Article

Time was—recent time, that is—sailors had two chances to pass a physical fitness assessment (PFA). Failing the first meant no promotion. Failing the second: No career. They could neither be promoted nor reenlist.

That’s changed; as of this month, the Navy now allows the sailor’s commanding officer to decide whether the sailor gets to go on, even after failing a second test.

In an administrative letter, Vice Adm. Rick Cheeseman, chief of naval personnel, said, "Commanding officers can now evaluate a sailor's physical readiness progress or lack of progress in performance evaluations, giving them the ability to manage risk, recognize earnest effort, and best take care of their people.”

According to the new policy, sailors who fail any PFA no longer need to have it noted on their annual evaluation (although they still may not advance until they pass another test). Enlisted sailors who fail a second consecutive PFA are no longer required to receive the lowest possible score in the "Military Bearing/Professionalism" category and are not denied the ability to reenlist.

In assessing eligibility for enlisted members, the memo states that commanders should consider a sailor’s ability to perform the functions of their rate without physical or medical limitation at sea, shore or isolated duty; their overall ability to contribute to Navy missions; and the likelihood of improvement in meeting PFA standards within the next 12 months.

“Building the bodies of great people,” Cheeseman wrote, “is more than annual (or biannual) testing and includes ensuring healthy food, adequate sleep, opportunities to exercise (especially outside), and medical readiness.”  

According to a report by Military.com, “critics have argued that many of the changes were the Navy relaxing its standards in the face of a challenging recruiting environment and an increasingly overweight population of Americans.” However, Navy data provided in November indicate that the number of sailors failing PFAs has remained very low. In 2017, nearly 98% of sailors passed the PFA, and 95.1% passed the first post-pandemic PFA in 2022.

The PFA policy changes are part of the Navy’s Culture of Excellence 2.0, initiated earlier this year, Cheeseman says. This initiative “charges our leaders to build great people, great leaders, and great teams: their minds, bodies, and spirits, eliminating barriers wherever possible.  In response, we are modernizing our PFA policy to acknowledge our diverse population, increase sailor trust, and enhance quality of service.”

Time was—recent time, that is—sailors had two chances to pass a physical fitness assessment (PFA). Failing the first meant no promotion. Failing the second: No career. They could neither be promoted nor reenlist.

That’s changed; as of this month, the Navy now allows the sailor’s commanding officer to decide whether the sailor gets to go on, even after failing a second test.

In an administrative letter, Vice Adm. Rick Cheeseman, chief of naval personnel, said, "Commanding officers can now evaluate a sailor's physical readiness progress or lack of progress in performance evaluations, giving them the ability to manage risk, recognize earnest effort, and best take care of their people.”

According to the new policy, sailors who fail any PFA no longer need to have it noted on their annual evaluation (although they still may not advance until they pass another test). Enlisted sailors who fail a second consecutive PFA are no longer required to receive the lowest possible score in the "Military Bearing/Professionalism" category and are not denied the ability to reenlist.

In assessing eligibility for enlisted members, the memo states that commanders should consider a sailor’s ability to perform the functions of their rate without physical or medical limitation at sea, shore or isolated duty; their overall ability to contribute to Navy missions; and the likelihood of improvement in meeting PFA standards within the next 12 months.

“Building the bodies of great people,” Cheeseman wrote, “is more than annual (or biannual) testing and includes ensuring healthy food, adequate sleep, opportunities to exercise (especially outside), and medical readiness.”  

According to a report by Military.com, “critics have argued that many of the changes were the Navy relaxing its standards in the face of a challenging recruiting environment and an increasingly overweight population of Americans.” However, Navy data provided in November indicate that the number of sailors failing PFAs has remained very low. In 2017, nearly 98% of sailors passed the PFA, and 95.1% passed the first post-pandemic PFA in 2022.

The PFA policy changes are part of the Navy’s Culture of Excellence 2.0, initiated earlier this year, Cheeseman says. This initiative “charges our leaders to build great people, great leaders, and great teams: their minds, bodies, and spirits, eliminating barriers wherever possible.  In response, we are modernizing our PFA policy to acknowledge our diverse population, increase sailor trust, and enhance quality of service.”

Time was—recent time, that is—sailors had two chances to pass a physical fitness assessment (PFA). Failing the first meant no promotion. Failing the second: No career. They could neither be promoted nor reenlist.

That’s changed; as of this month, the Navy now allows the sailor’s commanding officer to decide whether the sailor gets to go on, even after failing a second test.

In an administrative letter, Vice Adm. Rick Cheeseman, chief of naval personnel, said, "Commanding officers can now evaluate a sailor's physical readiness progress or lack of progress in performance evaluations, giving them the ability to manage risk, recognize earnest effort, and best take care of their people.”

According to the new policy, sailors who fail any PFA no longer need to have it noted on their annual evaluation (although they still may not advance until they pass another test). Enlisted sailors who fail a second consecutive PFA are no longer required to receive the lowest possible score in the "Military Bearing/Professionalism" category and are not denied the ability to reenlist.

In assessing eligibility for enlisted members, the memo states that commanders should consider a sailor’s ability to perform the functions of their rate without physical or medical limitation at sea, shore or isolated duty; their overall ability to contribute to Navy missions; and the likelihood of improvement in meeting PFA standards within the next 12 months.

“Building the bodies of great people,” Cheeseman wrote, “is more than annual (or biannual) testing and includes ensuring healthy food, adequate sleep, opportunities to exercise (especially outside), and medical readiness.”  

According to a report by Military.com, “critics have argued that many of the changes were the Navy relaxing its standards in the face of a challenging recruiting environment and an increasingly overweight population of Americans.” However, Navy data provided in November indicate that the number of sailors failing PFAs has remained very low. In 2017, nearly 98% of sailors passed the PFA, and 95.1% passed the first post-pandemic PFA in 2022.

The PFA policy changes are part of the Navy’s Culture of Excellence 2.0, initiated earlier this year, Cheeseman says. This initiative “charges our leaders to build great people, great leaders, and great teams: their minds, bodies, and spirits, eliminating barriers wherever possible.  In response, we are modernizing our PFA policy to acknowledge our diverse population, increase sailor trust, and enhance quality of service.”

The Diagnosis: Cutaneous Nocardiosis

The wound culture was positive for Nocardia farcinica. The patient received a 5-day course of intravenous sulfamethoxazole-trimethoprim in the hospital and was transitioned to oral sulfamethoxazoletrimethoprim (800 mg/160 mg taken as 1 tablet twice daily) for 6 months. Complete resolution of the infection was noted at 6-month follow-up (Figure).

Nocardia is a gram-positive, aerobic bacterium that typically is found in soil, water, and decaying organic matter.¹ There are more than 50 species; N farcinica, Nocardia nova, and Nocardia asteroides are the leading causes of infection in humans and animals. Nocardia asteroides is the most common cause of infection in humans.^1,2 Nocardiosis is an uncommon opportunistic infection that usually targets the skin, lungs, and central nervous system.³ Although it mainly affects individuals who are immunocompromised, up to 30% of infections can be seen in immunocompetent hosts who can contract cutaneous nocardiosis after experiencing traumatic injury to the skin.¹

Nocardiosis is difficult to diagnose due to its diverse clinical presentations. For example, cutaneous nocardiosis can manifest similar to mycetoma, sporotrichosis, spider bites, nontuberculous mycobacteria such as Mycobacterium marinum, or methicillin-resistant Staphylococcus aureus infections, thus making cutaneous nocardiosis one of the great imitators.¹ A culture is required for definitive diagnosis, as Nocardia grows well on nonselective media such as blood or Löwenstein-Jensen agar. It grows as waxy, pigmented, cerebriform colonies 3 to 5 days following incubation.³ The bacterium can be difficult to culture, and it is important to notify the microbiology laboratory if there is a high index of clinical suspicion for infection.

A history of exposure to gardening or handling animals can increase the risk for an individual contracting Nocardia.³ Although nocardiosis can be found across the world, it is native to tropical and subtropical climates such as those found in India, Africa, Latin America, and Southeast Asia.¹ Infections mostly are observed in individuals aged 20 to 40 years and tend to affect men more than women. Lesions typically are seen on the lower extremities, but localized infections also can be found on the torso, neck, and upper extremities.¹

Cutaneous nocardiosis is a granulomatous infection encompassing both cutaneous and subcutaneous tissue, which ultimately can lead to injury of bone and viscera.¹ Primary cutaneous nocardiosis can manifest as tumors or nodules that have a sporotrichoid pattern, in which they ascend along the lymphatics. Histopathology of infected tissue frequently shows a subcutaneous dermal infiltrate of neutrophils accompanied with abscess formation, and everlasting lesions may show signs of chronic inflammation and nonspecific granulomas.³

Treatment of nocardiosis should be guided by in vitro susceptibility tests. Sulfamethoxazole-trimethoprim 800 mg/160 mg taken as 1 tablet twice daily is the first-line option. The treatment duration is contingent on the extent, severity, and complications of infection but typically is 3 to 6 months.¹

The Diagnosis: Cutaneous Nocardiosis

The wound culture was positive for Nocardia farcinica. The patient received a 5-day course of intravenous sulfamethoxazole-trimethoprim in the hospital and was transitioned to oral sulfamethoxazoletrimethoprim (800 mg/160 mg taken as 1 tablet twice daily) for 6 months. Complete resolution of the infection was noted at 6-month follow-up (Figure).

Nocardia is a gram-positive, aerobic bacterium that typically is found in soil, water, and decaying organic matter.¹ There are more than 50 species; N farcinica, Nocardia nova, and Nocardia asteroides are the leading causes of infection in humans and animals. Nocardia asteroides is the most common cause of infection in humans.^1,2 Nocardiosis is an uncommon opportunistic infection that usually targets the skin, lungs, and central nervous system.³ Although it mainly affects individuals who are immunocompromised, up to 30% of infections can be seen in immunocompetent hosts who can contract cutaneous nocardiosis after experiencing traumatic injury to the skin.¹

Nocardiosis is difficult to diagnose due to its diverse clinical presentations. For example, cutaneous nocardiosis can manifest similar to mycetoma, sporotrichosis, spider bites, nontuberculous mycobacteria such as Mycobacterium marinum, or methicillin-resistant Staphylococcus aureus infections, thus making cutaneous nocardiosis one of the great imitators.¹ A culture is required for definitive diagnosis, as Nocardia grows well on nonselective media such as blood or Löwenstein-Jensen agar. It grows as waxy, pigmented, cerebriform colonies 3 to 5 days following incubation.³ The bacterium can be difficult to culture, and it is important to notify the microbiology laboratory if there is a high index of clinical suspicion for infection.

A history of exposure to gardening or handling animals can increase the risk for an individual contracting Nocardia.³ Although nocardiosis can be found across the world, it is native to tropical and subtropical climates such as those found in India, Africa, Latin America, and Southeast Asia.¹ Infections mostly are observed in individuals aged 20 to 40 years and tend to affect men more than women. Lesions typically are seen on the lower extremities, but localized infections also can be found on the torso, neck, and upper extremities.¹

Cutaneous nocardiosis is a granulomatous infection encompassing both cutaneous and subcutaneous tissue, which ultimately can lead to injury of bone and viscera.¹ Primary cutaneous nocardiosis can manifest as tumors or nodules that have a sporotrichoid pattern, in which they ascend along the lymphatics. Histopathology of infected tissue frequently shows a subcutaneous dermal infiltrate of neutrophils accompanied with abscess formation, and everlasting lesions may show signs of chronic inflammation and nonspecific granulomas.³

Treatment of nocardiosis should be guided by in vitro susceptibility tests. Sulfamethoxazole-trimethoprim 800 mg/160 mg taken as 1 tablet twice daily is the first-line option. The treatment duration is contingent on the extent, severity, and complications of infection but typically is 3 to 6 months.¹

The Diagnosis: Cutaneous Nocardiosis

The wound culture was positive for Nocardia farcinica. The patient received a 5-day course of intravenous sulfamethoxazole-trimethoprim in the hospital and was transitioned to oral sulfamethoxazoletrimethoprim (800 mg/160 mg taken as 1 tablet twice daily) for 6 months. Complete resolution of the infection was noted at 6-month follow-up (Figure).

Nocardia is a gram-positive, aerobic bacterium that typically is found in soil, water, and decaying organic matter.¹ There are more than 50 species; N farcinica, Nocardia nova, and Nocardia asteroides are the leading causes of infection in humans and animals. Nocardia asteroides is the most common cause of infection in humans.^1,2 Nocardiosis is an uncommon opportunistic infection that usually targets the skin, lungs, and central nervous system.³ Although it mainly affects individuals who are immunocompromised, up to 30% of infections can be seen in immunocompetent hosts who can contract cutaneous nocardiosis after experiencing traumatic injury to the skin.¹

Nocardiosis is difficult to diagnose due to its diverse clinical presentations. For example, cutaneous nocardiosis can manifest similar to mycetoma, sporotrichosis, spider bites, nontuberculous mycobacteria such as Mycobacterium marinum, or methicillin-resistant Staphylococcus aureus infections, thus making cutaneous nocardiosis one of the great imitators.¹ A culture is required for definitive diagnosis, as Nocardia grows well on nonselective media such as blood or Löwenstein-Jensen agar. It grows as waxy, pigmented, cerebriform colonies 3 to 5 days following incubation.³ The bacterium can be difficult to culture, and it is important to notify the microbiology laboratory if there is a high index of clinical suspicion for infection.

A history of exposure to gardening or handling animals can increase the risk for an individual contracting Nocardia.³ Although nocardiosis can be found across the world, it is native to tropical and subtropical climates such as those found in India, Africa, Latin America, and Southeast Asia.¹ Infections mostly are observed in individuals aged 20 to 40 years and tend to affect men more than women. Lesions typically are seen on the lower extremities, but localized infections also can be found on the torso, neck, and upper extremities.¹

Cutaneous nocardiosis is a granulomatous infection encompassing both cutaneous and subcutaneous tissue, which ultimately can lead to injury of bone and viscera.¹ Primary cutaneous nocardiosis can manifest as tumors or nodules that have a sporotrichoid pattern, in which they ascend along the lymphatics. Histopathology of infected tissue frequently shows a subcutaneous dermal infiltrate of neutrophils accompanied with abscess formation, and everlasting lesions may show signs of chronic inflammation and nonspecific granulomas.³

Treatment of nocardiosis should be guided by in vitro susceptibility tests. Sulfamethoxazole-trimethoprim 800 mg/160 mg taken as 1 tablet twice daily is the first-line option. The treatment duration is contingent on the extent, severity, and complications of infection but typically is 3 to 6 months.¹

To the Editor:

Neutrophilic dermatoses—a group of inflammatory cutaneous conditions—include acute febrile neutrophilic dermatosis (Sweet syndrome), pyoderma gangrenosum, and neutrophilic dermatosis of the dorsal hands. Histopathology shows a dense dermal infiltrate of mature neutrophils. In 2005, the histiocytoid subtype of Sweet syndrome was introduced with histopathologic findings of a dermal infiltrate composed of immature myeloid cells that resemble histiocytes in appearance but stain strongly with neutrophil markers on immunohistochemistry.¹ We present a case of histiocytoid pyoderma gangrenosum with histopathology that showed a dense dermal histiocytoid infiltrate with strong positivity for neutrophil markers on immunohistochemistry.

An 85-year-old man was seen by dermatology in the inpatient setting for a new-onset painful abdominal wound. He had a medical history of myelodysplastic syndrome (MDS), high-grade invasive papillary urothelial carcinoma of the bladder, and a recent diagnosis of low-grade invasive ascending colon adenocarcinoma. Ten days prior he underwent a right colectomy without intraoperative complications that was followed by septic shock. Workup with urinalysis and urine culture showed minimal pyuria with Pseudomonas aeruginosa. Additional studies, including blood cultures, abdominal wound cultures, computed tomography of the abdomen and pelvis, renal ultrasound, and chest radiographs, were unremarkable and showed no signs of surgical site infection, intra-abdominal or pelvic abscess formation, or pulmonary embolism. Broad-spectrum antibiotics—vancomycin and piperacillin-tazobactam—were started. Persistent fever (T_max of 102.3 °F [39.1 °C]) and leukocytosis (45.3×10⁹/L [4.2–10×10⁹/L]) despite antibiotic therapy, increasing pressor requirements, and progressive painful erythema and purulence at the abdominal surgical site led to debridement of the wound by the general surgery team on day 9 following the initial surgery due to suspected necrotizing infection. Within 24 hours, dermatology was consulted for continued rapid expansion of the wound. Physical examination of the abdomen revealed a large, well-demarcated, pink-red, indurated, ulcerated plaque with clear to purulent exudate and superficial erosions with violaceous undermined borders extending centrifugally from the abdominal surgical incision line (Figure 1A). Two punch biopsies sent for histopathologic evaluation and tissue culture showed dermal edema with a dense histiocytic infiltrate with nodular foci and admixed mature neutrophils to a lesser degree (Figure 2). Special staining was negative for bacteria, fungi, and mycobacteria. Immunohistochemistry revealed positive staining of the dermal inflammatory infiltrate with CD68, myeloperoxidase, and lysozyme, as well as negative staining with CD34 (Figure 3). These findings were suggestive of a histiocytoid neutrophilic dermatosis such as Sweet syndrome or pyoderma gangrenosum. Due to the morphology of the solitary lesion and the abrupt exacerbation shortly after surgical intervention, the patient was diagnosed with histiocytoid pyoderma gangrenosum. At the same time, the patient’s septic shock was treated with intravenous hydrocortisone (100 mg 3 times daily) for 2 days and also achieved a prompt response in the cutaneous symptoms (Figure 1B).

Sweet syndrome and pyoderma gangrenosum are considered distinct neutrophilic dermatoses that rarely coexist but share several clinical and histopathologic features, which can become a diagnostic challenge.² Both conditions can manifest clinically as abrupt-onset, tender, erythematous papules; vesiculopustular lesions; or bullae with ulcerative changes. They also exhibit pathergy; present with systemic symptoms such as pyrexia, malaise, and joint pain; are associated with underlying systemic conditions such as infections and/or malignancy; demonstrate a dense neutrophilic infiltrate in the dermis on histopathology; and respond promptly to systemic corticosteroids.^2-6 Bullous Sweet syndrome, which can present as vesicles, pustules, or bullae that progress to superficial ulcerations, may represent a variant of neutrophilic dermatosis characterized by features seen in both Sweet syndrome and pyoderma gangrenosum, suggesting that these 2 conditions may be on a spectrum.⁵Clinical features such as erythema with a blue, gray, or purple hue; undermined and ragged borders; and healing of skin lesions with atrophic or cribriform scarring may favor pyoderma gangrenosum, whereas a dull red or plum color and resolution of lesions without scarring may support the diagnosis of Sweet syndrome.⁷ Although both conditions can exhibit pathergy secondary to minor skin trauma such as venipuncture and biopsies,^2,3,5,8 Sweet syndrome rarely has been described to develop after surgery in a patient without a known history of the condition.⁹ In contrast, postsurgical pyoderma gangrenosum has been well described as secondary to the pathergy phenomenon.⁵

Our patient was favored to have pyoderma gangrenosum given the solitary lesion, its abrupt development after surgery, and the morphology of the lesion that exhibited a large violaceous to red ulcerative and exudative plaque with undermined borders with atrophic scarring. In patients with skin disease that cannot be distinguished with certainty as either Sweet syndrome or pyoderma gangrenosum, it is essential to recognize that, as neutrophilic dermatoses, both conditions can be managed with either the first-line treatment option of high-dose systemic steroids or one of the shared alternative first-line or second-line steroid-sparing treatments, such as dapsone and cyclosporine.²

Although the exact pathogenesis of pyoderma gangrenosum remains to be fully understood, paraneoplastic pyoderma gangrenosum is a frequently described phenomenon.^10,11 Our patient’s history of multiple malignancies, both solid and hematologic, supports the likelihood of malignancy-induced pyoderma gangrenosum; however, given his history of MDS, several other conditions were ruled out prior to making the diagnosis of pyoderma gangrenosum.

Classically, neutrophilic dermatoses such as pyoderma gangrenosum have a dense dermal neutrophilic infiltrate. Concurrent myeloproliferative disorders can alter the maturation of leukocytes, subsequently leading to an atypical appearance of the inflammatory cells on histopathology. Further, in the setting of myeloproliferative disorders, conditions such as leukemia cutis, in which there can be a cutaneous infiltrate of immature or mature myeloid or lymphocytic cells, must be considered. To ensure our patient’s abdominal skin changes were not a cutaneous manifestation of hematologic malignancy, immunohistochemical staining with CD20 and CD3 was performed and showed only the rare presence of B and T lymphocytes, respectively. Staining with CD34 for lymphocytic and myeloid progenitor cells was negative in the dermal infiltrate and further reduced the likelihood of leukemia cutis. Alternatively, patients can have aleukemic cutaneous myeloid sarcoma or leukemia cutis without an underlying hematologic condition or with latent peripheral blood or bone marrow myeloproliferative disorder, but our patient’s history of MDS eliminated this possibility.¹² After exclusion of cutaneous infiltration by malignant leukocytes, our patient was diagnosed with histiocytoid neutrophilic dermatosis.

To the Editor:

Neutrophilic dermatoses—a group of inflammatory cutaneous conditions—include acute febrile neutrophilic dermatosis (Sweet syndrome), pyoderma gangrenosum, and neutrophilic dermatosis of the dorsal hands. Histopathology shows a dense dermal infiltrate of mature neutrophils. In 2005, the histiocytoid subtype of Sweet syndrome was introduced with histopathologic findings of a dermal infiltrate composed of immature myeloid cells that resemble histiocytes in appearance but stain strongly with neutrophil markers on immunohistochemistry.¹ We present a case of histiocytoid pyoderma gangrenosum with histopathology that showed a dense dermal histiocytoid infiltrate with strong positivity for neutrophil markers on immunohistochemistry.

An 85-year-old man was seen by dermatology in the inpatient setting for a new-onset painful abdominal wound. He had a medical history of myelodysplastic syndrome (MDS), high-grade invasive papillary urothelial carcinoma of the bladder, and a recent diagnosis of low-grade invasive ascending colon adenocarcinoma. Ten days prior he underwent a right colectomy without intraoperative complications that was followed by septic shock. Workup with urinalysis and urine culture showed minimal pyuria with Pseudomonas aeruginosa. Additional studies, including blood cultures, abdominal wound cultures, computed tomography of the abdomen and pelvis, renal ultrasound, and chest radiographs, were unremarkable and showed no signs of surgical site infection, intra-abdominal or pelvic abscess formation, or pulmonary embolism. Broad-spectrum antibiotics—vancomycin and piperacillin-tazobactam—were started. Persistent fever (T_max of 102.3 °F [39.1 °C]) and leukocytosis (45.3×10⁹/L [4.2–10×10⁹/L]) despite antibiotic therapy, increasing pressor requirements, and progressive painful erythema and purulence at the abdominal surgical site led to debridement of the wound by the general surgery team on day 9 following the initial surgery due to suspected necrotizing infection. Within 24 hours, dermatology was consulted for continued rapid expansion of the wound. Physical examination of the abdomen revealed a large, well-demarcated, pink-red, indurated, ulcerated plaque with clear to purulent exudate and superficial erosions with violaceous undermined borders extending centrifugally from the abdominal surgical incision line (Figure 1A). Two punch biopsies sent for histopathologic evaluation and tissue culture showed dermal edema with a dense histiocytic infiltrate with nodular foci and admixed mature neutrophils to a lesser degree (Figure 2). Special staining was negative for bacteria, fungi, and mycobacteria. Immunohistochemistry revealed positive staining of the dermal inflammatory infiltrate with CD68, myeloperoxidase, and lysozyme, as well as negative staining with CD34 (Figure 3). These findings were suggestive of a histiocytoid neutrophilic dermatosis such as Sweet syndrome or pyoderma gangrenosum. Due to the morphology of the solitary lesion and the abrupt exacerbation shortly after surgical intervention, the patient was diagnosed with histiocytoid pyoderma gangrenosum. At the same time, the patient’s septic shock was treated with intravenous hydrocortisone (100 mg 3 times daily) for 2 days and also achieved a prompt response in the cutaneous symptoms (Figure 1B).

Sweet syndrome and pyoderma gangrenosum are considered distinct neutrophilic dermatoses that rarely coexist but share several clinical and histopathologic features, which can become a diagnostic challenge.² Both conditions can manifest clinically as abrupt-onset, tender, erythematous papules; vesiculopustular lesions; or bullae with ulcerative changes. They also exhibit pathergy; present with systemic symptoms such as pyrexia, malaise, and joint pain; are associated with underlying systemic conditions such as infections and/or malignancy; demonstrate a dense neutrophilic infiltrate in the dermis on histopathology; and respond promptly to systemic corticosteroids.^2-6 Bullous Sweet syndrome, which can present as vesicles, pustules, or bullae that progress to superficial ulcerations, may represent a variant of neutrophilic dermatosis characterized by features seen in both Sweet syndrome and pyoderma gangrenosum, suggesting that these 2 conditions may be on a spectrum.⁵Clinical features such as erythema with a blue, gray, or purple hue; undermined and ragged borders; and healing of skin lesions with atrophic or cribriform scarring may favor pyoderma gangrenosum, whereas a dull red or plum color and resolution of lesions without scarring may support the diagnosis of Sweet syndrome.⁷ Although both conditions can exhibit pathergy secondary to minor skin trauma such as venipuncture and biopsies,^2,3,5,8 Sweet syndrome rarely has been described to develop after surgery in a patient without a known history of the condition.⁹ In contrast, postsurgical pyoderma gangrenosum has been well described as secondary to the pathergy phenomenon.⁵

Our patient was favored to have pyoderma gangrenosum given the solitary lesion, its abrupt development after surgery, and the morphology of the lesion that exhibited a large violaceous to red ulcerative and exudative plaque with undermined borders with atrophic scarring. In patients with skin disease that cannot be distinguished with certainty as either Sweet syndrome or pyoderma gangrenosum, it is essential to recognize that, as neutrophilic dermatoses, both conditions can be managed with either the first-line treatment option of high-dose systemic steroids or one of the shared alternative first-line or second-line steroid-sparing treatments, such as dapsone and cyclosporine.²

Although the exact pathogenesis of pyoderma gangrenosum remains to be fully understood, paraneoplastic pyoderma gangrenosum is a frequently described phenomenon.^10,11 Our patient’s history of multiple malignancies, both solid and hematologic, supports the likelihood of malignancy-induced pyoderma gangrenosum; however, given his history of MDS, several other conditions were ruled out prior to making the diagnosis of pyoderma gangrenosum.

Classically, neutrophilic dermatoses such as pyoderma gangrenosum have a dense dermal neutrophilic infiltrate. Concurrent myeloproliferative disorders can alter the maturation of leukocytes, subsequently leading to an atypical appearance of the inflammatory cells on histopathology. Further, in the setting of myeloproliferative disorders, conditions such as leukemia cutis, in which there can be a cutaneous infiltrate of immature or mature myeloid or lymphocytic cells, must be considered. To ensure our patient’s abdominal skin changes were not a cutaneous manifestation of hematologic malignancy, immunohistochemical staining with CD20 and CD3 was performed and showed only the rare presence of B and T lymphocytes, respectively. Staining with CD34 for lymphocytic and myeloid progenitor cells was negative in the dermal infiltrate and further reduced the likelihood of leukemia cutis. Alternatively, patients can have aleukemic cutaneous myeloid sarcoma or leukemia cutis without an underlying hematologic condition or with latent peripheral blood or bone marrow myeloproliferative disorder, but our patient’s history of MDS eliminated this possibility.¹² After exclusion of cutaneous infiltration by malignant leukocytes, our patient was diagnosed with histiocytoid neutrophilic dermatosis.

To the Editor:

Neutrophilic dermatoses—a group of inflammatory cutaneous conditions—include acute febrile neutrophilic dermatosis (Sweet syndrome), pyoderma gangrenosum, and neutrophilic dermatosis of the dorsal hands. Histopathology shows a dense dermal infiltrate of mature neutrophils. In 2005, the histiocytoid subtype of Sweet syndrome was introduced with histopathologic findings of a dermal infiltrate composed of immature myeloid cells that resemble histiocytes in appearance but stain strongly with neutrophil markers on immunohistochemistry.¹ We present a case of histiocytoid pyoderma gangrenosum with histopathology that showed a dense dermal histiocytoid infiltrate with strong positivity for neutrophil markers on immunohistochemistry.

An 85-year-old man was seen by dermatology in the inpatient setting for a new-onset painful abdominal wound. He had a medical history of myelodysplastic syndrome (MDS), high-grade invasive papillary urothelial carcinoma of the bladder, and a recent diagnosis of low-grade invasive ascending colon adenocarcinoma. Ten days prior he underwent a right colectomy without intraoperative complications that was followed by septic shock. Workup with urinalysis and urine culture showed minimal pyuria with Pseudomonas aeruginosa. Additional studies, including blood cultures, abdominal wound cultures, computed tomography of the abdomen and pelvis, renal ultrasound, and chest radiographs, were unremarkable and showed no signs of surgical site infection, intra-abdominal or pelvic abscess formation, or pulmonary embolism. Broad-spectrum antibiotics—vancomycin and piperacillin-tazobactam—were started. Persistent fever (T_max of 102.3 °F [39.1 °C]) and leukocytosis (45.3×10⁹/L [4.2–10×10⁹/L]) despite antibiotic therapy, increasing pressor requirements, and progressive painful erythema and purulence at the abdominal surgical site led to debridement of the wound by the general surgery team on day 9 following the initial surgery due to suspected necrotizing infection. Within 24 hours, dermatology was consulted for continued rapid expansion of the wound. Physical examination of the abdomen revealed a large, well-demarcated, pink-red, indurated, ulcerated plaque with clear to purulent exudate and superficial erosions with violaceous undermined borders extending centrifugally from the abdominal surgical incision line (Figure 1A). Two punch biopsies sent for histopathologic evaluation and tissue culture showed dermal edema with a dense histiocytic infiltrate with nodular foci and admixed mature neutrophils to a lesser degree (Figure 2). Special staining was negative for bacteria, fungi, and mycobacteria. Immunohistochemistry revealed positive staining of the dermal inflammatory infiltrate with CD68, myeloperoxidase, and lysozyme, as well as negative staining with CD34 (Figure 3). These findings were suggestive of a histiocytoid neutrophilic dermatosis such as Sweet syndrome or pyoderma gangrenosum. Due to the morphology of the solitary lesion and the abrupt exacerbation shortly after surgical intervention, the patient was diagnosed with histiocytoid pyoderma gangrenosum. At the same time, the patient’s septic shock was treated with intravenous hydrocortisone (100 mg 3 times daily) for 2 days and also achieved a prompt response in the cutaneous symptoms (Figure 1B).

Sweet syndrome and pyoderma gangrenosum are considered distinct neutrophilic dermatoses that rarely coexist but share several clinical and histopathologic features, which can become a diagnostic challenge.² Both conditions can manifest clinically as abrupt-onset, tender, erythematous papules; vesiculopustular lesions; or bullae with ulcerative changes. They also exhibit pathergy; present with systemic symptoms such as pyrexia, malaise, and joint pain; are associated with underlying systemic conditions such as infections and/or malignancy; demonstrate a dense neutrophilic infiltrate in the dermis on histopathology; and respond promptly to systemic corticosteroids.^2-6 Bullous Sweet syndrome, which can present as vesicles, pustules, or bullae that progress to superficial ulcerations, may represent a variant of neutrophilic dermatosis characterized by features seen in both Sweet syndrome and pyoderma gangrenosum, suggesting that these 2 conditions may be on a spectrum.⁵Clinical features such as erythema with a blue, gray, or purple hue; undermined and ragged borders; and healing of skin lesions with atrophic or cribriform scarring may favor pyoderma gangrenosum, whereas a dull red or plum color and resolution of lesions without scarring may support the diagnosis of Sweet syndrome.⁷ Although both conditions can exhibit pathergy secondary to minor skin trauma such as venipuncture and biopsies,^2,3,5,8 Sweet syndrome rarely has been described to develop after surgery in a patient without a known history of the condition.⁹ In contrast, postsurgical pyoderma gangrenosum has been well described as secondary to the pathergy phenomenon.⁵

Our patient was favored to have pyoderma gangrenosum given the solitary lesion, its abrupt development after surgery, and the morphology of the lesion that exhibited a large violaceous to red ulcerative and exudative plaque with undermined borders with atrophic scarring. In patients with skin disease that cannot be distinguished with certainty as either Sweet syndrome or pyoderma gangrenosum, it is essential to recognize that, as neutrophilic dermatoses, both conditions can be managed with either the first-line treatment option of high-dose systemic steroids or one of the shared alternative first-line or second-line steroid-sparing treatments, such as dapsone and cyclosporine.²

Although the exact pathogenesis of pyoderma gangrenosum remains to be fully understood, paraneoplastic pyoderma gangrenosum is a frequently described phenomenon.^10,11 Our patient’s history of multiple malignancies, both solid and hematologic, supports the likelihood of malignancy-induced pyoderma gangrenosum; however, given his history of MDS, several other conditions were ruled out prior to making the diagnosis of pyoderma gangrenosum.

Classically, neutrophilic dermatoses such as pyoderma gangrenosum have a dense dermal neutrophilic infiltrate. Concurrent myeloproliferative disorders can alter the maturation of leukocytes, subsequently leading to an atypical appearance of the inflammatory cells on histopathology. Further, in the setting of myeloproliferative disorders, conditions such as leukemia cutis, in which there can be a cutaneous infiltrate of immature or mature myeloid or lymphocytic cells, must be considered. To ensure our patient’s abdominal skin changes were not a cutaneous manifestation of hematologic malignancy, immunohistochemical staining with CD20 and CD3 was performed and showed only the rare presence of B and T lymphocytes, respectively. Staining with CD34 for lymphocytic and myeloid progenitor cells was negative in the dermal infiltrate and further reduced the likelihood of leukemia cutis. Alternatively, patients can have aleukemic cutaneous myeloid sarcoma or leukemia cutis without an underlying hematologic condition or with latent peripheral blood or bone marrow myeloproliferative disorder, but our patient’s history of MDS eliminated this possibility.¹² After exclusion of cutaneous infiltration by malignant leukocytes, our patient was diagnosed with histiocytoid neutrophilic dermatosis.

A variety of skin problems can occur in musicians due to the repetitive movements of playing instruments.^1,2 Musicians’ nails are continuously exposed to the mechanical forces and chemical substances characteristic of their instruments.³ Occupational nail alterations in musicians caused by repetitive physical trauma, allergic contact dermatitis, and/or infection may lead to disability and compromise their professional career.³

We conducted a systematic review of the literature on the clinical features of musical instrument–related nail alterations to optimize the management and prevention of these conditions.

Methods

We conducted a systematic review of PubMed, Scopus, and Google Scholar databases for eligible publications on instrument-related nail alterations in musicians using the search terms musicians with nail, onychopathy, and Raynaud. No time or language criteria were applied. Reviews, editorials, and articles not related to the topic were excluded. Bibliographies/reference lists were checked to find any additional relevant publications. Relevant articles in English and French were screened by 2 independent reviewers (A.G. and N.L.), and the following data were extracted for qualitative synthesis: sex, age, musical instrument, clinical features, number of years practicing the instrument, laboratory investigations, and disease course.

Results

The literature search yielded 11 publications. Sixteen additional articles were identified by other methods (ie, references, related publications). Overall, 3 full-text articles described general nail alterations but did not describe the clinical data, and 11 publications were editorials, commentaries, reviews, or not relevant. Thirteen contributions fulfilled the inclusion criteria and were eligible for qualitative synthesis. The flow diagram illustrates the screening process (Figure 1).

Twenty-three patients were included. The instruments identified were divided into 2 groups: string instruments (ie, guitar, violin, harp) and percussion instruments (ie, drums, piano, slap bass). Nail alterations were clinically expressed as: (1) modifications of the nail surface; (2) nail bed, soft-tissue, and bone abnormalities; and (3) periungual tissue and distal pulp disorders. All cases are summarized in the Table.^4-16 Three articles described occupational Raynaud phenomenon.^12-14

Comment

Modifications of the Nail Surface—Onychodystrophy, such as deformity or discoloration of the nail plate, was described in 6 patients among a cohort of 295 musicians and an additional 6 patients among 199 musicians with induced skin lesions. This condition was most common in string instrument players and pianists due to injury and irritation.^4,5

One patient, who had been a professional violist for 27 years, presented with lamellar onychoschizia, which corresponds to a horizontal splitting of the nail toward its distal portion (Figure 2). The 3 fingernails of the dominant hand were involved with a V-shaped incision of the distal margin of the nail due to the repetitive friction of the nails with the strings.⁶

Striations of the nail plate were reported in a guitarist who played for 10 years.⁷ Physical examination revealed linear transverse ridges alternating with depressions on the central aspect of the nail plate of the right thumbnail, as the patient was right-handed. This condition, attributed to sustained pressure on the string applied by the thumb, also has been called habit tic deformity.⁷

Nail Bed, Soft-Tissue, and Bone Lesions—Purpura (or hemorrhage) of the nail bed was associated with a percussion instrument (ie, piano) in 1 patient, affecting the second, third, and fourth fingernails of the right hand.⁸ Especially when performing ascending glissando passages, the pianist applies pressure that may damage the finger and cause fingernail purpura. This condition improved after the patient stopping practicing glissandi.⁸

Conclusion

Healthy nails are essential for playing a musical instrument. This review highlights the occurrence of fingertip callosities, paronychia, onycholysis, and subungual hemorrhages among musicians who play instruments. Additionally, the transmission of string-vibratory movements can produce microvascular damage and occupational Raynaud phenomenon in some musicians. These occupational nail disorders are underrecognized and may be underdiagnosed. Thus, musicians and clinicians must be aware of these alterations to adopt preventive measures and to provide adequate treatment.

A variety of skin problems can occur in musicians due to the repetitive movements of playing instruments.^1,2 Musicians’ nails are continuously exposed to the mechanical forces and chemical substances characteristic of their instruments.³ Occupational nail alterations in musicians caused by repetitive physical trauma, allergic contact dermatitis, and/or infection may lead to disability and compromise their professional career.³

We conducted a systematic review of the literature on the clinical features of musical instrument–related nail alterations to optimize the management and prevention of these conditions.

Methods

We conducted a systematic review of PubMed, Scopus, and Google Scholar databases for eligible publications on instrument-related nail alterations in musicians using the search terms musicians with nail, onychopathy, and Raynaud. No time or language criteria were applied. Reviews, editorials, and articles not related to the topic were excluded. Bibliographies/reference lists were checked to find any additional relevant publications. Relevant articles in English and French were screened by 2 independent reviewers (A.G. and N.L.), and the following data were extracted for qualitative synthesis: sex, age, musical instrument, clinical features, number of years practicing the instrument, laboratory investigations, and disease course.

Results

The literature search yielded 11 publications. Sixteen additional articles were identified by other methods (ie, references, related publications). Overall, 3 full-text articles described general nail alterations but did not describe the clinical data, and 11 publications were editorials, commentaries, reviews, or not relevant. Thirteen contributions fulfilled the inclusion criteria and were eligible for qualitative synthesis. The flow diagram illustrates the screening process (Figure 1).

Twenty-three patients were included. The instruments identified were divided into 2 groups: string instruments (ie, guitar, violin, harp) and percussion instruments (ie, drums, piano, slap bass). Nail alterations were clinically expressed as: (1) modifications of the nail surface; (2) nail bed, soft-tissue, and bone abnormalities; and (3) periungual tissue and distal pulp disorders. All cases are summarized in the Table.^4-16 Three articles described occupational Raynaud phenomenon.^12-14

Comment

Modifications of the Nail Surface—Onychodystrophy, such as deformity or discoloration of the nail plate, was described in 6 patients among a cohort of 295 musicians and an additional 6 patients among 199 musicians with induced skin lesions. This condition was most common in string instrument players and pianists due to injury and irritation.^4,5

One patient, who had been a professional violist for 27 years, presented with lamellar onychoschizia, which corresponds to a horizontal splitting of the nail toward its distal portion (Figure 2). The 3 fingernails of the dominant hand were involved with a V-shaped incision of the distal margin of the nail due to the repetitive friction of the nails with the strings.⁶

Striations of the nail plate were reported in a guitarist who played for 10 years.⁷ Physical examination revealed linear transverse ridges alternating with depressions on the central aspect of the nail plate of the right thumbnail, as the patient was right-handed. This condition, attributed to sustained pressure on the string applied by the thumb, also has been called habit tic deformity.⁷

Nail Bed, Soft-Tissue, and Bone Lesions—Purpura (or hemorrhage) of the nail bed was associated with a percussion instrument (ie, piano) in 1 patient, affecting the second, third, and fourth fingernails of the right hand.⁸ Especially when performing ascending glissando passages, the pianist applies pressure that may damage the finger and cause fingernail purpura. This condition improved after the patient stopping practicing glissandi.⁸

Conclusion

Healthy nails are essential for playing a musical instrument. This review highlights the occurrence of fingertip callosities, paronychia, onycholysis, and subungual hemorrhages among musicians who play instruments. Additionally, the transmission of string-vibratory movements can produce microvascular damage and occupational Raynaud phenomenon in some musicians. These occupational nail disorders are underrecognized and may be underdiagnosed. Thus, musicians and clinicians must be aware of these alterations to adopt preventive measures and to provide adequate treatment.

A variety of skin problems can occur in musicians due to the repetitive movements of playing instruments.^1,2 Musicians’ nails are continuously exposed to the mechanical forces and chemical substances characteristic of their instruments.³ Occupational nail alterations in musicians caused by repetitive physical trauma, allergic contact dermatitis, and/or infection may lead to disability and compromise their professional career.³

We conducted a systematic review of the literature on the clinical features of musical instrument–related nail alterations to optimize the management and prevention of these conditions.

Methods

We conducted a systematic review of PubMed, Scopus, and Google Scholar databases for eligible publications on instrument-related nail alterations in musicians using the search terms musicians with nail, onychopathy, and Raynaud. No time or language criteria were applied. Reviews, editorials, and articles not related to the topic were excluded. Bibliographies/reference lists were checked to find any additional relevant publications. Relevant articles in English and French were screened by 2 independent reviewers (A.G. and N.L.), and the following data were extracted for qualitative synthesis: sex, age, musical instrument, clinical features, number of years practicing the instrument, laboratory investigations, and disease course.

Results

The literature search yielded 11 publications. Sixteen additional articles were identified by other methods (ie, references, related publications). Overall, 3 full-text articles described general nail alterations but did not describe the clinical data, and 11 publications were editorials, commentaries, reviews, or not relevant. Thirteen contributions fulfilled the inclusion criteria and were eligible for qualitative synthesis. The flow diagram illustrates the screening process (Figure 1).

Twenty-three patients were included. The instruments identified were divided into 2 groups: string instruments (ie, guitar, violin, harp) and percussion instruments (ie, drums, piano, slap bass). Nail alterations were clinically expressed as: (1) modifications of the nail surface; (2) nail bed, soft-tissue, and bone abnormalities; and (3) periungual tissue and distal pulp disorders. All cases are summarized in the Table.^4-16 Three articles described occupational Raynaud phenomenon.^12-14

Comment

Modifications of the Nail Surface—Onychodystrophy, such as deformity or discoloration of the nail plate, was described in 6 patients among a cohort of 295 musicians and an additional 6 patients among 199 musicians with induced skin lesions. This condition was most common in string instrument players and pianists due to injury and irritation.^4,5

One patient, who had been a professional violist for 27 years, presented with lamellar onychoschizia, which corresponds to a horizontal splitting of the nail toward its distal portion (Figure 2). The 3 fingernails of the dominant hand were involved with a V-shaped incision of the distal margin of the nail due to the repetitive friction of the nails with the strings.⁶

Striations of the nail plate were reported in a guitarist who played for 10 years.⁷ Physical examination revealed linear transverse ridges alternating with depressions on the central aspect of the nail plate of the right thumbnail, as the patient was right-handed. This condition, attributed to sustained pressure on the string applied by the thumb, also has been called habit tic deformity.⁷

Nail Bed, Soft-Tissue, and Bone Lesions—Purpura (or hemorrhage) of the nail bed was associated with a percussion instrument (ie, piano) in 1 patient, affecting the second, third, and fourth fingernails of the right hand.⁸ Especially when performing ascending glissando passages, the pianist applies pressure that may damage the finger and cause fingernail purpura. This condition improved after the patient stopping practicing glissandi.⁸

Conclusion

Healthy nails are essential for playing a musical instrument. This review highlights the occurrence of fingertip callosities, paronychia, onycholysis, and subungual hemorrhages among musicians who play instruments. Additionally, the transmission of string-vibratory movements can produce microvascular damage and occupational Raynaud phenomenon in some musicians. These occupational nail disorders are underrecognized and may be underdiagnosed. Thus, musicians and clinicians must be aware of these alterations to adopt preventive measures and to provide adequate treatment.

The Comparison

A Traction alopecia in a Hispanic woman who wears her hair in a tight bun.

B Traction alopecia in a Black adolescent girl who wears her hair in tight hairstyles.

Traction alopecia (TA) is a common type of alopecia that ultimately can result in permanent hair loss. It often is caused or worsened by repetitive and prolonged hairstyling practices such as tight ponytails, braids, or locs, or use of wigs or weaves.¹ Use of headwear, as in certain religious or ethnic groups, also can be contributory.² Individuals participating in or training for occupations involving military service or ballet are at risk for TA due to hairstyling-specific policies. Early stages of TA are reversible with proper treatment and avoidance of exacerbating factors, emphasizing the importance of prompt recognition.³

Epidemiology

Data on the true prevalence of TA are lacking. It can occur in individuals of any race or any hair type. However, it is most common in women of African descent, affecting approximately one-third of this population.⁴ Other commonly affected groups include ballerinas and active-duty service members due to tight ponytails and buns, as well as the Sikh population due to the use of turbans as a part of their religious practice.^2,5,6

Traction alopecia also impacts children, particularly those of African descent. A 2007 study of schoolchildren in South Africa determined that more than 17% of young African girls had evidence of TA—even some as young as 6 years of age.⁷

Traction alopecia can be caused or exacerbated by the use of hair clips and bobby pins that aid holding styles in place.⁸

Hair shaft morphology may contribute to the risk for TA, with more tightly coiled hair types being more susceptible.⁸ Variables such as use of chemical relaxers also increase the risk for disease, especially when combined with high-tension styling methods such as braids.⁹

Key clinical features

Patients with TA clinically present with hair loss and breakage in areas with tension, most commonly the marginal areas of the scalp as well as the frontal hairline and temporal scalp. Hair loss can result in a “fringe sign,” in which a patient may have preservation of a thin line of hairs at the frontal aspect of the hairline with a band of hair loss behind.¹⁰ This presentation may be used to differentiate TA from other forms of alopecia, including frontal fibrosing alopecia and female pattern hair loss. When the hair loss is not marginal, it may mimic other forms of patchy hair loss including alopecia areata and trichotillomania. Other clinical findings in TA may include broken hairs, pustules, and follicular papules.¹⁰ Patients also may describe symptoms such as scalp tenderness with specific hairstyles or headaches,¹¹ or they may be completely asymptomatic.

Trichoscopy can be helpful in guiding diagnosis and treatment. Patients with TA often have perifollicular erythema and hair casts (cylindrical structures that encircle the proximal hair shafts) in the earlier stages of the disease, with eventual loss of follicular ostia in the later stages.^10,12 Hair casts also may indicate ongoing traction.¹² The flambeau sign—white tracks seen on trichoscopy in the direction the hair is pulled—resembles a lit torch.¹³

Worth noting

Early-stage TA can be reversed by avoiding hair tension. However, patients may not be amenable to this due to personal hairstyling preferences, job duties, or religious practices. Treatment with topical or intralesional steroids or even oral antibiotics such as doxycycline for its anti-inflammatory ability may result in regrowth of lost hair if the follicles are not permanently lost and exacerbating factors are avoided.^3,14 Both topical and oral minoxidil have been used with success, with minoxidil thought to increase hair density by extending the anagen (growth) phase of hair follicles.^3,15 Culturally sensitive patient counseling on the condition and potential exacerbating factors is critical.¹⁶

At later stages of the disease—after loss of follicular ostia has occurred—surgical interventions should be considered,¹⁷ such as hair transplantation, which can be successful but remains a technical challenge due to variability in hair shaft curvature.¹⁸ Additionally, the cost of the procedure can limit use, and some patients may not be optimal candidates due to the extent of their hair loss. Traction alopecia may not be the only hair loss condition present. Examining the scalp is important even if the chief area of concern is the marginal scalp.

Health disparity highlight

Prevention, early identification, and treatment initiated in a timely fashion are crucial to prevent permanent hair loss. There are added societal and cultural pressures that impact hairstyle and hair care practices, especially for those with tightly coiled hair.¹⁹ Historically, tightly coiled hair has been unfairly viewed as “unprofessional,” “unkempt,” and a challenge to “manage” by some. Thus, heat, chemical relaxers, and tight hairstyles holding hair in one position have been used to straighten the hair permanently or temporarily or to keep it maintained in a style that did not necessitate excessive manipulation—often contributing to further tension on the hair.

Military service branches have evaluated and changed some hair-related policies to reflect the diverse hair types of military personnel.²⁰ The CROWN Act (www.thecrownact.com/about)—“Creating a Respectful and Open World for Natural Hair”—is a model law passed by 26 states that prohibits race-based hair discrimination, which is the denial of employment and educational opportunities because of hair texture. Although the law has not been passed in every state, it may help individuals with tightly coiled hair to embrace natural hairstyles. However, even hairstyles with one’s own natural curl pattern can contribute to tension and thus potential development of TA.

The Comparison

A Traction alopecia in a Hispanic woman who wears her hair in a tight bun.

B Traction alopecia in a Black adolescent girl who wears her hair in tight hairstyles.

Traction alopecia (TA) is a common type of alopecia that ultimately can result in permanent hair loss. It often is caused or worsened by repetitive and prolonged hairstyling practices such as tight ponytails, braids, or locs, or use of wigs or weaves.¹ Use of headwear, as in certain religious or ethnic groups, also can be contributory.² Individuals participating in or training for occupations involving military service or ballet are at risk for TA due to hairstyling-specific policies. Early stages of TA are reversible with proper treatment and avoidance of exacerbating factors, emphasizing the importance of prompt recognition.³

Epidemiology

Data on the true prevalence of TA are lacking. It can occur in individuals of any race or any hair type. However, it is most common in women of African descent, affecting approximately one-third of this population.⁴ Other commonly affected groups include ballerinas and active-duty service members due to tight ponytails and buns, as well as the Sikh population due to the use of turbans as a part of their religious practice.^2,5,6

Traction alopecia also impacts children, particularly those of African descent. A 2007 study of schoolchildren in South Africa determined that more than 17% of young African girls had evidence of TA—even some as young as 6 years of age.⁷

Traction alopecia can be caused or exacerbated by the use of hair clips and bobby pins that aid holding styles in place.⁸

Hair shaft morphology may contribute to the risk for TA, with more tightly coiled hair types being more susceptible.⁸ Variables such as use of chemical relaxers also increase the risk for disease, especially when combined with high-tension styling methods such as braids.⁹

Key clinical features

Patients with TA clinically present with hair loss and breakage in areas with tension, most commonly the marginal areas of the scalp as well as the frontal hairline and temporal scalp. Hair loss can result in a “fringe sign,” in which a patient may have preservation of a thin line of hairs at the frontal aspect of the hairline with a band of hair loss behind.¹⁰ This presentation may be used to differentiate TA from other forms of alopecia, including frontal fibrosing alopecia and female pattern hair loss. When the hair loss is not marginal, it may mimic other forms of patchy hair loss including alopecia areata and trichotillomania. Other clinical findings in TA may include broken hairs, pustules, and follicular papules.¹⁰ Patients also may describe symptoms such as scalp tenderness with specific hairstyles or headaches,¹¹ or they may be completely asymptomatic.

Trichoscopy can be helpful in guiding diagnosis and treatment. Patients with TA often have perifollicular erythema and hair casts (cylindrical structures that encircle the proximal hair shafts) in the earlier stages of the disease, with eventual loss of follicular ostia in the later stages.^10,12 Hair casts also may indicate ongoing traction.¹² The flambeau sign—white tracks seen on trichoscopy in the direction the hair is pulled—resembles a lit torch.¹³

Worth noting

Early-stage TA can be reversed by avoiding hair tension. However, patients may not be amenable to this due to personal hairstyling preferences, job duties, or religious practices. Treatment with topical or intralesional steroids or even oral antibiotics such as doxycycline for its anti-inflammatory ability may result in regrowth of lost hair if the follicles are not permanently lost and exacerbating factors are avoided.^3,14 Both topical and oral minoxidil have been used with success, with minoxidil thought to increase hair density by extending the anagen (growth) phase of hair follicles.^3,15 Culturally sensitive patient counseling on the condition and potential exacerbating factors is critical.¹⁶

At later stages of the disease—after loss of follicular ostia has occurred—surgical interventions should be considered,¹⁷ such as hair transplantation, which can be successful but remains a technical challenge due to variability in hair shaft curvature.¹⁸ Additionally, the cost of the procedure can limit use, and some patients may not be optimal candidates due to the extent of their hair loss. Traction alopecia may not be the only hair loss condition present. Examining the scalp is important even if the chief area of concern is the marginal scalp.

Health disparity highlight

Prevention, early identification, and treatment initiated in a timely fashion are crucial to prevent permanent hair loss. There are added societal and cultural pressures that impact hairstyle and hair care practices, especially for those with tightly coiled hair.¹⁹ Historically, tightly coiled hair has been unfairly viewed as “unprofessional,” “unkempt,” and a challenge to “manage” by some. Thus, heat, chemical relaxers, and tight hairstyles holding hair in one position have been used to straighten the hair permanently or temporarily or to keep it maintained in a style that did not necessitate excessive manipulation—often contributing to further tension on the hair.

Military service branches have evaluated and changed some hair-related policies to reflect the diverse hair types of military personnel.²⁰ The CROWN Act (www.thecrownact.com/about)—“Creating a Respectful and Open World for Natural Hair”—is a model law passed by 26 states that prohibits race-based hair discrimination, which is the denial of employment and educational opportunities because of hair texture. Although the law has not been passed in every state, it may help individuals with tightly coiled hair to embrace natural hairstyles. However, even hairstyles with one’s own natural curl pattern can contribute to tension and thus potential development of TA.

The Comparison

A Traction alopecia in a Hispanic woman who wears her hair in a tight bun.

B Traction alopecia in a Black adolescent girl who wears her hair in tight hairstyles.

Traction alopecia (TA) is a common type of alopecia that ultimately can result in permanent hair loss. It often is caused or worsened by repetitive and prolonged hairstyling practices such as tight ponytails, braids, or locs, or use of wigs or weaves.¹ Use of headwear, as in certain religious or ethnic groups, also can be contributory.² Individuals participating in or training for occupations involving military service or ballet are at risk for TA due to hairstyling-specific policies. Early stages of TA are reversible with proper treatment and avoidance of exacerbating factors, emphasizing the importance of prompt recognition.³

Epidemiology

Data on the true prevalence of TA are lacking. It can occur in individuals of any race or any hair type. However, it is most common in women of African descent, affecting approximately one-third of this population.⁴ Other commonly affected groups include ballerinas and active-duty service members due to tight ponytails and buns, as well as the Sikh population due to the use of turbans as a part of their religious practice.^2,5,6

Traction alopecia also impacts children, particularly those of African descent. A 2007 study of schoolchildren in South Africa determined that more than 17% of young African girls had evidence of TA—even some as young as 6 years of age.⁷

Traction alopecia can be caused or exacerbated by the use of hair clips and bobby pins that aid holding styles in place.⁸

Hair shaft morphology may contribute to the risk for TA, with more tightly coiled hair types being more susceptible.⁸ Variables such as use of chemical relaxers also increase the risk for disease, especially when combined with high-tension styling methods such as braids.⁹

Key clinical features

Patients with TA clinically present with hair loss and breakage in areas with tension, most commonly the marginal areas of the scalp as well as the frontal hairline and temporal scalp. Hair loss can result in a “fringe sign,” in which a patient may have preservation of a thin line of hairs at the frontal aspect of the hairline with a band of hair loss behind.¹⁰ This presentation may be used to differentiate TA from other forms of alopecia, including frontal fibrosing alopecia and female pattern hair loss. When the hair loss is not marginal, it may mimic other forms of patchy hair loss including alopecia areata and trichotillomania. Other clinical findings in TA may include broken hairs, pustules, and follicular papules.¹⁰ Patients also may describe symptoms such as scalp tenderness with specific hairstyles or headaches,¹¹ or they may be completely asymptomatic.

Trichoscopy can be helpful in guiding diagnosis and treatment. Patients with TA often have perifollicular erythema and hair casts (cylindrical structures that encircle the proximal hair shafts) in the earlier stages of the disease, with eventual loss of follicular ostia in the later stages.^10,12 Hair casts also may indicate ongoing traction.¹² The flambeau sign—white tracks seen on trichoscopy in the direction the hair is pulled—resembles a lit torch.¹³

Worth noting

Early-stage TA can be reversed by avoiding hair tension. However, patients may not be amenable to this due to personal hairstyling preferences, job duties, or religious practices. Treatment with topical or intralesional steroids or even oral antibiotics such as doxycycline for its anti-inflammatory ability may result in regrowth of lost hair if the follicles are not permanently lost and exacerbating factors are avoided.^3,14 Both topical and oral minoxidil have been used with success, with minoxidil thought to increase hair density by extending the anagen (growth) phase of hair follicles.^3,15 Culturally sensitive patient counseling on the condition and potential exacerbating factors is critical.¹⁶

At later stages of the disease—after loss of follicular ostia has occurred—surgical interventions should be considered,¹⁷ such as hair transplantation, which can be successful but remains a technical challenge due to variability in hair shaft curvature.¹⁸ Additionally, the cost of the procedure can limit use, and some patients may not be optimal candidates due to the extent of their hair loss. Traction alopecia may not be the only hair loss condition present. Examining the scalp is important even if the chief area of concern is the marginal scalp.

Health disparity highlight

Prevention, early identification, and treatment initiated in a timely fashion are crucial to prevent permanent hair loss. There are added societal and cultural pressures that impact hairstyle and hair care practices, especially for those with tightly coiled hair.¹⁹ Historically, tightly coiled hair has been unfairly viewed as “unprofessional,” “unkempt,” and a challenge to “manage” by some. Thus, heat, chemical relaxers, and tight hairstyles holding hair in one position have been used to straighten the hair permanently or temporarily or to keep it maintained in a style that did not necessitate excessive manipulation—often contributing to further tension on the hair.

Military service branches have evaluated and changed some hair-related policies to reflect the diverse hair types of military personnel.²⁰ The CROWN Act (www.thecrownact.com/about)—“Creating a Respectful and Open World for Natural Hair”—is a model law passed by 26 states that prohibits race-based hair discrimination, which is the denial of employment and educational opportunities because of hair texture. Although the law has not been passed in every state, it may help individuals with tightly coiled hair to embrace natural hairstyles. However, even hairstyles with one’s own natural curl pattern can contribute to tension and thus potential development of TA.

The Diagnosis: Folliculotropic Mycosis Fungoides

Folliculotropic mycosis fungoides (FMF) is a variant of mycosis fungoides (MF) characterized by folliculotropism and follicular-based lesions. The clinical manifestation of FMF can vary and includes patches, plaques, or tumors resembling nonfolliculotropic MF; acneform lesions including comedones and pustules; or areas of alopecia. Lesions commonly involve the head and neck but also can be seen on the trunk or extremities. Folliculotropic mycosis fungoides can be accompanied by pruritus or superimposed secondary infection.

Histologic features of FMF include follicular (perifollicular or intrafollicular) infiltration by atypical T cells showing cerebriform nuclei.¹ In early lesions, there may be only mild superficial perivascular inflammation without notable lymphocyte atypia, making diagnosis challenging. ^2,3 Mucinous degeneration of the follicles—termed follicular mucinosis—is a common histologic finding in FMF.^1,2 Follicular mucinosis is not exclusive to FMF; it can be primary/idiopathic or secondary to underlying inflammatory or neoplastic disorders such as FMF. On immunohistochemistry, FMF most commonly demonstrates a helper T cell phenotype that is positive for CD3 and CD4 and negative for CD8, with aberrant loss of CD7 and variably CD5, which is similar to classic MF. Occasionally, larger CD30+ cells also can be present in the dermis. T-cell gene rearrangement studies will demonstrate T-cell receptor clonality in most cases.²

Many large retrospective cohort studies have suggested that patients with FMF have a worse prognosis than classic MF, with a 5-year survival rate of 62% to 87% for early-stage FMF vs more than 90% for classic patchand plaque-stage MF.^4-7 However, a 2016 study suggested histologic evaluation may be able to further differentiate clinically identical cases into indolent and aggressive forms of FMF with considerably different outcomes based on the density of the perifollicular infiltrate.⁵ The presence of follicular mucinosis has no impact on prognosis compared to cases without follicular mucinosis.^1,2

Alopecia mucinosa is characterized by infiltrating, erythematous, scaling plaques localized to the head and neck.⁸ It is diagnosed clinically, and histopathology shows follicular mucinosis. The terms alopecia mucinosa and follicular mucinosis often are used interchangeably. Over the past few decades, 3 variants have been categorized: primary acute, primary chronic, and secondary. The primary acute form manifests in children and young adults as solitary lesions, which often resolve spontaneously. In contrast, the primary chronic form manifests in older adults as multiple disseminated lesions with a chronic relapsing course.^8,9 The secondary form can occur in the setting of other disorders, including lupus erythematosus, hypertrophic lichen planus, alopecia areata, and neoplasms such as MF or Hodgkin lymphoma.⁹ The histopathologic findings are similar for all types of alopecia mucinosa, with cystic pools of mucin deposition in the sebaceous glands and external root sheath of the follicles as well as associated inflammation composed of lymphocytes and eosinophils (Figure 1).^9,10 The inflammatory infiltrate rarely extends into the epidermis or upper portion of the hair follicle. Although histopathology alone cannot reliably distinguish between primary and secondary forms of alopecia mucinosa, MF (including follicular MF) or another underlying cutaneous T-cell lymphoma should be considered if inflammation extends into the upper dermis, epidermis, or follicles or is in a dense bandlike distribution.¹¹ On immunohistochemistry, lymphocytes should show positivity for CD3, CD4, and CD8. The CD4:CD8 ratio often is 1:1 in alopecia mucinosa, while in FMF it is approximately 3:1.10 CD7 commonly is negative but can be present in a small percentage of cases.¹² T-cell receptor gene rearrangement studies have detected clonality in both primary and secondary alopecia mucinosa and thus cannot be used alone to distinguish between the two.¹⁰ Given the overlap in histopathologic and immunohistochemical features of primary and secondary alopecia mucinosa, definitive diagnosis cannot be made with any single modality and should be based on correlating clinical presentation, histopathology, immunohistochemistry, and molecular analyses.

Inflammatory dermatoses including seborrheic dermatitis also are in the differential diagnosis for FMF. Seborrheic dermatitis is a common chronic inflammatory skin disorder affecting 1% to 3% of the general population. ¹³ Patients usually present with scaly and greasy plaques and papules localized to areas with increased sebaceous glands and high sebum production such as the face, scalp, and intertriginous regions. The distribution often is symmetrical, and the severity of disease can vary substantially.¹³ Sebopsoriasis is an entity with overlapping features of seborrheic dermatitis and psoriasis, including thicker, more erythematous plaques that are more elevated. Histopathology of seborrheic dermatitis reveals spongiotic inflammation in the epidermis characterized by rounding of the keratinocytes, widening of the intercellular spaces, and accumulation of intracellular edema, causing the formation of clear spaces in the epidermis (Figure 2). Focal parakeratosis, usually in the follicular ostia, and mounds of scaly crust often are present. ¹⁴ A periodic acid–Schiff stain should be performed to rule out infectious dermatophytes, which can show similar clinical and histologic features. More chronic cases of seborrheic dermatitis often can take on histologic features of psoriasis, namely epidermal hyperplasia with thinning over dermal papillae, though the hyperplasia in psoriasis is more regular.

Alopecia areata is an immune-mediated disorder characterized by nonscarring hair loss; it affects approximately 0.1% to 0.2% of the general population.¹⁵ The pathogenesis involves the premature transition of hair follicles in the anagen (growth) phase to the catagen ( nonproliferative/involution) and telogen (resting) phases, resulting in sudden hair shedding and decreased regrowth. Clinically, it is characterized by asymptomatic hair loss that occurs most frequently on the scalp and other areas of the head, including eyelashes, eyebrows, and facial hair, but also can occur on the extremities. There are several variants; the most common is patchy alopecia, which features smooth circular areas of hair loss that progress over several weeks. Some patients can progress to loss of all scalp hairs (alopecia totalis) or all hairs throughout the body (alopecia universalis). ¹⁵ Patients typically will have spontaneous regrowth of hair, with up to 50% of those with limited hair loss recovering within a year.¹⁶ The disease has a chronic/ relapsing course, and patients often will have multiple episodes of hair loss. Histopathologic features can vary depending on the stage of disease. In acute cases, a peribulbar lymphocytic infiltrate preferentially involving anagen-stage hair follicles is seen, with associated necrosis, edema, and pigment incontinence (Figure 3).¹⁶ In chronic alopecia areata, the inflammation may be less brisk, and follicular miniaturization often is seen. Additionally, increased proportions of catagen- or telogen-stage follicles are present.^16,17 On immunohistochemistry, lymphocytes express both CD4 and CD8, with a slightly increased CD4:CD8 ratio in active disease.¹⁸

Psoriatic alopecia describes hair loss that occurs in patients with psoriasis. Patients present with scaly, erythematous, psoriasiform plaques or patches, as well as decreased hair density, finer hairs, and increased dystrophic hair bulbs within the psoriatic plaques.¹⁹ It often is nonscarring and resolves with therapy, though scarring may occur with secondary infection. Psoriatic alopecia may occur in the setting of classic psoriasis and also may occur in psoriasiform drug eruptions, including those caused by tumor necrosis factor inhibitors.^20,21 Histologic features include atrophy of sebaceous glands, epidermal changes with hypogranulosis and psoriasiform hyperplasia, decreased hair follicle density, and neutrophils in the stratum spinosum (Figure 4). There often is associated perifollicular lymphocytic inflammation with small lymphocytes that do not have notable morphologic abnormalities.

The Diagnosis: Folliculotropic Mycosis Fungoides

Folliculotropic mycosis fungoides (FMF) is a variant of mycosis fungoides (MF) characterized by folliculotropism and follicular-based lesions. The clinical manifestation of FMF can vary and includes patches, plaques, or tumors resembling nonfolliculotropic MF; acneform lesions including comedones and pustules; or areas of alopecia. Lesions commonly involve the head and neck but also can be seen on the trunk or extremities. Folliculotropic mycosis fungoides can be accompanied by pruritus or superimposed secondary infection.

Histologic features of FMF include follicular (perifollicular or intrafollicular) infiltration by atypical T cells showing cerebriform nuclei.¹ In early lesions, there may be only mild superficial perivascular inflammation without notable lymphocyte atypia, making diagnosis challenging. ^2,3 Mucinous degeneration of the follicles—termed follicular mucinosis—is a common histologic finding in FMF.^1,2 Follicular mucinosis is not exclusive to FMF; it can be primary/idiopathic or secondary to underlying inflammatory or neoplastic disorders such as FMF. On immunohistochemistry, FMF most commonly demonstrates a helper T cell phenotype that is positive for CD3 and CD4 and negative for CD8, with aberrant loss of CD7 and variably CD5, which is similar to classic MF. Occasionally, larger CD30+ cells also can be present in the dermis. T-cell gene rearrangement studies will demonstrate T-cell receptor clonality in most cases.²

Many large retrospective cohort studies have suggested that patients with FMF have a worse prognosis than classic MF, with a 5-year survival rate of 62% to 87% for early-stage FMF vs more than 90% for classic patchand plaque-stage MF.^4-7 However, a 2016 study suggested histologic evaluation may be able to further differentiate clinically identical cases into indolent and aggressive forms of FMF with considerably different outcomes based on the density of the perifollicular infiltrate.⁵ The presence of follicular mucinosis has no impact on prognosis compared to cases without follicular mucinosis.^1,2

Alopecia mucinosa is characterized by infiltrating, erythematous, scaling plaques localized to the head and neck.⁸ It is diagnosed clinically, and histopathology shows follicular mucinosis. The terms alopecia mucinosa and follicular mucinosis often are used interchangeably. Over the past few decades, 3 variants have been categorized: primary acute, primary chronic, and secondary. The primary acute form manifests in children and young adults as solitary lesions, which often resolve spontaneously. In contrast, the primary chronic form manifests in older adults as multiple disseminated lesions with a chronic relapsing course.^8,9 The secondary form can occur in the setting of other disorders, including lupus erythematosus, hypertrophic lichen planus, alopecia areata, and neoplasms such as MF or Hodgkin lymphoma.⁹ The histopathologic findings are similar for all types of alopecia mucinosa, with cystic pools of mucin deposition in the sebaceous glands and external root sheath of the follicles as well as associated inflammation composed of lymphocytes and eosinophils (Figure 1).^9,10 The inflammatory infiltrate rarely extends into the epidermis or upper portion of the hair follicle. Although histopathology alone cannot reliably distinguish between primary and secondary forms of alopecia mucinosa, MF (including follicular MF) or another underlying cutaneous T-cell lymphoma should be considered if inflammation extends into the upper dermis, epidermis, or follicles or is in a dense bandlike distribution.¹¹ On immunohistochemistry, lymphocytes should show positivity for CD3, CD4, and CD8. The CD4:CD8 ratio often is 1:1 in alopecia mucinosa, while in FMF it is approximately 3:1.10 CD7 commonly is negative but can be present in a small percentage of cases.¹² T-cell receptor gene rearrangement studies have detected clonality in both primary and secondary alopecia mucinosa and thus cannot be used alone to distinguish between the two.¹⁰ Given the overlap in histopathologic and immunohistochemical features of primary and secondary alopecia mucinosa, definitive diagnosis cannot be made with any single modality and should be based on correlating clinical presentation, histopathology, immunohistochemistry, and molecular analyses.

Inflammatory dermatoses including seborrheic dermatitis also are in the differential diagnosis for FMF. Seborrheic dermatitis is a common chronic inflammatory skin disorder affecting 1% to 3% of the general population. ¹³ Patients usually present with scaly and greasy plaques and papules localized to areas with increased sebaceous glands and high sebum production such as the face, scalp, and intertriginous regions. The distribution often is symmetrical, and the severity of disease can vary substantially.¹³ Sebopsoriasis is an entity with overlapping features of seborrheic dermatitis and psoriasis, including thicker, more erythematous plaques that are more elevated. Histopathology of seborrheic dermatitis reveals spongiotic inflammation in the epidermis characterized by rounding of the keratinocytes, widening of the intercellular spaces, and accumulation of intracellular edema, causing the formation of clear spaces in the epidermis (Figure 2). Focal parakeratosis, usually in the follicular ostia, and mounds of scaly crust often are present. ¹⁴ A periodic acid–Schiff stain should be performed to rule out infectious dermatophytes, which can show similar clinical and histologic features. More chronic cases of seborrheic dermatitis often can take on histologic features of psoriasis, namely epidermal hyperplasia with thinning over dermal papillae, though the hyperplasia in psoriasis is more regular.

Alopecia areata is an immune-mediated disorder characterized by nonscarring hair loss; it affects approximately 0.1% to 0.2% of the general population.¹⁵ The pathogenesis involves the premature transition of hair follicles in the anagen (growth) phase to the catagen ( nonproliferative/involution) and telogen (resting) phases, resulting in sudden hair shedding and decreased regrowth. Clinically, it is characterized by asymptomatic hair loss that occurs most frequently on the scalp and other areas of the head, including eyelashes, eyebrows, and facial hair, but also can occur on the extremities. There are several variants; the most common is patchy alopecia, which features smooth circular areas of hair loss that progress over several weeks. Some patients can progress to loss of all scalp hairs (alopecia totalis) or all hairs throughout the body (alopecia universalis). ¹⁵ Patients typically will have spontaneous regrowth of hair, with up to 50% of those with limited hair loss recovering within a year.¹⁶ The disease has a chronic/ relapsing course, and patients often will have multiple episodes of hair loss. Histopathologic features can vary depending on the stage of disease. In acute cases, a peribulbar lymphocytic infiltrate preferentially involving anagen-stage hair follicles is seen, with associated necrosis, edema, and pigment incontinence (Figure 3).¹⁶ In chronic alopecia areata, the inflammation may be less brisk, and follicular miniaturization often is seen. Additionally, increased proportions of catagen- or telogen-stage follicles are present.^16,17 On immunohistochemistry, lymphocytes express both CD4 and CD8, with a slightly increased CD4:CD8 ratio in active disease.¹⁸

Psoriatic alopecia describes hair loss that occurs in patients with psoriasis. Patients present with scaly, erythematous, psoriasiform plaques or patches, as well as decreased hair density, finer hairs, and increased dystrophic hair bulbs within the psoriatic plaques.¹⁹ It often is nonscarring and resolves with therapy, though scarring may occur with secondary infection. Psoriatic alopecia may occur in the setting of classic psoriasis and also may occur in psoriasiform drug eruptions, including those caused by tumor necrosis factor inhibitors.^20,21 Histologic features include atrophy of sebaceous glands, epidermal changes with hypogranulosis and psoriasiform hyperplasia, decreased hair follicle density, and neutrophils in the stratum spinosum (Figure 4). There often is associated perifollicular lymphocytic inflammation with small lymphocytes that do not have notable morphologic abnormalities.

The Diagnosis: Folliculotropic Mycosis Fungoides

Folliculotropic mycosis fungoides (FMF) is a variant of mycosis fungoides (MF) characterized by folliculotropism and follicular-based lesions. The clinical manifestation of FMF can vary and includes patches, plaques, or tumors resembling nonfolliculotropic MF; acneform lesions including comedones and pustules; or areas of alopecia. Lesions commonly involve the head and neck but also can be seen on the trunk or extremities. Folliculotropic mycosis fungoides can be accompanied by pruritus or superimposed secondary infection.

Histologic features of FMF include follicular (perifollicular or intrafollicular) infiltration by atypical T cells showing cerebriform nuclei.¹ In early lesions, there may be only mild superficial perivascular inflammation without notable lymphocyte atypia, making diagnosis challenging. ^2,3 Mucinous degeneration of the follicles—termed follicular mucinosis—is a common histologic finding in FMF.^1,2 Follicular mucinosis is not exclusive to FMF; it can be primary/idiopathic or secondary to underlying inflammatory or neoplastic disorders such as FMF. On immunohistochemistry, FMF most commonly demonstrates a helper T cell phenotype that is positive for CD3 and CD4 and negative for CD8, with aberrant loss of CD7 and variably CD5, which is similar to classic MF. Occasionally, larger CD30+ cells also can be present in the dermis. T-cell gene rearrangement studies will demonstrate T-cell receptor clonality in most cases.²

Many large retrospective cohort studies have suggested that patients with FMF have a worse prognosis than classic MF, with a 5-year survival rate of 62% to 87% for early-stage FMF vs more than 90% for classic patchand plaque-stage MF.^4-7 However, a 2016 study suggested histologic evaluation may be able to further differentiate clinically identical cases into indolent and aggressive forms of FMF with considerably different outcomes based on the density of the perifollicular infiltrate.⁵ The presence of follicular mucinosis has no impact on prognosis compared to cases without follicular mucinosis.^1,2

Alopecia mucinosa is characterized by infiltrating, erythematous, scaling plaques localized to the head and neck.⁸ It is diagnosed clinically, and histopathology shows follicular mucinosis. The terms alopecia mucinosa and follicular mucinosis often are used interchangeably. Over the past few decades, 3 variants have been categorized: primary acute, primary chronic, and secondary. The primary acute form manifests in children and young adults as solitary lesions, which often resolve spontaneously. In contrast, the primary chronic form manifests in older adults as multiple disseminated lesions with a chronic relapsing course.^8,9 The secondary form can occur in the setting of other disorders, including lupus erythematosus, hypertrophic lichen planus, alopecia areata, and neoplasms such as MF or Hodgkin lymphoma.⁹ The histopathologic findings are similar for all types of alopecia mucinosa, with cystic pools of mucin deposition in the sebaceous glands and external root sheath of the follicles as well as associated inflammation composed of lymphocytes and eosinophils (Figure 1).^9,10 The inflammatory infiltrate rarely extends into the epidermis or upper portion of the hair follicle. Although histopathology alone cannot reliably distinguish between primary and secondary forms of alopecia mucinosa, MF (including follicular MF) or another underlying cutaneous T-cell lymphoma should be considered if inflammation extends into the upper dermis, epidermis, or follicles or is in a dense bandlike distribution.¹¹ On immunohistochemistry, lymphocytes should show positivity for CD3, CD4, and CD8. The CD4:CD8 ratio often is 1:1 in alopecia mucinosa, while in FMF it is approximately 3:1.10 CD7 commonly is negative but can be present in a small percentage of cases.¹² T-cell receptor gene rearrangement studies have detected clonality in both primary and secondary alopecia mucinosa and thus cannot be used alone to distinguish between the two.¹⁰ Given the overlap in histopathologic and immunohistochemical features of primary and secondary alopecia mucinosa, definitive diagnosis cannot be made with any single modality and should be based on correlating clinical presentation, histopathology, immunohistochemistry, and molecular analyses.

Inflammatory dermatoses including seborrheic dermatitis also are in the differential diagnosis for FMF. Seborrheic dermatitis is a common chronic inflammatory skin disorder affecting 1% to 3% of the general population. ¹³ Patients usually present with scaly and greasy plaques and papules localized to areas with increased sebaceous glands and high sebum production such as the face, scalp, and intertriginous regions. The distribution often is symmetrical, and the severity of disease can vary substantially.¹³ Sebopsoriasis is an entity with overlapping features of seborrheic dermatitis and psoriasis, including thicker, more erythematous plaques that are more elevated. Histopathology of seborrheic dermatitis reveals spongiotic inflammation in the epidermis characterized by rounding of the keratinocytes, widening of the intercellular spaces, and accumulation of intracellular edema, causing the formation of clear spaces in the epidermis (Figure 2). Focal parakeratosis, usually in the follicular ostia, and mounds of scaly crust often are present. ¹⁴ A periodic acid–Schiff stain should be performed to rule out infectious dermatophytes, which can show similar clinical and histologic features. More chronic cases of seborrheic dermatitis often can take on histologic features of psoriasis, namely epidermal hyperplasia with thinning over dermal papillae, though the hyperplasia in psoriasis is more regular.

Alopecia areata is an immune-mediated disorder characterized by nonscarring hair loss; it affects approximately 0.1% to 0.2% of the general population.¹⁵ The pathogenesis involves the premature transition of hair follicles in the anagen (growth) phase to the catagen ( nonproliferative/involution) and telogen (resting) phases, resulting in sudden hair shedding and decreased regrowth. Clinically, it is characterized by asymptomatic hair loss that occurs most frequently on the scalp and other areas of the head, including eyelashes, eyebrows, and facial hair, but also can occur on the extremities. There are several variants; the most common is patchy alopecia, which features smooth circular areas of hair loss that progress over several weeks. Some patients can progress to loss of all scalp hairs (alopecia totalis) or all hairs throughout the body (alopecia universalis). ¹⁵ Patients typically will have spontaneous regrowth of hair, with up to 50% of those with limited hair loss recovering within a year.¹⁶ The disease has a chronic/ relapsing course, and patients often will have multiple episodes of hair loss. Histopathologic features can vary depending on the stage of disease. In acute cases, a peribulbar lymphocytic infiltrate preferentially involving anagen-stage hair follicles is seen, with associated necrosis, edema, and pigment incontinence (Figure 3).¹⁶ In chronic alopecia areata, the inflammation may be less brisk, and follicular miniaturization often is seen. Additionally, increased proportions of catagen- or telogen-stage follicles are present.^16,17 On immunohistochemistry, lymphocytes express both CD4 and CD8, with a slightly increased CD4:CD8 ratio in active disease.¹⁸

Psoriatic alopecia describes hair loss that occurs in patients with psoriasis. Patients present with scaly, erythematous, psoriasiform plaques or patches, as well as decreased hair density, finer hairs, and increased dystrophic hair bulbs within the psoriatic plaques.¹⁹ It often is nonscarring and resolves with therapy, though scarring may occur with secondary infection. Psoriatic alopecia may occur in the setting of classic psoriasis and also may occur in psoriasiform drug eruptions, including those caused by tumor necrosis factor inhibitors.^20,21 Histologic features include atrophy of sebaceous glands, epidermal changes with hypogranulosis and psoriasiform hyperplasia, decreased hair follicle density, and neutrophils in the stratum spinosum (Figure 4). There often is associated perifollicular lymphocytic inflammation with small lymphocytes that do not have notable morphologic abnormalities.

The Diagnosis: Pigmented Nodular Basal Cell Carcinoma

Dermoscopy of our patient’s irregular dark brown papule revealed large blue clustered clods and radial lines converging to a central dot (middle quiz image). Histopathology revealed nests of basaloid cells with peripheral palisading, small horn pseudocysts, and deposits of melanin extending into the dermis (Figure). These findings were consistent with a diagnosis of pigmented nodular basal cell carcinoma (BCC).

Nodular BCC represents 60% to 80% of all BCC cases; pigmented BCC represents 6% of BCC cases.¹ Basal cell carcinomas frequently manifest as pearly papules with areas of pigment, surface telangiectases, and foci of ulceration. Dermoscopic features include fine arborizing vessels, blue-gray ovoid nests, spoke wheel–like structures, leaflike structures, and focal ulceration.¹ Histopathology shows well-defined dermal nodules comprising basaloid epithelial cells with peripheral palisading, mucinous stroma, focal melanin deposits, and surrounding clefting.² Arborizing vessels correspond to dilated vessels in the dermis.³ Blue-gray ovoid nests are wellcircumscribed ovoid or elongated structures that correspond histologically to well-defined large tumor nests with melanin aggregates invading the dermis. Spoke wheel–like structures are well-circumscribed radial projections connected to a pigmented central axis that correspond histologically to tumor nests near the epidermis and that appear as fingerlike projections with centrally located melanin deposits.³

The differential diagnosis of our patient’s lesion included nodular melanoma, lentigo maligna melanoma, deep penetrating nevus, and cellular blue nevus. Nodular melanoma is an invasive melanoma that lacks a radial growth phase. Dermoscopically, the more common features are a bluewhite veil, atypical vascular pattern, asymmetric pigmentation, atypical pigment network, and peripheral black globules.⁴ Histopathology reveals atypical melanocytes and architectural disorder.² Pigmented nodular BCC also can display dark globules on dermoscopy but typically has smaller and more arborizing blood vessels and does not have a pigmented network. Furthermore, BCC would not have atypical melanocytes on histopathology.^4,5

Dermoscopy of lentigo maligna melanoma displays hyperpigmented follicular openings, an annular-granular pattern, pigmented rhomboidal structures, and obliterated hair follicles.⁶ Histopathology demonstrates epidermal atrophy, increased pigmentation in basal keratinocytes, prominent solar elastosis, and an increased number of melanocytes that extend beyond the epidermis. ⁷ Pigmented nodular BCC can be distinguished from lentigo maligna melanoma dermoscopically by the presence of arborizing vessels, blue-gray ovoid nests, and lack of a pigment network.

Deep penetrating nevus is a darkly pigmented melanocytic lesion that infiltrates deeply into the reticular dermis.⁸ Specific dermoscopic features have not been well established; however, a uniformly dark blue or black pattern is common. Histologically, this type of nevus is symmetric and wedge shaped with a broad base extending to the deep dermis and subcutaneous fat.⁸ Melanocytes do not exhibit atypia or bizarre mitoses. Although pigmented nodular BCC can appear similar to deep penetrating nevus, histologically there will be atypical basaloid epithelial cells in BCC.

Blue nevi clinically appear as a smooth blue-gray lesion with a steel blue ground-glass pattern on dermoscopy. Histopathology shows spindle-shaped melanocytes in the dermis, which distinguishes this lesion from BCC.⁹

Consider pigmented BCC when a patient presents with a pigmented lesion. Dermoscopy can help appreciate a pigmented BCC by looking for features such as a spoke wheel– like pattern, blue ovoid nests, arborizing blood vessels, and lack of a pigment network. Because pigmented BCC constitutes a small fraction of all BCCs, it is important to be familiar with its presentation and dermoscopic features.

The Diagnosis: Pigmented Nodular Basal Cell Carcinoma

Dermoscopy of our patient’s irregular dark brown papule revealed large blue clustered clods and radial lines converging to a central dot (middle quiz image). Histopathology revealed nests of basaloid cells with peripheral palisading, small horn pseudocysts, and deposits of melanin extending into the dermis (Figure). These findings were consistent with a diagnosis of pigmented nodular basal cell carcinoma (BCC).

Nodular BCC represents 60% to 80% of all BCC cases; pigmented BCC represents 6% of BCC cases.¹ Basal cell carcinomas frequently manifest as pearly papules with areas of pigment, surface telangiectases, and foci of ulceration. Dermoscopic features include fine arborizing vessels, blue-gray ovoid nests, spoke wheel–like structures, leaflike structures, and focal ulceration.¹ Histopathology shows well-defined dermal nodules comprising basaloid epithelial cells with peripheral palisading, mucinous stroma, focal melanin deposits, and surrounding clefting.² Arborizing vessels correspond to dilated vessels in the dermis.³ Blue-gray ovoid nests are wellcircumscribed ovoid or elongated structures that correspond histologically to well-defined large tumor nests with melanin aggregates invading the dermis. Spoke wheel–like structures are well-circumscribed radial projections connected to a pigmented central axis that correspond histologically to tumor nests near the epidermis and that appear as fingerlike projections with centrally located melanin deposits.³

The differential diagnosis of our patient’s lesion included nodular melanoma, lentigo maligna melanoma, deep penetrating nevus, and cellular blue nevus. Nodular melanoma is an invasive melanoma that lacks a radial growth phase. Dermoscopically, the more common features are a bluewhite veil, atypical vascular pattern, asymmetric pigmentation, atypical pigment network, and peripheral black globules.⁴ Histopathology reveals atypical melanocytes and architectural disorder.² Pigmented nodular BCC also can display dark globules on dermoscopy but typically has smaller and more arborizing blood vessels and does not have a pigmented network. Furthermore, BCC would not have atypical melanocytes on histopathology.^4,5

Dermoscopy of lentigo maligna melanoma displays hyperpigmented follicular openings, an annular-granular pattern, pigmented rhomboidal structures, and obliterated hair follicles.⁶ Histopathology demonstrates epidermal atrophy, increased pigmentation in basal keratinocytes, prominent solar elastosis, and an increased number of melanocytes that extend beyond the epidermis. ⁷ Pigmented nodular BCC can be distinguished from lentigo maligna melanoma dermoscopically by the presence of arborizing vessels, blue-gray ovoid nests, and lack of a pigment network.

Deep penetrating nevus is a darkly pigmented melanocytic lesion that infiltrates deeply into the reticular dermis.⁸ Specific dermoscopic features have not been well established; however, a uniformly dark blue or black pattern is common. Histologically, this type of nevus is symmetric and wedge shaped with a broad base extending to the deep dermis and subcutaneous fat.⁸ Melanocytes do not exhibit atypia or bizarre mitoses. Although pigmented nodular BCC can appear similar to deep penetrating nevus, histologically there will be atypical basaloid epithelial cells in BCC.

Blue nevi clinically appear as a smooth blue-gray lesion with a steel blue ground-glass pattern on dermoscopy. Histopathology shows spindle-shaped melanocytes in the dermis, which distinguishes this lesion from BCC.⁹

Consider pigmented BCC when a patient presents with a pigmented lesion. Dermoscopy can help appreciate a pigmented BCC by looking for features such as a spoke wheel– like pattern, blue ovoid nests, arborizing blood vessels, and lack of a pigment network. Because pigmented BCC constitutes a small fraction of all BCCs, it is important to be familiar with its presentation and dermoscopic features.

The Diagnosis: Pigmented Nodular Basal Cell Carcinoma

Dermoscopy of our patient’s irregular dark brown papule revealed large blue clustered clods and radial lines converging to a central dot (middle quiz image). Histopathology revealed nests of basaloid cells with peripheral palisading, small horn pseudocysts, and deposits of melanin extending into the dermis (Figure). These findings were consistent with a diagnosis of pigmented nodular basal cell carcinoma (BCC).

Nodular BCC represents 60% to 80% of all BCC cases; pigmented BCC represents 6% of BCC cases.¹ Basal cell carcinomas frequently manifest as pearly papules with areas of pigment, surface telangiectases, and foci of ulceration. Dermoscopic features include fine arborizing vessels, blue-gray ovoid nests, spoke wheel–like structures, leaflike structures, and focal ulceration.¹ Histopathology shows well-defined dermal nodules comprising basaloid epithelial cells with peripheral palisading, mucinous stroma, focal melanin deposits, and surrounding clefting.² Arborizing vessels correspond to dilated vessels in the dermis.³ Blue-gray ovoid nests are wellcircumscribed ovoid or elongated structures that correspond histologically to well-defined large tumor nests with melanin aggregates invading the dermis. Spoke wheel–like structures are well-circumscribed radial projections connected to a pigmented central axis that correspond histologically to tumor nests near the epidermis and that appear as fingerlike projections with centrally located melanin deposits.³

The differential diagnosis of our patient’s lesion included nodular melanoma, lentigo maligna melanoma, deep penetrating nevus, and cellular blue nevus. Nodular melanoma is an invasive melanoma that lacks a radial growth phase. Dermoscopically, the more common features are a bluewhite veil, atypical vascular pattern, asymmetric pigmentation, atypical pigment network, and peripheral black globules.⁴ Histopathology reveals atypical melanocytes and architectural disorder.² Pigmented nodular BCC also can display dark globules on dermoscopy but typically has smaller and more arborizing blood vessels and does not have a pigmented network. Furthermore, BCC would not have atypical melanocytes on histopathology.^4,5

Dermoscopy of lentigo maligna melanoma displays hyperpigmented follicular openings, an annular-granular pattern, pigmented rhomboidal structures, and obliterated hair follicles.⁶ Histopathology demonstrates epidermal atrophy, increased pigmentation in basal keratinocytes, prominent solar elastosis, and an increased number of melanocytes that extend beyond the epidermis. ⁷ Pigmented nodular BCC can be distinguished from lentigo maligna melanoma dermoscopically by the presence of arborizing vessels, blue-gray ovoid nests, and lack of a pigment network.

Deep penetrating nevus is a darkly pigmented melanocytic lesion that infiltrates deeply into the reticular dermis.⁸ Specific dermoscopic features have not been well established; however, a uniformly dark blue or black pattern is common. Histologically, this type of nevus is symmetric and wedge shaped with a broad base extending to the deep dermis and subcutaneous fat.⁸ Melanocytes do not exhibit atypia or bizarre mitoses. Although pigmented nodular BCC can appear similar to deep penetrating nevus, histologically there will be atypical basaloid epithelial cells in BCC.

Blue nevi clinically appear as a smooth blue-gray lesion with a steel blue ground-glass pattern on dermoscopy. Histopathology shows spindle-shaped melanocytes in the dermis, which distinguishes this lesion from BCC.⁹

Consider pigmented BCC when a patient presents with a pigmented lesion. Dermoscopy can help appreciate a pigmented BCC by looking for features such as a spoke wheel– like pattern, blue ovoid nests, arborizing blood vessels, and lack of a pigment network. Because pigmented BCC constitutes a small fraction of all BCCs, it is important to be familiar with its presentation and dermoscopic features.

Although individuals with skin of color (SoC) are expected to become at least half of the US population by the year 2044, there remains a paucity of education and exposure to treatment of patients with SoC at many dermatology residency programs across the country.¹ One way to improve SoC education has been the formation of specialized clinics, centers, and programs. The first SoC center (SoCC) was established in 1999 at Mount Sinai–St. Luke’s Roosevelt in New York, New York²; since then, at least 13 additional formal SoCCs or SoC specialty clinics (SoCSCs) at US academic dermatology programs have been established.

Skin of color centers serve several important purposes: they improve dermatologic care in patients with SoC, increase research efforts focused on SoC dermatologic conditions, and educate dermatology resident and fellow trainees about SoC. Improving dermatologic care of patients with SoC in the United States is important in providing equitable health care and improving health disparities. Studies have shown that patient-physician racial and cultural concordance can positively impact patient care, increase patient trust and rapport, and improve patient-physician communication, and it can even influence patient decision-making to seek care.^3,4 Unfortunately, even though the US population continues to diversify, the racial/ethnic backgrounds of dermatologists do not parallel this trend; Hispanic and Black physicians comprise 18.9% and 13.6% of the general population, respectively, but represent only 4.2% and 3.0% of dermatologists, respectively.^5-7 This deficit is mirrored by resident and faculty representation, with Black and Latino representation ranging from 3% to 7%.^8-10

Many SoCC’s engage in research focused on dermatologic conditions affecting patients with SoC, which is vital to improving the dermatologic care in this underserved population. Despite increasing recognition of the importance of SoC research, there remains a paucity of clinical trials and research specifically focused on or demonstrating equitable representation of SoC.^11,12

The education and training of future dermatologists is another important area that can be improved by SoCCs. A 2008 study involving 63 chief residents showed that approximately half (52.4% [33/63]) of graduating dermatology residents reported receiving SoC-specific didactics, sessions, or lectures, and 30.2% (19/63) reported having a dedicated rotation where they gained specific experience treating patients with SoC.¹³ A later study in 2022 (N=125) found that 63.2% of graduating dermatology residents reported receiving SoC-specific didactics, sessions, or lectures, and only 11.2% reported having a dedicated rotation where they gained experience treating patients with SoC.¹⁴ These findings suggest that in the last 14 years, formal SoC education—specifically SoC clinical training—has not increased sufficiently.

We conducted a cross-sectional survey study to provide an in-depth analysis of SoCCs and SoCSCs in the United States, including their patient care focus, research, and program diversity.

Methods

We conducted an investigator-initiated, multicenter, cross-sectional survey study of all SoCCs in the United States and their respective academic residency programs. Fifteen formal SoCCs and/or SoCSCs were identified by dermatology program websites and an article by Tull et al² on the state of ethnic skin centers. All programs and centers identified were associated with a dermatology residency program accredited by the Accreditation Council for Graduate Medical Education.

A 42-item questionnaire was sent via email to the directors of these centers and clinics with the intent to collect descriptive information about each of the SoCCs, the diversity of the faculty and residents of the associated dermatology department, current research and funding, diversity and inclusion initiatives, and trainee education from March through April 2020. Data were analyzed using Excel and SPSS statistical software to obtain descriptive statistics including the mean value numeric trends across programs.

This study underwent expedited review and was approved by the University of Southern California (Los Angeles, California) institutional review board (IRB #HS-20-00113). Patient consent was not applicable, as no information was collected about patients.

Results

Fourteen directors from SoCCs/SoCSCs completed the questionnaire (93.3% response rate). Most centers were located in urban areas (12/14 [85.71%]), except for 2 in rural or suburban settings (Table). Most of the SoCCs/SoCSCs were located in the South (5/14 [35.71%]), followed by the Northeast (4/14 [28.57%]), West (3/14 [21.43%]), and Midwest (2/14 [14.29%])(Table). Six (42.86%) of the programs had a SoCSC, 3 (21.43%) had a formal SoCC, and 5 (35.71%) had both. Across all centers, the most common population seen and treated was Black/African American followed by Hispanic/Latino and Asian, respectively. The most commonly seen dermatologic conditions were acne, pigmentary disorders, alopecia, and atopic dermatitis (Figure). The most common cosmetic practice performed for patients with SoC was dermatosis papulosa nigra/seborrheic keratosis removal, followed by laser treatments, skin tag removal, chemical peels, and neuromodulator injections, respectively.

Faculty and Resident Demographics and Areas of Focus—The demographics and diversity of the dermatology faculty and residents at each individual institution also were assessed. The average number of full-time faculty at each institution was 19.4 (range, 2–48), while the average number of full-time faculty who identified as underrepresented in medicine (URiM) was 2.1 (range, 0–5). The average number of residents at each institution was 17.1 (range, 10–31), while the average number of URiM residents was 1.7 (range, 1–3).

Comment

As the number of SoCCs/SoCSCs in the United States continues to grow, it is important to highlight their programmatic, research, and educational accomplishments to show the benefits of such programs, including their ability to increase access to culturally competent and inclusive care for diverse patient populations. One study found that nearly 92% of patients in the United States seen by dermatologists are White.¹⁵ Although studies have shown that Hispanic/Latino and Black patients are less likely to seek care from a dermatologist,^16,17 there is no indication that these patients have a lesser need for such specialty care. Additionally, outcomes of common dermatologic conditions often are poorer in SoC populations.¹⁵ The dermatologists leading SoCCs/SoCSCs are actively working to reverse these trends, with Black and Hispanic/Latino patients representing the majority of their patients.

Faculty and Resident Demographics and Areas of Focus—Although there are increased diversity efforts in dermatology and the medical profession more broadly, there still is much work to be done. While individuals with SoC now comprise more than 35% of the US population, only 12% of dermatology residents and 6% of academic dermatology faculty identify as either Black or Hispanic/Latino.^5,8,10 These numbers are even more discouraging when considering other URiM racial groups such as Pacific Islander/Native Hawaiians or Native American/American Indians who represent 0% and 0.1% of dermatology faculty, respectively.^8,10 Academic programs with SoCCs/SoCSCs are working to create a space in which these discrepancies in representation can begin to be addressed. Compared to the national 6.8% rate of URiM faculty at academic institutions, those with SoCCs/SoCSCs report closer to 10% of faculty identifying as URiM.¹⁸ Moreover, almost all programs had faculty specialized in at least 1 condition that predominantly affects patients with SoC. This is of critical importance, as the conditions that most commonly affect SoC populations—such as CCCA, hidradenitis suppurativa, and cutaneous lupus—often are understudied, underfunded, underdiagnosed, and undertreated.^19-22

Faculty SoC Research—An important step in narrowing the knowledge gap and improving health care disparities in patients with SoC is to increase SoC research and/or to increase the representation of patients with SoC in research studies. In a 2021 study, a PubMed search of articles indexed for MEDLINE using the terms race/­ethnicity, dyschromia, atopic dermatitis, and acne was conducted to investigate publications pertaining to the top 3 most common chief concerns in patients with SoC. Only 1.6% of studies analyzed (N=74,941) had a specific focus on SoC.¹² A similar study found that among the top 5 ­dermatology-focused research journals, only 3.4% of all research (N=11,003) on the top 3 most common chief concerns in patients with SOC was conducted in patients with SoC.²³ Research efforts focused on dermatologic issues that affect patients with SoC are a priority at SoCCs/SoCSCs. In our study, all respondents indicated that they had at least 1 ongoing observational study; the most commonly studied conditions were CCCA, keloids/hypertrophic scarring, and atopic dermatitis, all of which are conditions that either occur in high frequency or primarily occur in SoC. Only 35.71% (5/14) of respondents had active clinical trials related to SoC, and only 21.43% (3/14) and 28.57% (4/14) had internal and external funding, respectively. Although research efforts are a priority at SoCCs/SoCSCs, our survey study highlights the continued paucity of formal clinical trials as well as funding for SoC-focused research. Improved research efforts for SoC must address these deficits in funding, academic support, and other resources.

It also is of great importance for institutions to provide support for trainees wanting to pursue SoC research. Encouragingly, more than half (57.14%) of SoCCs/SoCSCs have developed formal research opportunities for residents, and nearly 64.29% have formal opportunities for medical students. These efforts to provide early experiences in SoC research are especially impactful by cultivating interest in working with populations with SoC and hopefully inspiring future dermatologists to engage in further SoC research.

SoC Education and Diversity Initiatives—Although it is important to increase representation of URiM physicians in dermatology and to train more SoC specialists, it is imperative that all dermatologists feel comfortable recognizing and treating dermatologic conditions in patients of all skin tones and all racial/ethnic backgrounds; however, many studies suggest that residents not only lack formal didactics and education in SoC, but even more unsettling, they also lack confidence in treating SoC.^13,24 However, one study showed that this can be changed; Mhlaba et al²⁵ assessed a SoC curriculum for dermatology residents, and indeed all of the residents indicated that the curriculum improved their ability to treat SoC patients. This deficit in dermatology residency training is specifically addressed by SoCCs/SoCSCs. In our study, all respondents indicated that residents rotate through their centers. Moreover, our study found that most of the academic institutions with SoCCs/SoCSCs provide a SoC didactic curriculum for residents, and almost all of the programs invited SoC specialists to give guest lectures. This is in contrast to a 2022 study showing that 63.2% (N=125) of graduating dermatology residents reported receiving SoC-specific didactics, sessions, or lectures.¹⁴ These findings highlight the critical role that SoCCs/SoCSCs can provide in dermatology residency training.

Although SoCCs/SoCSCs have made considerable progress, there is still much room for improvement. Namely, only half of the respondents in our study indicated that their program has formally incorporated a SoC textbook into resident education (eTable 3). Representation of SoC in the textbooks that dermatology residents use is critically important because these images form the foundation of the morphologic aids of diagnosis. Numerous studies have analyzed popular dermatologic textbooks used by residency programs nationwide, finding the number of SoC images across dermatology textbooks ranging from 4% to 18%.^26,27 The use of standard dermatology textbooks is not enough to train residents to be competent in diagnosing and treating patients with SoC. There should be a concerted effort across the field of dermatology to encourage the development of a SoC educational curriculum at every academic dermatology program, including SoC textbooks, Kodachromes, and online/electronic resources.

Efforts to increase diversity in dermatology and dermatologic training should start in medical school preclinical curriculums and medical student rotations. Although our survey did not assess current medical student curricula, the benefits of academic institutions with SoCCs/SoCSCs are highlighted by the ability for both home and visiting medical students to rotate through the centers and gain early exposure to SoC dermatology. Most of the programs even provide scholarships and/or grants for URiM students to help fund their rotations, which is of critical importance considering the mounting data that the financial burden of visiting rotations disproportionately affects URiM students.²⁸

Study Limitations—Although we did an extensive search and believe to have correctly identified all 15 formal SoCCs/SoCSCs with a high response rate (93.3%), there are institutions that do not have formalized SoCCs/SoCSCs but are known to serve SoC populations. Likewise, there are private dermatology practices not associated with academic centers that have SoC specialists and positively contribute to SoC patient care, research, and education that were not included in this study. Additionally, the data for this study were collected in 2020 and analyzed in 2021, so it is possible that not all SoCCs, divisions, or clinics were included in this study, particularly if established after 2021.

Conclusion

As the United States continues to diversify, the proportion of patients with SoC will continue to grow, and it is imperative that this racial, ethnic, and cultural diversity is reflected in the dermatology workforce as well as research and training. The current deficits in medical training related to SoC populations and the importance for patients with SoC to find dermatologists who can appropriately treat them is well known.²⁹ Skin of color centers/SoCSCs strive to increase access to care for patients with SoC, improve cultural competency, promote diversity among faculty and trainees, and encourage SoC research and education at all levels. We urge academic dermatology training programs to make SoC education, research, and patient care a departmental priority. Important first steps include departmental diversification at all levels, incorporating SoC into curricula for residents, providing and securing funding for SoC research, and supporting the establishment of more formal SoCCs and/or SoCSCs to help reduce dermatologic health care disparities among patients with SoC and improve health equity.

Appendix

Although individuals with skin of color (SoC) are expected to become at least half of the US population by the year 2044, there remains a paucity of education and exposure to treatment of patients with SoC at many dermatology residency programs across the country.¹ One way to improve SoC education has been the formation of specialized clinics, centers, and programs. The first SoC center (SoCC) was established in 1999 at Mount Sinai–St. Luke’s Roosevelt in New York, New York²; since then, at least 13 additional formal SoCCs or SoC specialty clinics (SoCSCs) at US academic dermatology programs have been established.

Skin of color centers serve several important purposes: they improve dermatologic care in patients with SoC, increase research efforts focused on SoC dermatologic conditions, and educate dermatology resident and fellow trainees about SoC. Improving dermatologic care of patients with SoC in the United States is important in providing equitable health care and improving health disparities. Studies have shown that patient-physician racial and cultural concordance can positively impact patient care, increase patient trust and rapport, and improve patient-physician communication, and it can even influence patient decision-making to seek care.^3,4 Unfortunately, even though the US population continues to diversify, the racial/ethnic backgrounds of dermatologists do not parallel this trend; Hispanic and Black physicians comprise 18.9% and 13.6% of the general population, respectively, but represent only 4.2% and 3.0% of dermatologists, respectively.^5-7 This deficit is mirrored by resident and faculty representation, with Black and Latino representation ranging from 3% to 7%.^8-10

Many SoCC’s engage in research focused on dermatologic conditions affecting patients with SoC, which is vital to improving the dermatologic care in this underserved population. Despite increasing recognition of the importance of SoC research, there remains a paucity of clinical trials and research specifically focused on or demonstrating equitable representation of SoC.^11,12

The education and training of future dermatologists is another important area that can be improved by SoCCs. A 2008 study involving 63 chief residents showed that approximately half (52.4% [33/63]) of graduating dermatology residents reported receiving SoC-specific didactics, sessions, or lectures, and 30.2% (19/63) reported having a dedicated rotation where they gained specific experience treating patients with SoC.¹³ A later study in 2022 (N=125) found that 63.2% of graduating dermatology residents reported receiving SoC-specific didactics, sessions, or lectures, and only 11.2% reported having a dedicated rotation where they gained experience treating patients with SoC.¹⁴ These findings suggest that in the last 14 years, formal SoC education—specifically SoC clinical training—has not increased sufficiently.

We conducted a cross-sectional survey study to provide an in-depth analysis of SoCCs and SoCSCs in the United States, including their patient care focus, research, and program diversity.

Methods

We conducted an investigator-initiated, multicenter, cross-sectional survey study of all SoCCs in the United States and their respective academic residency programs. Fifteen formal SoCCs and/or SoCSCs were identified by dermatology program websites and an article by Tull et al² on the state of ethnic skin centers. All programs and centers identified were associated with a dermatology residency program accredited by the Accreditation Council for Graduate Medical Education.

A 42-item questionnaire was sent via email to the directors of these centers and clinics with the intent to collect descriptive information about each of the SoCCs, the diversity of the faculty and residents of the associated dermatology department, current research and funding, diversity and inclusion initiatives, and trainee education from March through April 2020. Data were analyzed using Excel and SPSS statistical software to obtain descriptive statistics including the mean value numeric trends across programs.

This study underwent expedited review and was approved by the University of Southern California (Los Angeles, California) institutional review board (IRB #HS-20-00113). Patient consent was not applicable, as no information was collected about patients.

Results

Fourteen directors from SoCCs/SoCSCs completed the questionnaire (93.3% response rate). Most centers were located in urban areas (12/14 [85.71%]), except for 2 in rural or suburban settings (Table). Most of the SoCCs/SoCSCs were located in the South (5/14 [35.71%]), followed by the Northeast (4/14 [28.57%]), West (3/14 [21.43%]), and Midwest (2/14 [14.29%])(Table). Six (42.86%) of the programs had a SoCSC, 3 (21.43%) had a formal SoCC, and 5 (35.71%) had both. Across all centers, the most common population seen and treated was Black/African American followed by Hispanic/Latino and Asian, respectively. The most commonly seen dermatologic conditions were acne, pigmentary disorders, alopecia, and atopic dermatitis (Figure). The most common cosmetic practice performed for patients with SoC was dermatosis papulosa nigra/seborrheic keratosis removal, followed by laser treatments, skin tag removal, chemical peels, and neuromodulator injections, respectively.

Faculty and Resident Demographics and Areas of Focus—The demographics and diversity of the dermatology faculty and residents at each individual institution also were assessed. The average number of full-time faculty at each institution was 19.4 (range, 2–48), while the average number of full-time faculty who identified as underrepresented in medicine (URiM) was 2.1 (range, 0–5). The average number of residents at each institution was 17.1 (range, 10–31), while the average number of URiM residents was 1.7 (range, 1–3).

Comment

As the number of SoCCs/SoCSCs in the United States continues to grow, it is important to highlight their programmatic, research, and educational accomplishments to show the benefits of such programs, including their ability to increase access to culturally competent and inclusive care for diverse patient populations. One study found that nearly 92% of patients in the United States seen by dermatologists are White.¹⁵ Although studies have shown that Hispanic/Latino and Black patients are less likely to seek care from a dermatologist,^16,17 there is no indication that these patients have a lesser need for such specialty care. Additionally, outcomes of common dermatologic conditions often are poorer in SoC populations.¹⁵ The dermatologists leading SoCCs/SoCSCs are actively working to reverse these trends, with Black and Hispanic/Latino patients representing the majority of their patients.

Faculty and Resident Demographics and Areas of Focus—Although there are increased diversity efforts in dermatology and the medical profession more broadly, there still is much work to be done. While individuals with SoC now comprise more than 35% of the US population, only 12% of dermatology residents and 6% of academic dermatology faculty identify as either Black or Hispanic/Latino.^5,8,10 These numbers are even more discouraging when considering other URiM racial groups such as Pacific Islander/Native Hawaiians or Native American/American Indians who represent 0% and 0.1% of dermatology faculty, respectively.^8,10 Academic programs with SoCCs/SoCSCs are working to create a space in which these discrepancies in representation can begin to be addressed. Compared to the national 6.8% rate of URiM faculty at academic institutions, those with SoCCs/SoCSCs report closer to 10% of faculty identifying as URiM.¹⁸ Moreover, almost all programs had faculty specialized in at least 1 condition that predominantly affects patients with SoC. This is of critical importance, as the conditions that most commonly affect SoC populations—such as CCCA, hidradenitis suppurativa, and cutaneous lupus—often are understudied, underfunded, underdiagnosed, and undertreated.^19-22

Faculty SoC Research—An important step in narrowing the knowledge gap and improving health care disparities in patients with SoC is to increase SoC research and/or to increase the representation of patients with SoC in research studies. In a 2021 study, a PubMed search of articles indexed for MEDLINE using the terms race/­ethnicity, dyschromia, atopic dermatitis, and acne was conducted to investigate publications pertaining to the top 3 most common chief concerns in patients with SoC. Only 1.6% of studies analyzed (N=74,941) had a specific focus on SoC.¹² A similar study found that among the top 5 ­dermatology-focused research journals, only 3.4% of all research (N=11,003) on the top 3 most common chief concerns in patients with SOC was conducted in patients with SoC.²³ Research efforts focused on dermatologic issues that affect patients with SoC are a priority at SoCCs/SoCSCs. In our study, all respondents indicated that they had at least 1 ongoing observational study; the most commonly studied conditions were CCCA, keloids/hypertrophic scarring, and atopic dermatitis, all of which are conditions that either occur in high frequency or primarily occur in SoC. Only 35.71% (5/14) of respondents had active clinical trials related to SoC, and only 21.43% (3/14) and 28.57% (4/14) had internal and external funding, respectively. Although research efforts are a priority at SoCCs/SoCSCs, our survey study highlights the continued paucity of formal clinical trials as well as funding for SoC-focused research. Improved research efforts for SoC must address these deficits in funding, academic support, and other resources.

It also is of great importance for institutions to provide support for trainees wanting to pursue SoC research. Encouragingly, more than half (57.14%) of SoCCs/SoCSCs have developed formal research opportunities for residents, and nearly 64.29% have formal opportunities for medical students. These efforts to provide early experiences in SoC research are especially impactful by cultivating interest in working with populations with SoC and hopefully inspiring future dermatologists to engage in further SoC research.

SoC Education and Diversity Initiatives—Although it is important to increase representation of URiM physicians in dermatology and to train more SoC specialists, it is imperative that all dermatologists feel comfortable recognizing and treating dermatologic conditions in patients of all skin tones and all racial/ethnic backgrounds; however, many studies suggest that residents not only lack formal didactics and education in SoC, but even more unsettling, they also lack confidence in treating SoC.^13,24 However, one study showed that this can be changed; Mhlaba et al²⁵ assessed a SoC curriculum for dermatology residents, and indeed all of the residents indicated that the curriculum improved their ability to treat SoC patients. This deficit in dermatology residency training is specifically addressed by SoCCs/SoCSCs. In our study, all respondents indicated that residents rotate through their centers. Moreover, our study found that most of the academic institutions with SoCCs/SoCSCs provide a SoC didactic curriculum for residents, and almost all of the programs invited SoC specialists to give guest lectures. This is in contrast to a 2022 study showing that 63.2% (N=125) of graduating dermatology residents reported receiving SoC-specific didactics, sessions, or lectures.¹⁴ These findings highlight the critical role that SoCCs/SoCSCs can provide in dermatology residency training.

Although SoCCs/SoCSCs have made considerable progress, there is still much room for improvement. Namely, only half of the respondents in our study indicated that their program has formally incorporated a SoC textbook into resident education (eTable 3). Representation of SoC in the textbooks that dermatology residents use is critically important because these images form the foundation of the morphologic aids of diagnosis. Numerous studies have analyzed popular dermatologic textbooks used by residency programs nationwide, finding the number of SoC images across dermatology textbooks ranging from 4% to 18%.^26,27 The use of standard dermatology textbooks is not enough to train residents to be competent in diagnosing and treating patients with SoC. There should be a concerted effort across the field of dermatology to encourage the development of a SoC educational curriculum at every academic dermatology program, including SoC textbooks, Kodachromes, and online/electronic resources.

Efforts to increase diversity in dermatology and dermatologic training should start in medical school preclinical curriculums and medical student rotations. Although our survey did not assess current medical student curricula, the benefits of academic institutions with SoCCs/SoCSCs are highlighted by the ability for both home and visiting medical students to rotate through the centers and gain early exposure to SoC dermatology. Most of the programs even provide scholarships and/or grants for URiM students to help fund their rotations, which is of critical importance considering the mounting data that the financial burden of visiting rotations disproportionately affects URiM students.²⁸

Study Limitations—Although we did an extensive search and believe to have correctly identified all 15 formal SoCCs/SoCSCs with a high response rate (93.3%), there are institutions that do not have formalized SoCCs/SoCSCs but are known to serve SoC populations. Likewise, there are private dermatology practices not associated with academic centers that have SoC specialists and positively contribute to SoC patient care, research, and education that were not included in this study. Additionally, the data for this study were collected in 2020 and analyzed in 2021, so it is possible that not all SoCCs, divisions, or clinics were included in this study, particularly if established after 2021.

Conclusion

As the United States continues to diversify, the proportion of patients with SoC will continue to grow, and it is imperative that this racial, ethnic, and cultural diversity is reflected in the dermatology workforce as well as research and training. The current deficits in medical training related to SoC populations and the importance for patients with SoC to find dermatologists who can appropriately treat them is well known.²⁹ Skin of color centers/SoCSCs strive to increase access to care for patients with SoC, improve cultural competency, promote diversity among faculty and trainees, and encourage SoC research and education at all levels. We urge academic dermatology training programs to make SoC education, research, and patient care a departmental priority. Important first steps include departmental diversification at all levels, incorporating SoC into curricula for residents, providing and securing funding for SoC research, and supporting the establishment of more formal SoCCs and/or SoCSCs to help reduce dermatologic health care disparities among patients with SoC and improve health equity.

Appendix

Although individuals with skin of color (SoC) are expected to become at least half of the US population by the year 2044, there remains a paucity of education and exposure to treatment of patients with SoC at many dermatology residency programs across the country.¹ One way to improve SoC education has been the formation of specialized clinics, centers, and programs. The first SoC center (SoCC) was established in 1999 at Mount Sinai–St. Luke’s Roosevelt in New York, New York²; since then, at least 13 additional formal SoCCs or SoC specialty clinics (SoCSCs) at US academic dermatology programs have been established.

Skin of color centers serve several important purposes: they improve dermatologic care in patients with SoC, increase research efforts focused on SoC dermatologic conditions, and educate dermatology resident and fellow trainees about SoC. Improving dermatologic care of patients with SoC in the United States is important in providing equitable health care and improving health disparities. Studies have shown that patient-physician racial and cultural concordance can positively impact patient care, increase patient trust and rapport, and improve patient-physician communication, and it can even influence patient decision-making to seek care.^3,4 Unfortunately, even though the US population continues to diversify, the racial/ethnic backgrounds of dermatologists do not parallel this trend; Hispanic and Black physicians comprise 18.9% and 13.6% of the general population, respectively, but represent only 4.2% and 3.0% of dermatologists, respectively.^5-7 This deficit is mirrored by resident and faculty representation, with Black and Latino representation ranging from 3% to 7%.^8-10

Many SoCC’s engage in research focused on dermatologic conditions affecting patients with SoC, which is vital to improving the dermatologic care in this underserved population. Despite increasing recognition of the importance of SoC research, there remains a paucity of clinical trials and research specifically focused on or demonstrating equitable representation of SoC.^11,12

The education and training of future dermatologists is another important area that can be improved by SoCCs. A 2008 study involving 63 chief residents showed that approximately half (52.4% [33/63]) of graduating dermatology residents reported receiving SoC-specific didactics, sessions, or lectures, and 30.2% (19/63) reported having a dedicated rotation where they gained specific experience treating patients with SoC.¹³ A later study in 2022 (N=125) found that 63.2% of graduating dermatology residents reported receiving SoC-specific didactics, sessions, or lectures, and only 11.2% reported having a dedicated rotation where they gained experience treating patients with SoC.¹⁴ These findings suggest that in the last 14 years, formal SoC education—specifically SoC clinical training—has not increased sufficiently.

We conducted a cross-sectional survey study to provide an in-depth analysis of SoCCs and SoCSCs in the United States, including their patient care focus, research, and program diversity.

Methods

We conducted an investigator-initiated, multicenter, cross-sectional survey study of all SoCCs in the United States and their respective academic residency programs. Fifteen formal SoCCs and/or SoCSCs were identified by dermatology program websites and an article by Tull et al² on the state of ethnic skin centers. All programs and centers identified were associated with a dermatology residency program accredited by the Accreditation Council for Graduate Medical Education.

A 42-item questionnaire was sent via email to the directors of these centers and clinics with the intent to collect descriptive information about each of the SoCCs, the diversity of the faculty and residents of the associated dermatology department, current research and funding, diversity and inclusion initiatives, and trainee education from March through April 2020. Data were analyzed using Excel and SPSS statistical software to obtain descriptive statistics including the mean value numeric trends across programs.

This study underwent expedited review and was approved by the University of Southern California (Los Angeles, California) institutional review board (IRB #HS-20-00113). Patient consent was not applicable, as no information was collected about patients.

Results

Fourteen directors from SoCCs/SoCSCs completed the questionnaire (93.3% response rate). Most centers were located in urban areas (12/14 [85.71%]), except for 2 in rural or suburban settings (Table). Most of the SoCCs/SoCSCs were located in the South (5/14 [35.71%]), followed by the Northeast (4/14 [28.57%]), West (3/14 [21.43%]), and Midwest (2/14 [14.29%])(Table). Six (42.86%) of the programs had a SoCSC, 3 (21.43%) had a formal SoCC, and 5 (35.71%) had both. Across all centers, the most common population seen and treated was Black/African American followed by Hispanic/Latino and Asian, respectively. The most commonly seen dermatologic conditions were acne, pigmentary disorders, alopecia, and atopic dermatitis (Figure). The most common cosmetic practice performed for patients with SoC was dermatosis papulosa nigra/seborrheic keratosis removal, followed by laser treatments, skin tag removal, chemical peels, and neuromodulator injections, respectively.

Faculty and Resident Demographics and Areas of Focus—The demographics and diversity of the dermatology faculty and residents at each individual institution also were assessed. The average number of full-time faculty at each institution was 19.4 (range, 2–48), while the average number of full-time faculty who identified as underrepresented in medicine (URiM) was 2.1 (range, 0–5). The average number of residents at each institution was 17.1 (range, 10–31), while the average number of URiM residents was 1.7 (range, 1–3).

Comment

As the number of SoCCs/SoCSCs in the United States continues to grow, it is important to highlight their programmatic, research, and educational accomplishments to show the benefits of such programs, including their ability to increase access to culturally competent and inclusive care for diverse patient populations. One study found that nearly 92% of patients in the United States seen by dermatologists are White.¹⁵ Although studies have shown that Hispanic/Latino and Black patients are less likely to seek care from a dermatologist,^16,17 there is no indication that these patients have a lesser need for such specialty care. Additionally, outcomes of common dermatologic conditions often are poorer in SoC populations.¹⁵ The dermatologists leading SoCCs/SoCSCs are actively working to reverse these trends, with Black and Hispanic/Latino patients representing the majority of their patients.

Faculty and Resident Demographics and Areas of Focus—Although there are increased diversity efforts in dermatology and the medical profession more broadly, there still is much work to be done. While individuals with SoC now comprise more than 35% of the US population, only 12% of dermatology residents and 6% of academic dermatology faculty identify as either Black or Hispanic/Latino.^5,8,10 These numbers are even more discouraging when considering other URiM racial groups such as Pacific Islander/Native Hawaiians or Native American/American Indians who represent 0% and 0.1% of dermatology faculty, respectively.^8,10 Academic programs with SoCCs/SoCSCs are working to create a space in which these discrepancies in representation can begin to be addressed. Compared to the national 6.8% rate of URiM faculty at academic institutions, those with SoCCs/SoCSCs report closer to 10% of faculty identifying as URiM.¹⁸ Moreover, almost all programs had faculty specialized in at least 1 condition that predominantly affects patients with SoC. This is of critical importance, as the conditions that most commonly affect SoC populations—such as CCCA, hidradenitis suppurativa, and cutaneous lupus—often are understudied, underfunded, underdiagnosed, and undertreated.^19-22

Faculty SoC Research—An important step in narrowing the knowledge gap and improving health care disparities in patients with SoC is to increase SoC research and/or to increase the representation of patients with SoC in research studies. In a 2021 study, a PubMed search of articles indexed for MEDLINE using the terms race/­ethnicity, dyschromia, atopic dermatitis, and acne was conducted to investigate publications pertaining to the top 3 most common chief concerns in patients with SoC. Only 1.6% of studies analyzed (N=74,941) had a specific focus on SoC.¹² A similar study found that among the top 5 ­dermatology-focused research journals, only 3.4% of all research (N=11,003) on the top 3 most common chief concerns in patients with SOC was conducted in patients with SoC.²³ Research efforts focused on dermatologic issues that affect patients with SoC are a priority at SoCCs/SoCSCs. In our study, all respondents indicated that they had at least 1 ongoing observational study; the most commonly studied conditions were CCCA, keloids/hypertrophic scarring, and atopic dermatitis, all of which are conditions that either occur in high frequency or primarily occur in SoC. Only 35.71% (5/14) of respondents had active clinical trials related to SoC, and only 21.43% (3/14) and 28.57% (4/14) had internal and external funding, respectively. Although research efforts are a priority at SoCCs/SoCSCs, our survey study highlights the continued paucity of formal clinical trials as well as funding for SoC-focused research. Improved research efforts for SoC must address these deficits in funding, academic support, and other resources.

It also is of great importance for institutions to provide support for trainees wanting to pursue SoC research. Encouragingly, more than half (57.14%) of SoCCs/SoCSCs have developed formal research opportunities for residents, and nearly 64.29% have formal opportunities for medical students. These efforts to provide early experiences in SoC research are especially impactful by cultivating interest in working with populations with SoC and hopefully inspiring future dermatologists to engage in further SoC research.

SoC Education and Diversity Initiatives—Although it is important to increase representation of URiM physicians in dermatology and to train more SoC specialists, it is imperative that all dermatologists feel comfortable recognizing and treating dermatologic conditions in patients of all skin tones and all racial/ethnic backgrounds; however, many studies suggest that residents not only lack formal didactics and education in SoC, but even more unsettling, they also lack confidence in treating SoC.^13,24 However, one study showed that this can be changed; Mhlaba et al²⁵ assessed a SoC curriculum for dermatology residents, and indeed all of the residents indicated that the curriculum improved their ability to treat SoC patients. This deficit in dermatology residency training is specifically addressed by SoCCs/SoCSCs. In our study, all respondents indicated that residents rotate through their centers. Moreover, our study found that most of the academic institutions with SoCCs/SoCSCs provide a SoC didactic curriculum for residents, and almost all of the programs invited SoC specialists to give guest lectures. This is in contrast to a 2022 study showing that 63.2% (N=125) of graduating dermatology residents reported receiving SoC-specific didactics, sessions, or lectures.¹⁴ These findings highlight the critical role that SoCCs/SoCSCs can provide in dermatology residency training.

Although SoCCs/SoCSCs have made considerable progress, there is still much room for improvement. Namely, only half of the respondents in our study indicated that their program has formally incorporated a SoC textbook into resident education (eTable 3). Representation of SoC in the textbooks that dermatology residents use is critically important because these images form the foundation of the morphologic aids of diagnosis. Numerous studies have analyzed popular dermatologic textbooks used by residency programs nationwide, finding the number of SoC images across dermatology textbooks ranging from 4% to 18%.^26,27 The use of standard dermatology textbooks is not enough to train residents to be competent in diagnosing and treating patients with SoC. There should be a concerted effort across the field of dermatology to encourage the development of a SoC educational curriculum at every academic dermatology program, including SoC textbooks, Kodachromes, and online/electronic resources.

Efforts to increase diversity in dermatology and dermatologic training should start in medical school preclinical curriculums and medical student rotations. Although our survey did not assess current medical student curricula, the benefits of academic institutions with SoCCs/SoCSCs are highlighted by the ability for both home and visiting medical students to rotate through the centers and gain early exposure to SoC dermatology. Most of the programs even provide scholarships and/or grants for URiM students to help fund their rotations, which is of critical importance considering the mounting data that the financial burden of visiting rotations disproportionately affects URiM students.²⁸

Study Limitations—Although we did an extensive search and believe to have correctly identified all 15 formal SoCCs/SoCSCs with a high response rate (93.3%), there are institutions that do not have formalized SoCCs/SoCSCs but are known to serve SoC populations. Likewise, there are private dermatology practices not associated with academic centers that have SoC specialists and positively contribute to SoC patient care, research, and education that were not included in this study. Additionally, the data for this study were collected in 2020 and analyzed in 2021, so it is possible that not all SoCCs, divisions, or clinics were included in this study, particularly if established after 2021.

Conclusion

As the United States continues to diversify, the proportion of patients with SoC will continue to grow, and it is imperative that this racial, ethnic, and cultural diversity is reflected in the dermatology workforce as well as research and training. The current deficits in medical training related to SoC populations and the importance for patients with SoC to find dermatologists who can appropriately treat them is well known.²⁹ Skin of color centers/SoCSCs strive to increase access to care for patients with SoC, improve cultural competency, promote diversity among faculty and trainees, and encourage SoC research and education at all levels. We urge academic dermatology training programs to make SoC education, research, and patient care a departmental priority. Important first steps include departmental diversification at all levels, incorporating SoC into curricula for residents, providing and securing funding for SoC research, and supporting the establishment of more formal SoCCs and/or SoCSCs to help reduce dermatologic health care disparities among patients with SoC and improve health equity.

Appendix

To the Editor:

Prescriptions for isotretinoin may be influenced by patient demographics, medical comorbidities, and drug safety programs.^1,2 In 1982, isotretinoin was approved by the US Food and Drug Administration for treatment of severe recalcitrant nodulocystic acne that is nonresponsive to conventional therapies such as antibiotics; however, prescriber beliefs regarding the necessity of oral antibiotic failure before isotretinoin is prescribed may be influenced by the provider’s generational age.³ Currently, there is a knowledge gap regarding the impact of provider characteristics, including the year providers completed training, on isotretinoin utilization. The aim of our cross-sectional study was to characterize generational isotretinoin prescribing habits in a large-scale midwestern private practice dermatology group.

Modernizing Medicine (https://www.modmed.com), an electronic medical record software, was queried for all encounters that included both an International Classification of Diseases, Tenth Revision, Clinical Modification diagnosis code L70.0 (acne vulgaris) and a medication prescription from May 2021 to May 2022. Data were collected from a large private practice group with locations across the state of Ohio. Exclusion criteria included provider-patient prescription pairs that included non–acne medication prescriptions, patients seen by multiple providers, and providers who treated fewer than 5 patients with acne during the study period. A mixed-effect multiple logistic regression was performed to analyze whether a patient was ever prescribed isotretinoin, adjusting for individual prescriber, prescriber generation (millennial [1981–1996], Generation X [1965–1980], and baby boomer [1946–1964]),⁴ and patient sex; spironolactone and oral antibiotic prescriptions during the study period were included as additional covariates in a subsequent post hoc analysis. This study utilized data that was fully deidentified in accordance with the US Health Insurance Portability and Accountability Act (HIPAA) Privacy Rule. Approval from an institutional review board was not required.

A total of 18,089 provider-patient prescription pairs were included in our analysis (Table). In our most robust model, female patients were significantly less likely to receive isotretinoin compared with male patients (adjusted OR [aOR], 0.394; P<.01). Millennial providers were significantly more likely to utilize isotretinoin in patients who did not receive antibiotics compared with patients who did receive antibiotics (aOR, 1.693; P<.01). When compared with both Generation X and baby boomers, millennial providers were more likely to prescribe isotretinoin in patients who received antibiotics (aOR, 2.227 [P=.02] and 3.638 [P<.01], respectively).

To the Editor:

Prescriptions for isotretinoin may be influenced by patient demographics, medical comorbidities, and drug safety programs.^1,2 In 1982, isotretinoin was approved by the US Food and Drug Administration for treatment of severe recalcitrant nodulocystic acne that is nonresponsive to conventional therapies such as antibiotics; however, prescriber beliefs regarding the necessity of oral antibiotic failure before isotretinoin is prescribed may be influenced by the provider’s generational age.³ Currently, there is a knowledge gap regarding the impact of provider characteristics, including the year providers completed training, on isotretinoin utilization. The aim of our cross-sectional study was to characterize generational isotretinoin prescribing habits in a large-scale midwestern private practice dermatology group.

Modernizing Medicine (https://www.modmed.com), an electronic medical record software, was queried for all encounters that included both an International Classification of Diseases, Tenth Revision, Clinical Modification diagnosis code L70.0 (acne vulgaris) and a medication prescription from May 2021 to May 2022. Data were collected from a large private practice group with locations across the state of Ohio. Exclusion criteria included provider-patient prescription pairs that included non–acne medication prescriptions, patients seen by multiple providers, and providers who treated fewer than 5 patients with acne during the study period. A mixed-effect multiple logistic regression was performed to analyze whether a patient was ever prescribed isotretinoin, adjusting for individual prescriber, prescriber generation (millennial [1981–1996], Generation X [1965–1980], and baby boomer [1946–1964]),⁴ and patient sex; spironolactone and oral antibiotic prescriptions during the study period were included as additional covariates in a subsequent post hoc analysis. This study utilized data that was fully deidentified in accordance with the US Health Insurance Portability and Accountability Act (HIPAA) Privacy Rule. Approval from an institutional review board was not required.

A total of 18,089 provider-patient prescription pairs were included in our analysis (Table). In our most robust model, female patients were significantly less likely to receive isotretinoin compared with male patients (adjusted OR [aOR], 0.394; P<.01). Millennial providers were significantly more likely to utilize isotretinoin in patients who did not receive antibiotics compared with patients who did receive antibiotics (aOR, 1.693; P<.01). When compared with both Generation X and baby boomers, millennial providers were more likely to prescribe isotretinoin in patients who received antibiotics (aOR, 2.227 [P=.02] and 3.638 [P<.01], respectively).

To the Editor:

Prescriptions for isotretinoin may be influenced by patient demographics, medical comorbidities, and drug safety programs.^1,2 In 1982, isotretinoin was approved by the US Food and Drug Administration for treatment of severe recalcitrant nodulocystic acne that is nonresponsive to conventional therapies such as antibiotics; however, prescriber beliefs regarding the necessity of oral antibiotic failure before isotretinoin is prescribed may be influenced by the provider’s generational age.³ Currently, there is a knowledge gap regarding the impact of provider characteristics, including the year providers completed training, on isotretinoin utilization. The aim of our cross-sectional study was to characterize generational isotretinoin prescribing habits in a large-scale midwestern private practice dermatology group.

Modernizing Medicine (https://www.modmed.com), an electronic medical record software, was queried for all encounters that included both an International Classification of Diseases, Tenth Revision, Clinical Modification diagnosis code L70.0 (acne vulgaris) and a medication prescription from May 2021 to May 2022. Data were collected from a large private practice group with locations across the state of Ohio. Exclusion criteria included provider-patient prescription pairs that included non–acne medication prescriptions, patients seen by multiple providers, and providers who treated fewer than 5 patients with acne during the study period. A mixed-effect multiple logistic regression was performed to analyze whether a patient was ever prescribed isotretinoin, adjusting for individual prescriber, prescriber generation (millennial [1981–1996], Generation X [1965–1980], and baby boomer [1946–1964]),⁴ and patient sex; spironolactone and oral antibiotic prescriptions during the study period were included as additional covariates in a subsequent post hoc analysis. This study utilized data that was fully deidentified in accordance with the US Health Insurance Portability and Accountability Act (HIPAA) Privacy Rule. Approval from an institutional review board was not required.

A total of 18,089 provider-patient prescription pairs were included in our analysis (Table). In our most robust model, female patients were significantly less likely to receive isotretinoin compared with male patients (adjusted OR [aOR], 0.394; P<.01). Millennial providers were significantly more likely to utilize isotretinoin in patients who did not receive antibiotics compared with patients who did receive antibiotics (aOR, 1.693; P<.01). When compared with both Generation X and baby boomers, millennial providers were more likely to prescribe isotretinoin in patients who received antibiotics (aOR, 2.227 [P=.02] and 3.638 [P<.01], respectively).