young girl with a lighter skin tone. The fine white vellus hairs are signs of regrowth. 

B. Alopecia areata in a 49-year-old man with tightly coiled hair and darker skin tone. Coiled white hairs are noted in the alopecia patches.

Alopecia areata (AA) is a common autoimmune condition characterized by hair loss resulting from a T cell–mediated attack on the hair follicles. It manifests as nonscarring patches of hair loss on the scalp, eyebrows, eyelashes, and beard area as well as more extensive complete loss of scalp and body hair. While AA may affect individuals of any age, most patients develop their first patch(es) of hair loss during childhood.¹ The treatment landscape for AA has evolved considerably in recent years, but barriers to access to newer treatments persist. 

Epidemiology 

AA is most prevalent among pediatric and adult individuals of African, Asian, or Hispanic/Latino descent.^2-4 In some studies, Black individuals had higher odds and Asian individuals had lower odds of developing AA, while other studies have reported the highest standardized prevalence among Asian individuals.⁵ In the United States, AA affects about 1.47% of adults and as many as 0.11% of children.^6-8 In Black patients, AA often manifests early with a female predominance.⁵ 

AA frequently is associated with autoimmune comorbidities, the most common being thyroid disease.^3,5 In Black patients, AA is associated with more atopic comorbidities, including asthma, atopic dermatitis, and allergic rhinitis.⁵ 

Key Clinical Features 

AA clinically manifests similarly across different skin tones; however, in patients with more tightly coiled or curly hair, the extent of scalp hair loss may be underestimated without a full examination. Culturally sensitive approaches to hair and scalp evaluation are essential, especially for Black women, whose hair care practices and scalp conditions may be overlooked or misunderstood during visits to evaluate hair loss. A thoughtful history and gentle examination of the hair and scalp that considers hair texture, cultural practices such as head coverings (eg, headwraps, turbans, hijabs), use of hair adornments (eg, clips, beads, bows), traditional braiding, and use of natural oils or herbal treatments, as well as styling methods including tight hairstyles, use of heat styling tools (eg, flat irons, curling irons), chemical application (eg, straighteners, hair color), and washing or styling frequency can improve diagnostic accuracy and help build trust in the patient-provider relationship. 

Classic signs of AA visualized with dermoscopy include yellow and/or black dots on the scalp and exclamation point hairs. The appearance of fine white vellus hairs within the alopecic patches also may indicate early regrowth. On scalp trichoscopy, black dots are more prominent, and yellow dots are less prominent, in individuals with darker skin tones vs lighter skin tones.⁹ 

Worth Noting 

In addition to a full examination of the scalp, documenting the extent of hair loss using validated severity scales, including the severity of alopecia tool (SALT), AA severity index (AASI), clinician-reported outcome assessment, and patient-reported outcome measures, can standardize disease severity assessment, facilitate timely insurance or medication approvals, and support objective tracking of treatment response, which may ultimately enhance access to care.¹⁰ 

Prompt treatment of AA is essential. Not surprisingly, patients given a diagnosis of AA may experience considerable emotional and psychological distress—regardless of the extent of the loss.¹¹ Treatment options include mid- to high-potency topical or intralesional corticosteroids and newer and more targeted systemic options, including 3 Janus kinase (JAK) inhibitors—baricitinib, ritlecitinib, and deuruxolitinib—for more extensive disease.¹² Treatment with intralesional corticosteroids may cause transient hypopigmentation, which may be more noticeable in patients with darker skin tones. Delays in treatment with JAK inhibitors can lead to a less-than-optimal response. Of the 3 JAK inhibitors that are approved by the US Food and Drug Administration for AA, only ritlecitinib is approved for children 12 years and older, leaving a therapeutic gap for younger patients that often leads to uncomfortable scalp injections, delayed or no treatment, off-label use of JAK inhibitors as well as the pairing of off-label dupilumab with oral minoxidil.¹² 

Based on adult data, patients with severe disease and a shorter duration of hair loss (ie, < 4 years) tend to respond better to JAK inhibitors than those experiencing hair loss for longer periods. Also, those with more severe AA tend to have poorer outcomes than those with less severe disease.¹³ If treatment proves less than optimal, wigs and hair pieces may need to be considered. It is worth noting that some insurance companies will cover the cost of wigs for patients when prescribed as cranial prostheses. 

Health Disparity Highlight 

Health disparities in AA can be influenced by socioeconomic status and access to care. Patients from lower-income backgrounds often face barriers to accessing dermatologic care and treatments such as JAK inhibitors, which may remain inaccessible due to high costs and insurance limitations.¹⁴ These barriers can intersect with other factors such as age, sex, and race, potentially exacerbating disparities. Women with skin of color in underserved communities may experience delayed diagnosis, limited treatment options, and greater psychosocial distress from hair loss.¹⁴ Addressing these inequities requires advocacy, education for both patients and clinicians, and improved access to treatment to ensure comprehensive care for all patients. 

The Comparison

A. Alopecia areata in a young girl with a lighter skin tone. The fine white vellus hairs are signs of regrowth. 

B. Alopecia areata in a 49-year-old man with tightly coiled hair and darker skin tone. Coiled white hairs are noted in the alopecia patches.

Alopecia areata (AA) is a common autoimmune condition characterized by hair loss resulting from a T cell–mediated attack on the hair follicles. It manifests as nonscarring patches of hair loss on the scalp, eyebrows, eyelashes, and beard area as well as more extensive complete loss of scalp and body hair. While AA may affect individuals of any age, most patients develop their first patch(es) of hair loss during childhood.¹ The treatment landscape for AA has evolved considerably in recent years, but barriers to access to newer treatments persist. 

Epidemiology 

AA is most prevalent among pediatric and adult individuals of African, Asian, or Hispanic/Latino descent.^2-4 In some studies, Black individuals had higher odds and Asian individuals had lower odds of developing AA, while other studies have reported the highest standardized prevalence among Asian individuals.⁵ In the United States, AA affects about 1.47% of adults and as many as 0.11% of children.^6-8 In Black patients, AA often manifests early with a female predominance.⁵ 

AA frequently is associated with autoimmune comorbidities, the most common being thyroid disease.^3,5 In Black patients, AA is associated with more atopic comorbidities, including asthma, atopic dermatitis, and allergic rhinitis.⁵ 

Key Clinical Features 

AA clinically manifests similarly across different skin tones; however, in patients with more tightly coiled or curly hair, the extent of scalp hair loss may be underestimated without a full examination. Culturally sensitive approaches to hair and scalp evaluation are essential, especially for Black women, whose hair care practices and scalp conditions may be overlooked or misunderstood during visits to evaluate hair loss. A thoughtful history and gentle examination of the hair and scalp that considers hair texture, cultural practices such as head coverings (eg, headwraps, turbans, hijabs), use of hair adornments (eg, clips, beads, bows), traditional braiding, and use of natural oils or herbal treatments, as well as styling methods including tight hairstyles, use of heat styling tools (eg, flat irons, curling irons), chemical application (eg, straighteners, hair color), and washing or styling frequency can improve diagnostic accuracy and help build trust in the patient-provider relationship. 

Classic signs of AA visualized with dermoscopy include yellow and/or black dots on the scalp and exclamation point hairs. The appearance of fine white vellus hairs within the alopecic patches also may indicate early regrowth. On scalp trichoscopy, black dots are more prominent, and yellow dots are less prominent, in individuals with darker skin tones vs lighter skin tones.⁹ 

Worth Noting 

In addition to a full examination of the scalp, documenting the extent of hair loss using validated severity scales, including the severity of alopecia tool (SALT), AA severity index (AASI), clinician-reported outcome assessment, and patient-reported outcome measures, can standardize disease severity assessment, facilitate timely insurance or medication approvals, and support objective tracking of treatment response, which may ultimately enhance access to care.¹⁰ 

Prompt treatment of AA is essential. Not surprisingly, patients given a diagnosis of AA may experience considerable emotional and psychological distress—regardless of the extent of the loss.¹¹ Treatment options include mid- to high-potency topical or intralesional corticosteroids and newer and more targeted systemic options, including 3 Janus kinase (JAK) inhibitors—baricitinib, ritlecitinib, and deuruxolitinib—for more extensive disease.¹² Treatment with intralesional corticosteroids may cause transient hypopigmentation, which may be more noticeable in patients with darker skin tones. Delays in treatment with JAK inhibitors can lead to a less-than-optimal response. Of the 3 JAK inhibitors that are approved by the US Food and Drug Administration for AA, only ritlecitinib is approved for children 12 years and older, leaving a therapeutic gap for younger patients that often leads to uncomfortable scalp injections, delayed or no treatment, off-label use of JAK inhibitors as well as the pairing of off-label dupilumab with oral minoxidil.¹² 

Based on adult data, patients with severe disease and a shorter duration of hair loss (ie, < 4 years) tend to respond better to JAK inhibitors than those experiencing hair loss for longer periods. Also, those with more severe AA tend to have poorer outcomes than those with less severe disease.¹³ If treatment proves less than optimal, wigs and hair pieces may need to be considered. It is worth noting that some insurance companies will cover the cost of wigs for patients when prescribed as cranial prostheses. 

Health Disparity Highlight 

Health disparities in AA can be influenced by socioeconomic status and access to care. Patients from lower-income backgrounds often face barriers to accessing dermatologic care and treatments such as JAK inhibitors, which may remain inaccessible due to high costs and insurance limitations.¹⁴ These barriers can intersect with other factors such as age, sex, and race, potentially exacerbating disparities. Women with skin of color in underserved communities may experience delayed diagnosis, limited treatment options, and greater psychosocial distress from hair loss.¹⁴ Addressing these inequities requires advocacy, education for both patients and clinicians, and improved access to treatment to ensure comprehensive care for all patients. 

Patients often ask dermatologists how to best care for their specific hair type; however, there are no formal recommendations that apply to the many different hair care practices utilized by Black patients, as hair types in this community can range from wavy to tightly coiled.¹ Understanding the the history of hair care in those of African ancestry and various styling practices in this population is necessary to adequately counsel patients and gain trust in the doctor-patient relationship. In this article, we provide an overview of hair care recommendations based on common styling practices in Black women.

A PubMed search of articles indexed for MEDLINE using the terms Black hair care, African American hair management, hair loss prevention, hair care practices, natural hair, natural-hair styles, alopecia, hairdressing, hair breakage, hair fragility, heat-stressed hair, traction alopecia, and natural hair care yielded 305 results; 107 duplicates were identified and removed, leaving 198 articles to be screened for eligibility (ie, English-language studies created in the past 15 years). Sixty-eight full-text articles were screened against the exclusion criteria, which included case reports and case series, articles not focused on Afro-textured hair, and cancer-related hair loss. Three additional fulltext articles were identified via resources from Wayne State University library (Detroit, Michigan) that were not available on PubMed. A total of 29 full-text articles were included in our review.

Background on Hair Care and Styling in African Populations

It is difficult to understand the history of hair in those of African ancestry in the United States.² Prior to slavery, hair styling was considered a way of identification, classification, and communication as well as a medium through which to connect with the spiritual world in many parts of Africa. Hair-styling practices in Africa included elaborate cornrows, threading, and braiding with many accessories. Notable hair-styling products included natural butters, herbs, and powders to assist with moisture retention. Scarves also were used during this time for ceremonies or protection.³ During the mass enslavement of African populations and their transportation to the Americas by Europeans, slaveholders routinely cut off all the hair of both men and women in order to objectify and erase the culture of African hair styling passed down through generations.^4,5 Hair texture then was weaponized to create a caste system in plantation life, in which Black slaves with straight hair textures were granted the “privilege” of domestic work, while those with kinky hair were relegated to arduous manual labor in the fields.⁴ Years later, during the 1800s, laws were enacted in the United States to prohibit Black women from wearing tightly coiled natural hair in public places.⁵ Over the next few centuries from the 1800s to the early 2000s, various hair-styling trends such as the use of hot combs, perms, afros, and Jheri curls developed as a means for Black individuals to conform to societal pressure to adopt more European features; however, as time progressed, afros, braids, locs, and natural hair would become more dominant as statements against these same societal pressures.⁵

The natural hair movement, which emerged in the United States in the 2000s, encouraged Black women to abandon the use of toxic chemical hair straighteners, cultivate healthier hair care practices, disrupt Eurocentric standards of wearing straightened hair, and facilitate self-definition of beauty ideals from the Civil Rights Movement of the 1960s.^4,5 It is estimated that between 30% and 70% of all Black women in the United States wear natural hair, including 79% of millennial Black women younger than 30 years⁶; however, several new trends such as wigs and weaves have grown in popularity since the early 2000s due to mainstream pop culture and improvements in creating natural hairlines.^7,8

Key Features of Afro-Textured Hair

Individuals of African descent have the most diverse hair texture phenotypes, ranging from straight to tightly coiled.⁹ Although hair is chemically similar across various racial groups, differences are noted mainly in the shape of the hair shaft, with elliptical and curved shapes seen in Afrotextured hair. These differences yield more tightly curled strands than in other hair types; however, these features also contribute to fragility, as it creates points of weakness and decreases the tensile strength of the hair shaft.¹⁰ This inherent fragility leads to higher rates of hair breakage as well as lower moisture content and slower growth rates, which is why Afro-textured hair requires special care.⁹

Afro-textured hair generally falls into 2 main categories of the Andre Walker hair typing system: 4A-4C and 3A-3C.¹¹ In the 4A-4C category, hair is described as coily or kinky. Common concerns related to this hair type include dryness and brittleness with increased susceptibility to breakage. The 3A-3C category is described as loose to corkscrew curls, with a common concern of dryness.^11,12 Additionally, Loussouarn et al¹³ established a method to further define natural hair curliness using curve diameter and curl meters on glass plates to measure the curvature of hair strands. This method allows for assessing diversity and range of curliness within various races without relying on ethnic origin.¹³

Common Hair Care Practices

A description of each hair type and recommended styling practices with their levels of evidence can be found in the eTable.

Natural Hair—Natural hair is classified as hair that has not been chemically changed by perms, heat, or other straightening treatments.^12,14 For natural hair, retaining the moisture of the hair shaft should be the main focus, as moisture loss leads to considerable dryness.¹⁴ Generally, it is recommended to wash natural hair once per week or every other week; however, this can change based on hair length and oil production on the scalp. Washing daily may be ideal for shorter hair and monthly for longer hair to help prevent product build-up that can have a drying effect.¹⁵ Avoid shampoos that are drying (eg, sulfate and silicone products). The co-washing method also can be utilized, which entails washing the hair with a conditioning cleanser instead of shampoo and conditioner. However, this technique is not meant to completely replace shampoo.¹⁶ In fact, a clarifying shampoo is recommended after co-washing 3 or 4 times.¹⁶ The use of a hot oil treatment twice per month can promote moisture retention and reduce split-end formation.¹⁷ For maintenance between washes, many utilize the liquid, oil, cream (LOC) or liquid, cream, oil (LCO) methods, which describe regimens that utilize water, an oil of choice, and cream such as shea butter to lock in moisture.¹⁸ This method can be used as often as needed for dry hair.

Due to the susceptibility of Afro-textured hair to tangle and knot, using a wide-tooth comb, detangling brush, or detangling conditioners is a grade B recommendation for care (eTable). Though not widely documented in the literature, many of our patients have had anecdotal success detangling their hair simply by pulling hair strands apart by hand or “finger detangling” as well as using wide-tooth combs. Although both hair types are healthier in their natural states, kinky hair (type 4A-4C) is extremely fragile and more difficult to manage than less kinky hair (type 3A-3C).¹⁸

Special care is needed when detangling due to strands being weaker when wet.¹⁹ Detangling should be performed in a retrograde fashion. Deep conditioning can aid in moisture retention and should be performed weekly or biweekly.^17-20 Depending on the health of the hair, protein treatments can be considered on a monthly basis to help preserve the cuticle. Styling with braids, twists, or other protective styles can then be completed on an individual basis.

Thermal Straightening—A blowout involves straightening the hair after a wash with the use of a hair dryer.²¹ This common hair-styling method does not employ the use of chemicals beyond light hair oils and heat-protectant creams or sprays, typically resulting in a less kinky afro or semi-straight hair. Thermal straightening utilizes heat to temporarily straighten hair strands. Flat irons with heated metal plates then can be used after blow-drying the hair to fully straighten and smooth the strands. These processes combined commonly are known as a silk press.^21-22

For thermally straightened hair, it is recommended to either wrap the hair around the scalp to keep it flat or pin curl the hair and cover with a bonnet to sleep. Safe straightening techniques with the use of a flat iron include setting the temperature no higher than 175 °F or a low/medium setting while also limiting use to once per week if possible.²³ The number of passes of the flat iron also should be limited to 1 to 2 to reduce breakage. A heat-protectant cream or spray also can be applied to the hair before flat ironing to minimize damage. Applying heat protectant to the hair prior to styling will help minimize heat damage by distributing the heat along the hair fiber surface, avoiding water boiling in the hair shaft and the development of bubble hair leading to damage.²⁴

Chemical Straightening—Similar to how relaxers, perms, and Jheri curl treatments chemically modify hair texture using distinct chemicals yielding different curl patterns, the Brazilian blowout similarly straightens hair using a hair dryer and chemicals applied to hair strands after washing.^21-24 Relaxers utilize sodium or guanidine hydroxide for straightening, perms use ammonium thioglycolate for curling, and Jheri curl treatments employ thioglycolates or mercaptans for defined curls. However, these treatments generally are cautioned against due to potential hair damage and recent associations with uterine and breast cancer in Black women. Research has suggested that endocrine disrupters in these products, especially those marketed to Black women, contribute to hormone-related disease processes.^25,26 One study found higher concentrations of alkylphenols, the fragrance marker diethyl phthalate, and parabens in relaxers²⁷; however, more research is needed to determine specific chemicals associated with these cancers.

Braids and Locs—Braiding is a technique that involves interlocking 3 or more sections of hair that may or may not be fixated to the scalp like a cornrow,¹¹ and one can utilize extensions or natural hair depending on the desired outcome. Intended for long-term wear (ie, weeks to months), braids minimize breakage and reduce daily styling needs. Two popular styles—cornrows and individual braids—differ in preparation and weaving techniques. Cornrows are an Afro-centric style involving uniform, tightly woven braids that are close to the scalp, creating distinct patterns. Conversely, individual braids weave separate hair sections, offering diverse styling possibilities. Braiding practices should exclude hairline edges—often termed baby hairs—to prevent traction alopecia. Minimal use of edge gel, which helps to tame the vellus hairs at the frontotemporal scalp, as well as mindful weave volume, weight, and length are recommended to avert breakage. Braids that cause pain are too tight, can damage hair, and may cause traction alopecia.¹¹ Braids should not be worn for longer than 3 months at a time and require biweekly washing with diluted shampoo and conditioner. Proper drying by wringing the hair with a microfiber towel is essential to avoid frizz and mold formation.

Locs are a low-maintenance hairstyle considered permanent until cut.²⁸ This style involves twisting, palm rolling, or using tools such as crochet hooks to “lock” the hair. Regular maintenance with retwisting and cleaning is vital for loc health. Increased weight and tight twisting of locs can cause damage to the scalp and hair strands; however, locs are known to increase hair volume over time, often due to the accumulation of hairs that would otherwise have been shed in the telogen phase.²⁸

Wigs and Weaves—Wigs consist of synthetic or human hair that can be strapped to the head with an adjustable band or glued to the scalp depending on the desired style.²⁹ Wigs are removed daily, which allows for quick access to hair for cleansing and moisturizing. In contrast, weaves typically are sewn into the natural hair, which may make it difficult to reach the scalp for cleansing, leading to dryness and product build-up.²⁹ Notably, there is evidence of a relationship between long-term use of weaves and traction alopecia.³⁰

Wigs can have a fully synthetic hair line or lace hair line and can range from very affordable to expensive. When applied correctly, both styles offer an easy way to cover and protect the natural hair by reducing the amount of physical trauma related to daily hair styling. A lace-front wig contains a frontal thin mesh or lace that camouflages the natural frontal hairline.^29,30 A risk of lace-front wigs is that they can cause friction alopecia secondary to repeated use of adhesives and repeated friction against the hairline. Generally, wigs and weaves should be cared for as one would care for one’s own hair.

Hair Care in Black Children—Children’s hair care begins with washing the hair and scalp with shampoo, applying conditioner, and detangling as needed.³¹ After rinsing out the conditioner, a leave-in conditioner can assist with moisture retention and further detangling. The hair is then styled, either wet or dry. Recommendations for hair care practices in Black children include loose hairstyles that do not strain hair roots and nightly removal of root-securing accessories (eg, barrettes, elastic hairbeads). Frequent cornrow styling and friction on chemically straightened hair were identified by a survey as considerable traction alopecia risk factors.³² Thus, educating caregivers on appropriate hair-grooming practices for children is important.

Hair Protection—Proactive steps to reduce hair loss include wearing satin bonnets and/or using satin pillowcases while sleeping regardless of hairstyle. Although evidence is limited, it is thought that satin and silk allow the hair to retain its moisture and natural oils, preventing breakage and friction.^33,34 Frequent hair trimming every 2 to 4 months can reduce breakage when doing thermal treatments.^35,36 When prolonged or repetitive styles are used, it is encouraged to give the hair a break between styles to recover from the repeated stress. Wearing an intermittent updo or high bun—a hairstyle in which the hair is pulled upward—can prevent breakage by reducing heavy strain on the hair; however, it is important to avoid the use of rubber bands due to friction and risk for tangling of hair strands. Instead, the use of covered elastic ties and/or those without metal is preferred.¹¹ Alternatively, if a polished and neat appearance with slicked-back hair is desired, the practice of tautly pulling the hair is not recommended. Instead, use of an alcohol-free gel is suggested along with a satin scarf wrapped around the hairline to facilitate the setting of the hair in place.¹¹

A common practice to preserve curly hairstyles while sleeping is known as the pineapple method, which protects the hair and aids in preserving the freshness and style of the curls.³⁷ It consists of a loosely tied high ponytail at the top of the head allowing the curls to fall forward. This minimizes frizz and prevents the curls from forming knots.

Conclusion

Hair care recommendations in Black women can be complex due to a wide range of personal care preferences and styling techniques in this population. While evidence in the literature is limited, it still is important for dermatologists to be familiar with the different hair care practices utilized by Black women so they can effectively counsel patients and improve hair health. Knowledge of optimal hair care practices can aid in the prevention of common hair disorders that disproportionately affect this patient population, such as traction alopecia and trichorrhexis nodosa or breakage.

Patients often ask dermatologists how to best care for their specific hair type; however, there are no formal recommendations that apply to the many different hair care practices utilized by Black patients, as hair types in this community can range from wavy to tightly coiled.¹ Understanding the the history of hair care in those of African ancestry and various styling practices in this population is necessary to adequately counsel patients and gain trust in the doctor-patient relationship. In this article, we provide an overview of hair care recommendations based on common styling practices in Black women.

A PubMed search of articles indexed for MEDLINE using the terms Black hair care, African American hair management, hair loss prevention, hair care practices, natural hair, natural-hair styles, alopecia, hairdressing, hair breakage, hair fragility, heat-stressed hair, traction alopecia, and natural hair care yielded 305 results; 107 duplicates were identified and removed, leaving 198 articles to be screened for eligibility (ie, English-language studies created in the past 15 years). Sixty-eight full-text articles were screened against the exclusion criteria, which included case reports and case series, articles not focused on Afro-textured hair, and cancer-related hair loss. Three additional fulltext articles were identified via resources from Wayne State University library (Detroit, Michigan) that were not available on PubMed. A total of 29 full-text articles were included in our review.

Background on Hair Care and Styling in African Populations

It is difficult to understand the history of hair in those of African ancestry in the United States.² Prior to slavery, hair styling was considered a way of identification, classification, and communication as well as a medium through which to connect with the spiritual world in many parts of Africa. Hair-styling practices in Africa included elaborate cornrows, threading, and braiding with many accessories. Notable hair-styling products included natural butters, herbs, and powders to assist with moisture retention. Scarves also were used during this time for ceremonies or protection.³ During the mass enslavement of African populations and their transportation to the Americas by Europeans, slaveholders routinely cut off all the hair of both men and women in order to objectify and erase the culture of African hair styling passed down through generations.^4,5 Hair texture then was weaponized to create a caste system in plantation life, in which Black slaves with straight hair textures were granted the “privilege” of domestic work, while those with kinky hair were relegated to arduous manual labor in the fields.⁴ Years later, during the 1800s, laws were enacted in the United States to prohibit Black women from wearing tightly coiled natural hair in public places.⁵ Over the next few centuries from the 1800s to the early 2000s, various hair-styling trends such as the use of hot combs, perms, afros, and Jheri curls developed as a means for Black individuals to conform to societal pressure to adopt more European features; however, as time progressed, afros, braids, locs, and natural hair would become more dominant as statements against these same societal pressures.⁵

The natural hair movement, which emerged in the United States in the 2000s, encouraged Black women to abandon the use of toxic chemical hair straighteners, cultivate healthier hair care practices, disrupt Eurocentric standards of wearing straightened hair, and facilitate self-definition of beauty ideals from the Civil Rights Movement of the 1960s.^4,5 It is estimated that between 30% and 70% of all Black women in the United States wear natural hair, including 79% of millennial Black women younger than 30 years⁶; however, several new trends such as wigs and weaves have grown in popularity since the early 2000s due to mainstream pop culture and improvements in creating natural hairlines.^7,8

Key Features of Afro-Textured Hair

Individuals of African descent have the most diverse hair texture phenotypes, ranging from straight to tightly coiled.⁹ Although hair is chemically similar across various racial groups, differences are noted mainly in the shape of the hair shaft, with elliptical and curved shapes seen in Afrotextured hair. These differences yield more tightly curled strands than in other hair types; however, these features also contribute to fragility, as it creates points of weakness and decreases the tensile strength of the hair shaft.¹⁰ This inherent fragility leads to higher rates of hair breakage as well as lower moisture content and slower growth rates, which is why Afro-textured hair requires special care.⁹

Afro-textured hair generally falls into 2 main categories of the Andre Walker hair typing system: 4A-4C and 3A-3C.¹¹ In the 4A-4C category, hair is described as coily or kinky. Common concerns related to this hair type include dryness and brittleness with increased susceptibility to breakage. The 3A-3C category is described as loose to corkscrew curls, with a common concern of dryness.^11,12 Additionally, Loussouarn et al¹³ established a method to further define natural hair curliness using curve diameter and curl meters on glass plates to measure the curvature of hair strands. This method allows for assessing diversity and range of curliness within various races without relying on ethnic origin.¹³

Common Hair Care Practices

A description of each hair type and recommended styling practices with their levels of evidence can be found in the eTable.

Natural Hair—Natural hair is classified as hair that has not been chemically changed by perms, heat, or other straightening treatments.^12,14 For natural hair, retaining the moisture of the hair shaft should be the main focus, as moisture loss leads to considerable dryness.¹⁴ Generally, it is recommended to wash natural hair once per week or every other week; however, this can change based on hair length and oil production on the scalp. Washing daily may be ideal for shorter hair and monthly for longer hair to help prevent product build-up that can have a drying effect.¹⁵ Avoid shampoos that are drying (eg, sulfate and silicone products). The co-washing method also can be utilized, which entails washing the hair with a conditioning cleanser instead of shampoo and conditioner. However, this technique is not meant to completely replace shampoo.¹⁶ In fact, a clarifying shampoo is recommended after co-washing 3 or 4 times.¹⁶ The use of a hot oil treatment twice per month can promote moisture retention and reduce split-end formation.¹⁷ For maintenance between washes, many utilize the liquid, oil, cream (LOC) or liquid, cream, oil (LCO) methods, which describe regimens that utilize water, an oil of choice, and cream such as shea butter to lock in moisture.¹⁸ This method can be used as often as needed for dry hair.

Due to the susceptibility of Afro-textured hair to tangle and knot, using a wide-tooth comb, detangling brush, or detangling conditioners is a grade B recommendation for care (eTable). Though not widely documented in the literature, many of our patients have had anecdotal success detangling their hair simply by pulling hair strands apart by hand or “finger detangling” as well as using wide-tooth combs. Although both hair types are healthier in their natural states, kinky hair (type 4A-4C) is extremely fragile and more difficult to manage than less kinky hair (type 3A-3C).¹⁸

Special care is needed when detangling due to strands being weaker when wet.¹⁹ Detangling should be performed in a retrograde fashion. Deep conditioning can aid in moisture retention and should be performed weekly or biweekly.^17-20 Depending on the health of the hair, protein treatments can be considered on a monthly basis to help preserve the cuticle. Styling with braids, twists, or other protective styles can then be completed on an individual basis.

Thermal Straightening—A blowout involves straightening the hair after a wash with the use of a hair dryer.²¹ This common hair-styling method does not employ the use of chemicals beyond light hair oils and heat-protectant creams or sprays, typically resulting in a less kinky afro or semi-straight hair. Thermal straightening utilizes heat to temporarily straighten hair strands. Flat irons with heated metal plates then can be used after blow-drying the hair to fully straighten and smooth the strands. These processes combined commonly are known as a silk press.^21-22

For thermally straightened hair, it is recommended to either wrap the hair around the scalp to keep it flat or pin curl the hair and cover with a bonnet to sleep. Safe straightening techniques with the use of a flat iron include setting the temperature no higher than 175 °F or a low/medium setting while also limiting use to once per week if possible.²³ The number of passes of the flat iron also should be limited to 1 to 2 to reduce breakage. A heat-protectant cream or spray also can be applied to the hair before flat ironing to minimize damage. Applying heat protectant to the hair prior to styling will help minimize heat damage by distributing the heat along the hair fiber surface, avoiding water boiling in the hair shaft and the development of bubble hair leading to damage.²⁴

Chemical Straightening—Similar to how relaxers, perms, and Jheri curl treatments chemically modify hair texture using distinct chemicals yielding different curl patterns, the Brazilian blowout similarly straightens hair using a hair dryer and chemicals applied to hair strands after washing.^21-24 Relaxers utilize sodium or guanidine hydroxide for straightening, perms use ammonium thioglycolate for curling, and Jheri curl treatments employ thioglycolates or mercaptans for defined curls. However, these treatments generally are cautioned against due to potential hair damage and recent associations with uterine and breast cancer in Black women. Research has suggested that endocrine disrupters in these products, especially those marketed to Black women, contribute to hormone-related disease processes.^25,26 One study found higher concentrations of alkylphenols, the fragrance marker diethyl phthalate, and parabens in relaxers²⁷; however, more research is needed to determine specific chemicals associated with these cancers.

Braids and Locs—Braiding is a technique that involves interlocking 3 or more sections of hair that may or may not be fixated to the scalp like a cornrow,¹¹ and one can utilize extensions or natural hair depending on the desired outcome. Intended for long-term wear (ie, weeks to months), braids minimize breakage and reduce daily styling needs. Two popular styles—cornrows and individual braids—differ in preparation and weaving techniques. Cornrows are an Afro-centric style involving uniform, tightly woven braids that are close to the scalp, creating distinct patterns. Conversely, individual braids weave separate hair sections, offering diverse styling possibilities. Braiding practices should exclude hairline edges—often termed baby hairs—to prevent traction alopecia. Minimal use of edge gel, which helps to tame the vellus hairs at the frontotemporal scalp, as well as mindful weave volume, weight, and length are recommended to avert breakage. Braids that cause pain are too tight, can damage hair, and may cause traction alopecia.¹¹ Braids should not be worn for longer than 3 months at a time and require biweekly washing with diluted shampoo and conditioner. Proper drying by wringing the hair with a microfiber towel is essential to avoid frizz and mold formation.

Locs are a low-maintenance hairstyle considered permanent until cut.²⁸ This style involves twisting, palm rolling, or using tools such as crochet hooks to “lock” the hair. Regular maintenance with retwisting and cleaning is vital for loc health. Increased weight and tight twisting of locs can cause damage to the scalp and hair strands; however, locs are known to increase hair volume over time, often due to the accumulation of hairs that would otherwise have been shed in the telogen phase.²⁸

Wigs and Weaves—Wigs consist of synthetic or human hair that can be strapped to the head with an adjustable band or glued to the scalp depending on the desired style.²⁹ Wigs are removed daily, which allows for quick access to hair for cleansing and moisturizing. In contrast, weaves typically are sewn into the natural hair, which may make it difficult to reach the scalp for cleansing, leading to dryness and product build-up.²⁹ Notably, there is evidence of a relationship between long-term use of weaves and traction alopecia.³⁰

Wigs can have a fully synthetic hair line or lace hair line and can range from very affordable to expensive. When applied correctly, both styles offer an easy way to cover and protect the natural hair by reducing the amount of physical trauma related to daily hair styling. A lace-front wig contains a frontal thin mesh or lace that camouflages the natural frontal hairline.^29,30 A risk of lace-front wigs is that they can cause friction alopecia secondary to repeated use of adhesives and repeated friction against the hairline. Generally, wigs and weaves should be cared for as one would care for one’s own hair.

Hair Care in Black Children—Children’s hair care begins with washing the hair and scalp with shampoo, applying conditioner, and detangling as needed.³¹ After rinsing out the conditioner, a leave-in conditioner can assist with moisture retention and further detangling. The hair is then styled, either wet or dry. Recommendations for hair care practices in Black children include loose hairstyles that do not strain hair roots and nightly removal of root-securing accessories (eg, barrettes, elastic hairbeads). Frequent cornrow styling and friction on chemically straightened hair were identified by a survey as considerable traction alopecia risk factors.³² Thus, educating caregivers on appropriate hair-grooming practices for children is important.

Hair Protection—Proactive steps to reduce hair loss include wearing satin bonnets and/or using satin pillowcases while sleeping regardless of hairstyle. Although evidence is limited, it is thought that satin and silk allow the hair to retain its moisture and natural oils, preventing breakage and friction.^33,34 Frequent hair trimming every 2 to 4 months can reduce breakage when doing thermal treatments.^35,36 When prolonged or repetitive styles are used, it is encouraged to give the hair a break between styles to recover from the repeated stress. Wearing an intermittent updo or high bun—a hairstyle in which the hair is pulled upward—can prevent breakage by reducing heavy strain on the hair; however, it is important to avoid the use of rubber bands due to friction and risk for tangling of hair strands. Instead, the use of covered elastic ties and/or those without metal is preferred.¹¹ Alternatively, if a polished and neat appearance with slicked-back hair is desired, the practice of tautly pulling the hair is not recommended. Instead, use of an alcohol-free gel is suggested along with a satin scarf wrapped around the hairline to facilitate the setting of the hair in place.¹¹

A common practice to preserve curly hairstyles while sleeping is known as the pineapple method, which protects the hair and aids in preserving the freshness and style of the curls.³⁷ It consists of a loosely tied high ponytail at the top of the head allowing the curls to fall forward. This minimizes frizz and prevents the curls from forming knots.

Conclusion

Hair care recommendations in Black women can be complex due to a wide range of personal care preferences and styling techniques in this population. While evidence in the literature is limited, it still is important for dermatologists to be familiar with the different hair care practices utilized by Black women so they can effectively counsel patients and improve hair health. Knowledge of optimal hair care practices can aid in the prevention of common hair disorders that disproportionately affect this patient population, such as traction alopecia and trichorrhexis nodosa or breakage.

Patients often ask dermatologists how to best care for their specific hair type; however, there are no formal recommendations that apply to the many different hair care practices utilized by Black patients, as hair types in this community can range from wavy to tightly coiled.¹ Understanding the the history of hair care in those of African ancestry and various styling practices in this population is necessary to adequately counsel patients and gain trust in the doctor-patient relationship. In this article, we provide an overview of hair care recommendations based on common styling practices in Black women.

A PubMed search of articles indexed for MEDLINE using the terms Black hair care, African American hair management, hair loss prevention, hair care practices, natural hair, natural-hair styles, alopecia, hairdressing, hair breakage, hair fragility, heat-stressed hair, traction alopecia, and natural hair care yielded 305 results; 107 duplicates were identified and removed, leaving 198 articles to be screened for eligibility (ie, English-language studies created in the past 15 years). Sixty-eight full-text articles were screened against the exclusion criteria, which included case reports and case series, articles not focused on Afro-textured hair, and cancer-related hair loss. Three additional fulltext articles were identified via resources from Wayne State University library (Detroit, Michigan) that were not available on PubMed. A total of 29 full-text articles were included in our review.

Background on Hair Care and Styling in African Populations

It is difficult to understand the history of hair in those of African ancestry in the United States.² Prior to slavery, hair styling was considered a way of identification, classification, and communication as well as a medium through which to connect with the spiritual world in many parts of Africa. Hair-styling practices in Africa included elaborate cornrows, threading, and braiding with many accessories. Notable hair-styling products included natural butters, herbs, and powders to assist with moisture retention. Scarves also were used during this time for ceremonies or protection.³ During the mass enslavement of African populations and their transportation to the Americas by Europeans, slaveholders routinely cut off all the hair of both men and women in order to objectify and erase the culture of African hair styling passed down through generations.^4,5 Hair texture then was weaponized to create a caste system in plantation life, in which Black slaves with straight hair textures were granted the “privilege” of domestic work, while those with kinky hair were relegated to arduous manual labor in the fields.⁴ Years later, during the 1800s, laws were enacted in the United States to prohibit Black women from wearing tightly coiled natural hair in public places.⁵ Over the next few centuries from the 1800s to the early 2000s, various hair-styling trends such as the use of hot combs, perms, afros, and Jheri curls developed as a means for Black individuals to conform to societal pressure to adopt more European features; however, as time progressed, afros, braids, locs, and natural hair would become more dominant as statements against these same societal pressures.⁵

The natural hair movement, which emerged in the United States in the 2000s, encouraged Black women to abandon the use of toxic chemical hair straighteners, cultivate healthier hair care practices, disrupt Eurocentric standards of wearing straightened hair, and facilitate self-definition of beauty ideals from the Civil Rights Movement of the 1960s.^4,5 It is estimated that between 30% and 70% of all Black women in the United States wear natural hair, including 79% of millennial Black women younger than 30 years⁶; however, several new trends such as wigs and weaves have grown in popularity since the early 2000s due to mainstream pop culture and improvements in creating natural hairlines.^7,8

Key Features of Afro-Textured Hair

Individuals of African descent have the most diverse hair texture phenotypes, ranging from straight to tightly coiled.⁹ Although hair is chemically similar across various racial groups, differences are noted mainly in the shape of the hair shaft, with elliptical and curved shapes seen in Afrotextured hair. These differences yield more tightly curled strands than in other hair types; however, these features also contribute to fragility, as it creates points of weakness and decreases the tensile strength of the hair shaft.¹⁰ This inherent fragility leads to higher rates of hair breakage as well as lower moisture content and slower growth rates, which is why Afro-textured hair requires special care.⁹

Afro-textured hair generally falls into 2 main categories of the Andre Walker hair typing system: 4A-4C and 3A-3C.¹¹ In the 4A-4C category, hair is described as coily or kinky. Common concerns related to this hair type include dryness and brittleness with increased susceptibility to breakage. The 3A-3C category is described as loose to corkscrew curls, with a common concern of dryness.^11,12 Additionally, Loussouarn et al¹³ established a method to further define natural hair curliness using curve diameter and curl meters on glass plates to measure the curvature of hair strands. This method allows for assessing diversity and range of curliness within various races without relying on ethnic origin.¹³

Common Hair Care Practices

A description of each hair type and recommended styling practices with their levels of evidence can be found in the eTable.

Natural Hair—Natural hair is classified as hair that has not been chemically changed by perms, heat, or other straightening treatments.^12,14 For natural hair, retaining the moisture of the hair shaft should be the main focus, as moisture loss leads to considerable dryness.¹⁴ Generally, it is recommended to wash natural hair once per week or every other week; however, this can change based on hair length and oil production on the scalp. Washing daily may be ideal for shorter hair and monthly for longer hair to help prevent product build-up that can have a drying effect.¹⁵ Avoid shampoos that are drying (eg, sulfate and silicone products). The co-washing method also can be utilized, which entails washing the hair with a conditioning cleanser instead of shampoo and conditioner. However, this technique is not meant to completely replace shampoo.¹⁶ In fact, a clarifying shampoo is recommended after co-washing 3 or 4 times.¹⁶ The use of a hot oil treatment twice per month can promote moisture retention and reduce split-end formation.¹⁷ For maintenance between washes, many utilize the liquid, oil, cream (LOC) or liquid, cream, oil (LCO) methods, which describe regimens that utilize water, an oil of choice, and cream such as shea butter to lock in moisture.¹⁸ This method can be used as often as needed for dry hair.

Due to the susceptibility of Afro-textured hair to tangle and knot, using a wide-tooth comb, detangling brush, or detangling conditioners is a grade B recommendation for care (eTable). Though not widely documented in the literature, many of our patients have had anecdotal success detangling their hair simply by pulling hair strands apart by hand or “finger detangling” as well as using wide-tooth combs. Although both hair types are healthier in their natural states, kinky hair (type 4A-4C) is extremely fragile and more difficult to manage than less kinky hair (type 3A-3C).¹⁸

Special care is needed when detangling due to strands being weaker when wet.¹⁹ Detangling should be performed in a retrograde fashion. Deep conditioning can aid in moisture retention and should be performed weekly or biweekly.^17-20 Depending on the health of the hair, protein treatments can be considered on a monthly basis to help preserve the cuticle. Styling with braids, twists, or other protective styles can then be completed on an individual basis.

Thermal Straightening—A blowout involves straightening the hair after a wash with the use of a hair dryer.²¹ This common hair-styling method does not employ the use of chemicals beyond light hair oils and heat-protectant creams or sprays, typically resulting in a less kinky afro or semi-straight hair. Thermal straightening utilizes heat to temporarily straighten hair strands. Flat irons with heated metal plates then can be used after blow-drying the hair to fully straighten and smooth the strands. These processes combined commonly are known as a silk press.^21-22

For thermally straightened hair, it is recommended to either wrap the hair around the scalp to keep it flat or pin curl the hair and cover with a bonnet to sleep. Safe straightening techniques with the use of a flat iron include setting the temperature no higher than 175 °F or a low/medium setting while also limiting use to once per week if possible.²³ The number of passes of the flat iron also should be limited to 1 to 2 to reduce breakage. A heat-protectant cream or spray also can be applied to the hair before flat ironing to minimize damage. Applying heat protectant to the hair prior to styling will help minimize heat damage by distributing the heat along the hair fiber surface, avoiding water boiling in the hair shaft and the development of bubble hair leading to damage.²⁴

Chemical Straightening—Similar to how relaxers, perms, and Jheri curl treatments chemically modify hair texture using distinct chemicals yielding different curl patterns, the Brazilian blowout similarly straightens hair using a hair dryer and chemicals applied to hair strands after washing.^21-24 Relaxers utilize sodium or guanidine hydroxide for straightening, perms use ammonium thioglycolate for curling, and Jheri curl treatments employ thioglycolates or mercaptans for defined curls. However, these treatments generally are cautioned against due to potential hair damage and recent associations with uterine and breast cancer in Black women. Research has suggested that endocrine disrupters in these products, especially those marketed to Black women, contribute to hormone-related disease processes.^25,26 One study found higher concentrations of alkylphenols, the fragrance marker diethyl phthalate, and parabens in relaxers²⁷; however, more research is needed to determine specific chemicals associated with these cancers.

Braids and Locs—Braiding is a technique that involves interlocking 3 or more sections of hair that may or may not be fixated to the scalp like a cornrow,¹¹ and one can utilize extensions or natural hair depending on the desired outcome. Intended for long-term wear (ie, weeks to months), braids minimize breakage and reduce daily styling needs. Two popular styles—cornrows and individual braids—differ in preparation and weaving techniques. Cornrows are an Afro-centric style involving uniform, tightly woven braids that are close to the scalp, creating distinct patterns. Conversely, individual braids weave separate hair sections, offering diverse styling possibilities. Braiding practices should exclude hairline edges—often termed baby hairs—to prevent traction alopecia. Minimal use of edge gel, which helps to tame the vellus hairs at the frontotemporal scalp, as well as mindful weave volume, weight, and length are recommended to avert breakage. Braids that cause pain are too tight, can damage hair, and may cause traction alopecia.¹¹ Braids should not be worn for longer than 3 months at a time and require biweekly washing with diluted shampoo and conditioner. Proper drying by wringing the hair with a microfiber towel is essential to avoid frizz and mold formation.

Locs are a low-maintenance hairstyle considered permanent until cut.²⁸ This style involves twisting, palm rolling, or using tools such as crochet hooks to “lock” the hair. Regular maintenance with retwisting and cleaning is vital for loc health. Increased weight and tight twisting of locs can cause damage to the scalp and hair strands; however, locs are known to increase hair volume over time, often due to the accumulation of hairs that would otherwise have been shed in the telogen phase.²⁸

Wigs and Weaves—Wigs consist of synthetic or human hair that can be strapped to the head with an adjustable band or glued to the scalp depending on the desired style.²⁹ Wigs are removed daily, which allows for quick access to hair for cleansing and moisturizing. In contrast, weaves typically are sewn into the natural hair, which may make it difficult to reach the scalp for cleansing, leading to dryness and product build-up.²⁹ Notably, there is evidence of a relationship between long-term use of weaves and traction alopecia.³⁰

Wigs can have a fully synthetic hair line or lace hair line and can range from very affordable to expensive. When applied correctly, both styles offer an easy way to cover and protect the natural hair by reducing the amount of physical trauma related to daily hair styling. A lace-front wig contains a frontal thin mesh or lace that camouflages the natural frontal hairline.^29,30 A risk of lace-front wigs is that they can cause friction alopecia secondary to repeated use of adhesives and repeated friction against the hairline. Generally, wigs and weaves should be cared for as one would care for one’s own hair.

Hair Care in Black Children—Children’s hair care begins with washing the hair and scalp with shampoo, applying conditioner, and detangling as needed.³¹ After rinsing out the conditioner, a leave-in conditioner can assist with moisture retention and further detangling. The hair is then styled, either wet or dry. Recommendations for hair care practices in Black children include loose hairstyles that do not strain hair roots and nightly removal of root-securing accessories (eg, barrettes, elastic hairbeads). Frequent cornrow styling and friction on chemically straightened hair were identified by a survey as considerable traction alopecia risk factors.³² Thus, educating caregivers on appropriate hair-grooming practices for children is important.

Hair Protection—Proactive steps to reduce hair loss include wearing satin bonnets and/or using satin pillowcases while sleeping regardless of hairstyle. Although evidence is limited, it is thought that satin and silk allow the hair to retain its moisture and natural oils, preventing breakage and friction.^33,34 Frequent hair trimming every 2 to 4 months can reduce breakage when doing thermal treatments.^35,36 When prolonged or repetitive styles are used, it is encouraged to give the hair a break between styles to recover from the repeated stress. Wearing an intermittent updo or high bun—a hairstyle in which the hair is pulled upward—can prevent breakage by reducing heavy strain on the hair; however, it is important to avoid the use of rubber bands due to friction and risk for tangling of hair strands. Instead, the use of covered elastic ties and/or those without metal is preferred.¹¹ Alternatively, if a polished and neat appearance with slicked-back hair is desired, the practice of tautly pulling the hair is not recommended. Instead, use of an alcohol-free gel is suggested along with a satin scarf wrapped around the hairline to facilitate the setting of the hair in place.¹¹

A common practice to preserve curly hairstyles while sleeping is known as the pineapple method, which protects the hair and aids in preserving the freshness and style of the curls.³⁷ It consists of a loosely tied high ponytail at the top of the head allowing the curls to fall forward. This minimizes frizz and prevents the curls from forming knots.

Conclusion

Hair care recommendations in Black women can be complex due to a wide range of personal care preferences and styling techniques in this population. While evidence in the literature is limited, it still is important for dermatologists to be familiar with the different hair care practices utilized by Black women so they can effectively counsel patients and improve hair health. Knowledge of optimal hair care practices can aid in the prevention of common hair disorders that disproportionately affect this patient population, such as traction alopecia and trichorrhexis nodosa or breakage.

THE DIAGNOSIS: Nail-Patella Syndrome

Nail-patella syndrome (NPS) is an autosomaldominant disorder that is present in approximately 1 in 50,000 live births worldwide.^1,2 It manifests with a spectrum of clinical findings affecting the nails, skeletal system, kidneys, and eyes.³ Most cases of NPS are caused by loss-of-function mutations in LMX1B,¹ a gene encoding the LIM homeobox transcription factor.⁴ The LMX1B gene plays a critical role in the dorsoventral patterning of developing limbs.⁵ Mutations of this gene impair the development and function of podocytes and glomerular filtration slits⁶ and have been found to affect the development of the dopaminergic and mesencephalic serotoninergic neurons.² Approximately 5% of patients with NPS have an unexplained genetic cause, suggesting an alternate mechanism for disease.¹ Loss-of-function mutations also were observed in the Wnt inhibitory factor 1 gene (WIF1) in a family with an NPS-like presentation and could represent a novel cause of the condition.¹ Regardless, NPS may be diagnosed clinically based on characteristic medical history, imaging, and physical examination findings.

Nail changes are the most consistent feature of NPS. The nails may be absent, hypoplastic, dystrophic, ridged (horizontally or vertically), or pitted or may demonstrate characteristic triangular lacunae. Nail findings often are congenital, bilateral, and symmetrical. The first digits typically are most severely affected, with progressive improvement appreciated toward the fifth fingers, as seen in our patient. The nail changes can be subtle, sometimes manifesting only as a single triangular lacuna on both thumbnails. Toenail involvement is less common and, when present, tends to be even more discreet. In contrast to the fingernails, the fifth toenails are most commonly affected.⁷

There are many skeletal manifestations of NPS. Patellae may be absent, hypoplastic, or irregularly shaped on physical examination or imaging, and changes may involve one or both knees. The Figure shows plain radiographs of the knees with bilateral patellar subluxation. Elbow dysplasia or radial head subluxation may result in physical limitations in extension, pronation, or supination of the joint.⁷ In approximately 70% of patients seen with the disorder, imaging may reveal symmetric posterior and lateral bony projections from the iliac crests, known as iliac horns; when present, these are considered pathognomonic.⁸

Open-angle glaucoma is the most common ocular finding in NPS. Other less commonly associated eye abnormalities include hyperpigmentation of the pupillary margin (Lester iris).⁶ Renal involvement occurs in 30% to 50% of patients with NPS and is the main predictor of mortality, with percentages as high as 5% to 14%.⁷ Defects occur in the glomerular basement membrane and manifest clinically with hematuria and/or proteinuria. The course of proteinuria is unpredictable. Some cases remit spontaneously, while others remain asymptomatic, progress to nephrotic syndrome, or, although rare, advance to renal failure.^7,9

Bowel symptoms, neurologic problems, vasomotor concerns, thin dental enamel, attention-deficit disorder or attention-deficit/hyperactivity disorder, and major depressive disorder all have been reported in association with NPS.^2,7

Nail psoriasis typically exhibits nail pitting and onycholysis. Other manifestations include subungual hyperkeratosis, oil drop discoloration, and splinter hemorrhages. Topical and intralesional treatments are used to manage symptoms of the disease, as it can become debilitating if left untreated, unlike the nail disease seen in NPS.¹⁰ Onychomycosis can have a similar manifestation to psoriasis with sublingual hyperkeratosis of the nail, but it usually is caused by dermatophytes or yeasts such as Candida albicans. Onycholysis and thickening of the subungual region also can be seen. Diagnosis relies on direct microscopy and fungal culture, and a thorough patient history will help distinguish fungal vs nonfungal etiology. New-generation antifungals are used to eradicate the infection.¹¹ Leukonychia manifests with white-appearing nails due to nail-plate or nail-bed abnormalities. Leukonychia can have multisystem involvement, but nails demonstrate a white discoloration rather than the other abnormalities discussed here.¹² Hypohidrotic ectodermal dysplasia is a rare hereditary congenital disease that affects ectodermal structures and manifests with a triad of symptoms: hypotrichosis, hypohidrosis, and hypodontia. The condition often manifests in childhood with characteristic features such as light-pigmented sparse and fine hair. Physical growth as well as psychomotor development are within normal limits. Neither bone nor renal involvement is typical for hypohidrotic ectodermal dysplasia.¹³

Our case highlights the typical manifestation of NPS with multisystem involvement, demonstrating the complexity of the disease. For cases in which a clinical diagnosis of NPS is uncertain, gene-targeted or comprehensive genomic testing is recommended, as well as genetic counseling. Given the broad spectrum of clinical manifestations, it is imperative that patients undergo screening for musculoskeletal, renal, and ophthalmologic involvement. Treatment is targeted at symptom management and prevention of long-term complications, reliant on clinical presentation, and specific to each patient.

THE DIAGNOSIS: Nail-Patella Syndrome

Nail-patella syndrome (NPS) is an autosomaldominant disorder that is present in approximately 1 in 50,000 live births worldwide.^1,2 It manifests with a spectrum of clinical findings affecting the nails, skeletal system, kidneys, and eyes.³ Most cases of NPS are caused by loss-of-function mutations in LMX1B,¹ a gene encoding the LIM homeobox transcription factor.⁴ The LMX1B gene plays a critical role in the dorsoventral patterning of developing limbs.⁵ Mutations of this gene impair the development and function of podocytes and glomerular filtration slits⁶ and have been found to affect the development of the dopaminergic and mesencephalic serotoninergic neurons.² Approximately 5% of patients with NPS have an unexplained genetic cause, suggesting an alternate mechanism for disease.¹ Loss-of-function mutations also were observed in the Wnt inhibitory factor 1 gene (WIF1) in a family with an NPS-like presentation and could represent a novel cause of the condition.¹ Regardless, NPS may be diagnosed clinically based on characteristic medical history, imaging, and physical examination findings.

Nail changes are the most consistent feature of NPS. The nails may be absent, hypoplastic, dystrophic, ridged (horizontally or vertically), or pitted or may demonstrate characteristic triangular lacunae. Nail findings often are congenital, bilateral, and symmetrical. The first digits typically are most severely affected, with progressive improvement appreciated toward the fifth fingers, as seen in our patient. The nail changes can be subtle, sometimes manifesting only as a single triangular lacuna on both thumbnails. Toenail involvement is less common and, when present, tends to be even more discreet. In contrast to the fingernails, the fifth toenails are most commonly affected.⁷

There are many skeletal manifestations of NPS. Patellae may be absent, hypoplastic, or irregularly shaped on physical examination or imaging, and changes may involve one or both knees. The Figure shows plain radiographs of the knees with bilateral patellar subluxation. Elbow dysplasia or radial head subluxation may result in physical limitations in extension, pronation, or supination of the joint.⁷ In approximately 70% of patients seen with the disorder, imaging may reveal symmetric posterior and lateral bony projections from the iliac crests, known as iliac horns; when present, these are considered pathognomonic.⁸

Open-angle glaucoma is the most common ocular finding in NPS. Other less commonly associated eye abnormalities include hyperpigmentation of the pupillary margin (Lester iris).⁶ Renal involvement occurs in 30% to 50% of patients with NPS and is the main predictor of mortality, with percentages as high as 5% to 14%.⁷ Defects occur in the glomerular basement membrane and manifest clinically with hematuria and/or proteinuria. The course of proteinuria is unpredictable. Some cases remit spontaneously, while others remain asymptomatic, progress to nephrotic syndrome, or, although rare, advance to renal failure.^7,9

Bowel symptoms, neurologic problems, vasomotor concerns, thin dental enamel, attention-deficit disorder or attention-deficit/hyperactivity disorder, and major depressive disorder all have been reported in association with NPS.^2,7

Nail psoriasis typically exhibits nail pitting and onycholysis. Other manifestations include subungual hyperkeratosis, oil drop discoloration, and splinter hemorrhages. Topical and intralesional treatments are used to manage symptoms of the disease, as it can become debilitating if left untreated, unlike the nail disease seen in NPS.¹⁰ Onychomycosis can have a similar manifestation to psoriasis with sublingual hyperkeratosis of the nail, but it usually is caused by dermatophytes or yeasts such as Candida albicans. Onycholysis and thickening of the subungual region also can be seen. Diagnosis relies on direct microscopy and fungal culture, and a thorough patient history will help distinguish fungal vs nonfungal etiology. New-generation antifungals are used to eradicate the infection.¹¹ Leukonychia manifests with white-appearing nails due to nail-plate or nail-bed abnormalities. Leukonychia can have multisystem involvement, but nails demonstrate a white discoloration rather than the other abnormalities discussed here.¹² Hypohidrotic ectodermal dysplasia is a rare hereditary congenital disease that affects ectodermal structures and manifests with a triad of symptoms: hypotrichosis, hypohidrosis, and hypodontia. The condition often manifests in childhood with characteristic features such as light-pigmented sparse and fine hair. Physical growth as well as psychomotor development are within normal limits. Neither bone nor renal involvement is typical for hypohidrotic ectodermal dysplasia.¹³

Our case highlights the typical manifestation of NPS with multisystem involvement, demonstrating the complexity of the disease. For cases in which a clinical diagnosis of NPS is uncertain, gene-targeted or comprehensive genomic testing is recommended, as well as genetic counseling. Given the broad spectrum of clinical manifestations, it is imperative that patients undergo screening for musculoskeletal, renal, and ophthalmologic involvement. Treatment is targeted at symptom management and prevention of long-term complications, reliant on clinical presentation, and specific to each patient.

THE DIAGNOSIS: Nail-Patella Syndrome

Nail-patella syndrome (NPS) is an autosomaldominant disorder that is present in approximately 1 in 50,000 live births worldwide.^1,2 It manifests with a spectrum of clinical findings affecting the nails, skeletal system, kidneys, and eyes.³ Most cases of NPS are caused by loss-of-function mutations in LMX1B,¹ a gene encoding the LIM homeobox transcription factor.⁴ The LMX1B gene plays a critical role in the dorsoventral patterning of developing limbs.⁵ Mutations of this gene impair the development and function of podocytes and glomerular filtration slits⁶ and have been found to affect the development of the dopaminergic and mesencephalic serotoninergic neurons.² Approximately 5% of patients with NPS have an unexplained genetic cause, suggesting an alternate mechanism for disease.¹ Loss-of-function mutations also were observed in the Wnt inhibitory factor 1 gene (WIF1) in a family with an NPS-like presentation and could represent a novel cause of the condition.¹ Regardless, NPS may be diagnosed clinically based on characteristic medical history, imaging, and physical examination findings.

Nail changes are the most consistent feature of NPS. The nails may be absent, hypoplastic, dystrophic, ridged (horizontally or vertically), or pitted or may demonstrate characteristic triangular lacunae. Nail findings often are congenital, bilateral, and symmetrical. The first digits typically are most severely affected, with progressive improvement appreciated toward the fifth fingers, as seen in our patient. The nail changes can be subtle, sometimes manifesting only as a single triangular lacuna on both thumbnails. Toenail involvement is less common and, when present, tends to be even more discreet. In contrast to the fingernails, the fifth toenails are most commonly affected.⁷

There are many skeletal manifestations of NPS. Patellae may be absent, hypoplastic, or irregularly shaped on physical examination or imaging, and changes may involve one or both knees. The Figure shows plain radiographs of the knees with bilateral patellar subluxation. Elbow dysplasia or radial head subluxation may result in physical limitations in extension, pronation, or supination of the joint.⁷ In approximately 70% of patients seen with the disorder, imaging may reveal symmetric posterior and lateral bony projections from the iliac crests, known as iliac horns; when present, these are considered pathognomonic.⁸

Open-angle glaucoma is the most common ocular finding in NPS. Other less commonly associated eye abnormalities include hyperpigmentation of the pupillary margin (Lester iris).⁶ Renal involvement occurs in 30% to 50% of patients with NPS and is the main predictor of mortality, with percentages as high as 5% to 14%.⁷ Defects occur in the glomerular basement membrane and manifest clinically with hematuria and/or proteinuria. The course of proteinuria is unpredictable. Some cases remit spontaneously, while others remain asymptomatic, progress to nephrotic syndrome, or, although rare, advance to renal failure.^7,9

Bowel symptoms, neurologic problems, vasomotor concerns, thin dental enamel, attention-deficit disorder or attention-deficit/hyperactivity disorder, and major depressive disorder all have been reported in association with NPS.^2,7

Nail psoriasis typically exhibits nail pitting and onycholysis. Other manifestations include subungual hyperkeratosis, oil drop discoloration, and splinter hemorrhages. Topical and intralesional treatments are used to manage symptoms of the disease, as it can become debilitating if left untreated, unlike the nail disease seen in NPS.¹⁰ Onychomycosis can have a similar manifestation to psoriasis with sublingual hyperkeratosis of the nail, but it usually is caused by dermatophytes or yeasts such as Candida albicans. Onycholysis and thickening of the subungual region also can be seen. Diagnosis relies on direct microscopy and fungal culture, and a thorough patient history will help distinguish fungal vs nonfungal etiology. New-generation antifungals are used to eradicate the infection.¹¹ Leukonychia manifests with white-appearing nails due to nail-plate or nail-bed abnormalities. Leukonychia can have multisystem involvement, but nails demonstrate a white discoloration rather than the other abnormalities discussed here.¹² Hypohidrotic ectodermal dysplasia is a rare hereditary congenital disease that affects ectodermal structures and manifests with a triad of symptoms: hypotrichosis, hypohidrosis, and hypodontia. The condition often manifests in childhood with characteristic features such as light-pigmented sparse and fine hair. Physical growth as well as psychomotor development are within normal limits. Neither bone nor renal involvement is typical for hypohidrotic ectodermal dysplasia.¹³

Our case highlights the typical manifestation of NPS with multisystem involvement, demonstrating the complexity of the disease. For cases in which a clinical diagnosis of NPS is uncertain, gene-targeted or comprehensive genomic testing is recommended, as well as genetic counseling. Given the broad spectrum of clinical manifestations, it is imperative that patients undergo screening for musculoskeletal, renal, and ophthalmologic involvement. Treatment is targeted at symptom management and prevention of long-term complications, reliant on clinical presentation, and specific to each patient.

Formaldehyde (FA) is a colorless, flammable, highly pungent gas that remains ubiquitous in the environment despite being a known carcinogen and allergen.¹ In the cosmetic industry, FA commonly is used as both a preservative and active ingredient in hairstraightening products. Due to its toxicity and the thermal instability of FA releasers (ie, the release of FA at high temperatures), the US Food and Drug Administration has proposed a ban on formaldehyde and other FA-releasing chemicals (eg, methylene glycol) as an ingredient in hairsmoothing or hair-straightening products marketed in the United States.² However, the implementation of this ban is not yet in effect.

Hair-straightening products that are referred to as chemical relaxers typically contain alkaline derivatives. Alkaline hair straighteners—which include lye relaxers (active ingredient: sodium hydroxide), nolye relaxers (active ingredients: potassium hydroxide, lithium hydroxide, calcium hydroxide, guanidine hydroxide, or ammonium thioglycolate), and the Japanese hair straightening process (active ingredient: ammonium thioglycolate)—do not contain FA or FA-derivatives as active ingredients.³ Alternatively, acidic hair straighteners—popularly known as keratin treatments—contain either FA or FA-releasers and will be the primary focus of this discussion. As many patients are exposed to these products, we aim to highlight the cutaneous and systemic manifestations of acute and chronic exposure.

How Hair-Straightening Products Work

Hair straighteners that include FA or its derivatives generally contain high and low molecular weights of keratin peptides. The keratin peptides with high molecular weights diffuse into the cuticle while the low-molecular-weight peptides can penetrate further into the cortex of the hair shaft.⁴ Formaldehyde forms cross-links with the keratin amino acids (eg, tyrosine, arginine), and the application of heat via blow-drying enhances its ability to cross-link the hydrolyzed keratin from the straightening product to the natural keratin in the hair fibers; the use of a heated flat iron further enhances the cross-linking and seals the cuticle.⁵ The same mechanism of action applies for “safe keratin” (marketing terminology used for FA releasers) treatments, whereby the hydrogen and salt bonds of the hair are weakened, allowing for interconversion of the cysteine bonds of the hair fibers. This chemical conversion allows for the hair shafts to have a stable straight configuration. Of note, this mechanism of action differs from the action of chemical relaxers, which have a high pH and straighten the hair by opening the cuticles and permanently breaking the disulfide bonds in the cortex of the hair shaft—a process that restructures the keratin bonds without requiring heat application.⁵

The outcome of a keratin treatment, as seen on light microscopy, is the replenishment of gaps in the hair’s cuticle, therefore increasing its mechanical and thermal properties.⁶ This can give the appearance of increased shine, softness, and tensile strength. However, Sanad et al⁶ report that, as viewed on transmission electron microscopy, these keratin treatments do not repair lost cuticles, cuticle splitting, or detached cuticle layers from damaged strands.

Lastly, some patients notice lightening of their hair color after a hair-straightening treatment, which is possibly due to inhibition of the enzymatic synthesis of melanin, decomposition of melanin granules, or a direct reaction from chemical neutralizers with a high pH.⁶ Knowledge of the mechanism of action of hair-straightening treatments will aid dermatologists in educating patients about their immediate and long-term effects. This education subsequently will help patients avoid inappropriate hair care techniques that further damage the hair.

Environmental Distribution and Systemic Absorption of Formaldehyde

Atmospheric FA is absorbed via cutaneous and mucosal surfaces. Atmospheric FA concentrations produced when hair-straightening products are used cannot routinely be predicted because the amount generated depends on factors such as the pH of the preparation, the temperature to which the product is heated during straightening, duration of storage, and aeration and size of the environment in which the product is being used, among others.⁷

Peteffi et al⁷ and Aglan et al⁸ detected a moderate positive correlation between environmental FA concentrations and those in cosmetic products, particularly after blow-drying the hair or using other heat applications; however, the products examined by Peteffi et al⁷ contained exceedingly high concentrations of FA (up to 5.9%, which is higher than the legal limit of 0.1% in the United States).⁹ Of note, some products in this study were labelled as “formaldehyde free” but still contained high concentrations of FA.⁷ This is consistent with data published by the Occupational Health and Safety Administration, which citied salons with exposure limits outside the national recommendations (2.0 FA ppm/air).¹⁰ These findings highlight the inadvertent exposure that consumers face from products that are not regulated consistently.

Interestingly, Henault et al¹¹ observed that products with a high concentration of FA dispersed more airborne particles during hair brushing than hair straightening/ironing.¹¹ Further studies are needed to clarify the different routes and methods contributing to FA dispersion and the molecular instability of FA-releasers.

Clinical Correlation

Products that contain low (ie, less than the legal limit) levels of FA are not mandated to declare its presence on the product label; however, many products are contaminated with FA or inappropriately omit FA from the ingredient list, even at elevated concentrations. Consumers therefore may be inadvertently exposed to FA particles. Additionally, occupations with frequent exposure to FA include hairdressers, barbers, beauticians and related workers (33.6% exposure rate); sewers and embroiderers (26.1%); and cooks (19.1%).¹²

Adverse health effects associated with acute FA exposure include but are not limited to headache, eye irritation, allergic/irritant contact dermatitis, psoriasiform reactions, and acute kidney and respiratory tract injuries. Frontal fibrosing alopecia; non-Hodgkin lymphoma; and cancers of the upper digestive tract, lungs, and bladder also have been associated with chronic FA exposure.^7,13 In a cohort of female hairdressers, a longer duration of FA exposure (>8 years) as well as cumulative exposure were associated with an increase in ovarian cancer (OR, 1.48 [0.88 to 2.51]).¹² Formalin, the aqueous derivative of FA, also contains phenolic products that can mediate inflammatory response, DNA methylation, and carcinogenesis even with chronic low-level exposure.¹⁴ However, evidence supporting a direct correlation of FA exposure with breast carcinoma in both hairstylists and consumers remains controversial.⁷

Sanchez-Duenas et al¹⁵ described a case series of patients who were found to have psoriasiform scalp reactions after exposure to keratin treatments containing FA. The time to development of the lesions was inversely correlated with the number of treatments received, although the mean time to development was 12 months postprocedure.¹⁵ These researchers also identified no allergies to the substance on contact testing, which suggests an alternate pathogenesis as a consequence of FA exposure, resulting in the development of a psoriasiform reaction.¹⁵

Following adjustment for sex, age, menopause status, and skin color, frontal fibrosing alopecia also has been associated with the use of formalin and FA in hair straighteners.¹⁴ This is possibly related to the ability of FA and many phenolic products to induce chronic inflammation; however, a cumulative effect has not been noted consistently across the literature.

Future Directives

Continuous industry regulation is needed to ensure that use of FA is reduced and it is eventually eliminated from consumer products. Additionally, strict regulations are required to ensure products containing FA and FA-releasers are accurately labeled. Physicians and consumers should be aware of the potential health hazards associated with FA and advocate for effective legislation. While there is controversy regarding the level of absorption from environmental exposure and the subsequent biologic effects of absorption, both consumers and workers in industries such as hairdressing and barbering should reduce exposure time to FA and limit the application of heat and contact with products containing FA and FA releasers.

Formaldehyde (FA) is a colorless, flammable, highly pungent gas that remains ubiquitous in the environment despite being a known carcinogen and allergen.¹ In the cosmetic industry, FA commonly is used as both a preservative and active ingredient in hairstraightening products. Due to its toxicity and the thermal instability of FA releasers (ie, the release of FA at high temperatures), the US Food and Drug Administration has proposed a ban on formaldehyde and other FA-releasing chemicals (eg, methylene glycol) as an ingredient in hairsmoothing or hair-straightening products marketed in the United States.² However, the implementation of this ban is not yet in effect.

Hair-straightening products that are referred to as chemical relaxers typically contain alkaline derivatives. Alkaline hair straighteners—which include lye relaxers (active ingredient: sodium hydroxide), nolye relaxers (active ingredients: potassium hydroxide, lithium hydroxide, calcium hydroxide, guanidine hydroxide, or ammonium thioglycolate), and the Japanese hair straightening process (active ingredient: ammonium thioglycolate)—do not contain FA or FA-derivatives as active ingredients.³ Alternatively, acidic hair straighteners—popularly known as keratin treatments—contain either FA or FA-releasers and will be the primary focus of this discussion. As many patients are exposed to these products, we aim to highlight the cutaneous and systemic manifestations of acute and chronic exposure.

How Hair-Straightening Products Work

Hair straighteners that include FA or its derivatives generally contain high and low molecular weights of keratin peptides. The keratin peptides with high molecular weights diffuse into the cuticle while the low-molecular-weight peptides can penetrate further into the cortex of the hair shaft.⁴ Formaldehyde forms cross-links with the keratin amino acids (eg, tyrosine, arginine), and the application of heat via blow-drying enhances its ability to cross-link the hydrolyzed keratin from the straightening product to the natural keratin in the hair fibers; the use of a heated flat iron further enhances the cross-linking and seals the cuticle.⁵ The same mechanism of action applies for “safe keratin” (marketing terminology used for FA releasers) treatments, whereby the hydrogen and salt bonds of the hair are weakened, allowing for interconversion of the cysteine bonds of the hair fibers. This chemical conversion allows for the hair shafts to have a stable straight configuration. Of note, this mechanism of action differs from the action of chemical relaxers, which have a high pH and straighten the hair by opening the cuticles and permanently breaking the disulfide bonds in the cortex of the hair shaft—a process that restructures the keratin bonds without requiring heat application.⁵

The outcome of a keratin treatment, as seen on light microscopy, is the replenishment of gaps in the hair’s cuticle, therefore increasing its mechanical and thermal properties.⁶ This can give the appearance of increased shine, softness, and tensile strength. However, Sanad et al⁶ report that, as viewed on transmission electron microscopy, these keratin treatments do not repair lost cuticles, cuticle splitting, or detached cuticle layers from damaged strands.

Lastly, some patients notice lightening of their hair color after a hair-straightening treatment, which is possibly due to inhibition of the enzymatic synthesis of melanin, decomposition of melanin granules, or a direct reaction from chemical neutralizers with a high pH.⁶ Knowledge of the mechanism of action of hair-straightening treatments will aid dermatologists in educating patients about their immediate and long-term effects. This education subsequently will help patients avoid inappropriate hair care techniques that further damage the hair.

Environmental Distribution and Systemic Absorption of Formaldehyde

Atmospheric FA is absorbed via cutaneous and mucosal surfaces. Atmospheric FA concentrations produced when hair-straightening products are used cannot routinely be predicted because the amount generated depends on factors such as the pH of the preparation, the temperature to which the product is heated during straightening, duration of storage, and aeration and size of the environment in which the product is being used, among others.⁷

Peteffi et al⁷ and Aglan et al⁸ detected a moderate positive correlation between environmental FA concentrations and those in cosmetic products, particularly after blow-drying the hair or using other heat applications; however, the products examined by Peteffi et al⁷ contained exceedingly high concentrations of FA (up to 5.9%, which is higher than the legal limit of 0.1% in the United States).⁹ Of note, some products in this study were labelled as “formaldehyde free” but still contained high concentrations of FA.⁷ This is consistent with data published by the Occupational Health and Safety Administration, which citied salons with exposure limits outside the national recommendations (2.0 FA ppm/air).¹⁰ These findings highlight the inadvertent exposure that consumers face from products that are not regulated consistently.

Interestingly, Henault et al¹¹ observed that products with a high concentration of FA dispersed more airborne particles during hair brushing than hair straightening/ironing.¹¹ Further studies are needed to clarify the different routes and methods contributing to FA dispersion and the molecular instability of FA-releasers.

Clinical Correlation

Products that contain low (ie, less than the legal limit) levels of FA are not mandated to declare its presence on the product label; however, many products are contaminated with FA or inappropriately omit FA from the ingredient list, even at elevated concentrations. Consumers therefore may be inadvertently exposed to FA particles. Additionally, occupations with frequent exposure to FA include hairdressers, barbers, beauticians and related workers (33.6% exposure rate); sewers and embroiderers (26.1%); and cooks (19.1%).¹²

Adverse health effects associated with acute FA exposure include but are not limited to headache, eye irritation, allergic/irritant contact dermatitis, psoriasiform reactions, and acute kidney and respiratory tract injuries. Frontal fibrosing alopecia; non-Hodgkin lymphoma; and cancers of the upper digestive tract, lungs, and bladder also have been associated with chronic FA exposure.^7,13 In a cohort of female hairdressers, a longer duration of FA exposure (>8 years) as well as cumulative exposure were associated with an increase in ovarian cancer (OR, 1.48 [0.88 to 2.51]).¹² Formalin, the aqueous derivative of FA, also contains phenolic products that can mediate inflammatory response, DNA methylation, and carcinogenesis even with chronic low-level exposure.¹⁴ However, evidence supporting a direct correlation of FA exposure with breast carcinoma in both hairstylists and consumers remains controversial.⁷

Sanchez-Duenas et al¹⁵ described a case series of patients who were found to have psoriasiform scalp reactions after exposure to keratin treatments containing FA. The time to development of the lesions was inversely correlated with the number of treatments received, although the mean time to development was 12 months postprocedure.¹⁵ These researchers also identified no allergies to the substance on contact testing, which suggests an alternate pathogenesis as a consequence of FA exposure, resulting in the development of a psoriasiform reaction.¹⁵

Following adjustment for sex, age, menopause status, and skin color, frontal fibrosing alopecia also has been associated with the use of formalin and FA in hair straighteners.¹⁴ This is possibly related to the ability of FA and many phenolic products to induce chronic inflammation; however, a cumulative effect has not been noted consistently across the literature.

Future Directives

Continuous industry regulation is needed to ensure that use of FA is reduced and it is eventually eliminated from consumer products. Additionally, strict regulations are required to ensure products containing FA and FA-releasers are accurately labeled. Physicians and consumers should be aware of the potential health hazards associated with FA and advocate for effective legislation. While there is controversy regarding the level of absorption from environmental exposure and the subsequent biologic effects of absorption, both consumers and workers in industries such as hairdressing and barbering should reduce exposure time to FA and limit the application of heat and contact with products containing FA and FA releasers.

Formaldehyde (FA) is a colorless, flammable, highly pungent gas that remains ubiquitous in the environment despite being a known carcinogen and allergen.¹ In the cosmetic industry, FA commonly is used as both a preservative and active ingredient in hairstraightening products. Due to its toxicity and the thermal instability of FA releasers (ie, the release of FA at high temperatures), the US Food and Drug Administration has proposed a ban on formaldehyde and other FA-releasing chemicals (eg, methylene glycol) as an ingredient in hairsmoothing or hair-straightening products marketed in the United States.² However, the implementation of this ban is not yet in effect.

Hair-straightening products that are referred to as chemical relaxers typically contain alkaline derivatives. Alkaline hair straighteners—which include lye relaxers (active ingredient: sodium hydroxide), nolye relaxers (active ingredients: potassium hydroxide, lithium hydroxide, calcium hydroxide, guanidine hydroxide, or ammonium thioglycolate), and the Japanese hair straightening process (active ingredient: ammonium thioglycolate)—do not contain FA or FA-derivatives as active ingredients.³ Alternatively, acidic hair straighteners—popularly known as keratin treatments—contain either FA or FA-releasers and will be the primary focus of this discussion. As many patients are exposed to these products, we aim to highlight the cutaneous and systemic manifestations of acute and chronic exposure.

How Hair-Straightening Products Work

Hair straighteners that include FA or its derivatives generally contain high and low molecular weights of keratin peptides. The keratin peptides with high molecular weights diffuse into the cuticle while the low-molecular-weight peptides can penetrate further into the cortex of the hair shaft.⁴ Formaldehyde forms cross-links with the keratin amino acids (eg, tyrosine, arginine), and the application of heat via blow-drying enhances its ability to cross-link the hydrolyzed keratin from the straightening product to the natural keratin in the hair fibers; the use of a heated flat iron further enhances the cross-linking and seals the cuticle.⁵ The same mechanism of action applies for “safe keratin” (marketing terminology used for FA releasers) treatments, whereby the hydrogen and salt bonds of the hair are weakened, allowing for interconversion of the cysteine bonds of the hair fibers. This chemical conversion allows for the hair shafts to have a stable straight configuration. Of note, this mechanism of action differs from the action of chemical relaxers, which have a high pH and straighten the hair by opening the cuticles and permanently breaking the disulfide bonds in the cortex of the hair shaft—a process that restructures the keratin bonds without requiring heat application.⁵

The outcome of a keratin treatment, as seen on light microscopy, is the replenishment of gaps in the hair’s cuticle, therefore increasing its mechanical and thermal properties.⁶ This can give the appearance of increased shine, softness, and tensile strength. However, Sanad et al⁶ report that, as viewed on transmission electron microscopy, these keratin treatments do not repair lost cuticles, cuticle splitting, or detached cuticle layers from damaged strands.

Lastly, some patients notice lightening of their hair color after a hair-straightening treatment, which is possibly due to inhibition of the enzymatic synthesis of melanin, decomposition of melanin granules, or a direct reaction from chemical neutralizers with a high pH.⁶ Knowledge of the mechanism of action of hair-straightening treatments will aid dermatologists in educating patients about their immediate and long-term effects. This education subsequently will help patients avoid inappropriate hair care techniques that further damage the hair.

Environmental Distribution and Systemic Absorption of Formaldehyde

Atmospheric FA is absorbed via cutaneous and mucosal surfaces. Atmospheric FA concentrations produced when hair-straightening products are used cannot routinely be predicted because the amount generated depends on factors such as the pH of the preparation, the temperature to which the product is heated during straightening, duration of storage, and aeration and size of the environment in which the product is being used, among others.⁷

Peteffi et al⁷ and Aglan et al⁸ detected a moderate positive correlation between environmental FA concentrations and those in cosmetic products, particularly after blow-drying the hair or using other heat applications; however, the products examined by Peteffi et al⁷ contained exceedingly high concentrations of FA (up to 5.9%, which is higher than the legal limit of 0.1% in the United States).⁹ Of note, some products in this study were labelled as “formaldehyde free” but still contained high concentrations of FA.⁷ This is consistent with data published by the Occupational Health and Safety Administration, which citied salons with exposure limits outside the national recommendations (2.0 FA ppm/air).¹⁰ These findings highlight the inadvertent exposure that consumers face from products that are not regulated consistently.

Interestingly, Henault et al¹¹ observed that products with a high concentration of FA dispersed more airborne particles during hair brushing than hair straightening/ironing.¹¹ Further studies are needed to clarify the different routes and methods contributing to FA dispersion and the molecular instability of FA-releasers.

Clinical Correlation

Products that contain low (ie, less than the legal limit) levels of FA are not mandated to declare its presence on the product label; however, many products are contaminated with FA or inappropriately omit FA from the ingredient list, even at elevated concentrations. Consumers therefore may be inadvertently exposed to FA particles. Additionally, occupations with frequent exposure to FA include hairdressers, barbers, beauticians and related workers (33.6% exposure rate); sewers and embroiderers (26.1%); and cooks (19.1%).¹²

Adverse health effects associated with acute FA exposure include but are not limited to headache, eye irritation, allergic/irritant contact dermatitis, psoriasiform reactions, and acute kidney and respiratory tract injuries. Frontal fibrosing alopecia; non-Hodgkin lymphoma; and cancers of the upper digestive tract, lungs, and bladder also have been associated with chronic FA exposure.^7,13 In a cohort of female hairdressers, a longer duration of FA exposure (>8 years) as well as cumulative exposure were associated with an increase in ovarian cancer (OR, 1.48 [0.88 to 2.51]).¹² Formalin, the aqueous derivative of FA, also contains phenolic products that can mediate inflammatory response, DNA methylation, and carcinogenesis even with chronic low-level exposure.¹⁴ However, evidence supporting a direct correlation of FA exposure with breast carcinoma in both hairstylists and consumers remains controversial.⁷

Sanchez-Duenas et al¹⁵ described a case series of patients who were found to have psoriasiform scalp reactions after exposure to keratin treatments containing FA. The time to development of the lesions was inversely correlated with the number of treatments received, although the mean time to development was 12 months postprocedure.¹⁵ These researchers also identified no allergies to the substance on contact testing, which suggests an alternate pathogenesis as a consequence of FA exposure, resulting in the development of a psoriasiform reaction.¹⁵

Following adjustment for sex, age, menopause status, and skin color, frontal fibrosing alopecia also has been associated with the use of formalin and FA in hair straighteners.¹⁴ This is possibly related to the ability of FA and many phenolic products to induce chronic inflammation; however, a cumulative effect has not been noted consistently across the literature.

Future Directives

Continuous industry regulation is needed to ensure that use of FA is reduced and it is eventually eliminated from consumer products. Additionally, strict regulations are required to ensure products containing FA and FA-releasers are accurately labeled. Physicians and consumers should be aware of the potential health hazards associated with FA and advocate for effective legislation. While there is controversy regarding the level of absorption from environmental exposure and the subsequent biologic effects of absorption, both consumers and workers in industries such as hairdressing and barbering should reduce exposure time to FA and limit the application of heat and contact with products containing FA and FA releasers.