Cutis

In this era of biologics for psoriasis with ever-increasing effectiveness and safety as well as patients who have less and less time to visit the physician's office, it would seem that the days of in-office UV treatments would be numbered. However, rumors of the demise of phototherapy may be greatly exaggerated. Phototherapy is still one of the safest and most cost-effective treatments for psoriasis and other dermatoses.1 Its use often is a prerequisite for biologic therapy, and it may be the only therapeutic option for certain subsets of patients, such as children, pregnant women, and immunosuppressed patients. Moreover, narrowband UVB technology has breathed new life into phototherapy, with better efficacy and less long-term risk. Although the utilization of psoralen plus UVA (PUVA) light therapy has indeed decreased over the last 2 decades, the use of UVB therapies continues to increase dramatically.²

Phototherapy Codes

There are 4 chief Current Procedural Terminology (CPT) codes for reporting phototherapy services: (1) 96900: actinotherapy (UV light treatment); (2) 96910: photochemotherapy, tar, and UVB (Goeckerman treatment) or petrolatum and UVB; (3) 96912: photochemotherapy and PUVA; and (4) 96913: photochemotherapy (Goeckerman and/or PUVA) for severe photoresponsive dermatoses requiring at least 4 to 8 hours of care under direct supervision of the physician.³

There is lack of specificity of the CPT code descriptions for phototherapy. Moreover, insurer guidance for documentation for phototherapy is vague to nonexistent, and of course whenever the use of any medical service increases, insurer scrutiny is sure to follow. Therefore, it is not surprising that dermatology practices have reported that private insurers as well as Medicare are auditing medical records for phototherapy treatments.⁴ In fact, recently we have seen a Midwest private insurer demand payment from dermatologists for hundreds of 96910 phototherapy services, which the insurer asserted should have been coded as 96900 because topical therapies were not applied by the dermatology staff. The insurer did not just evaluate medical records but also contacted patients directly and asked how services had been provided. Clearly, more detailed guidance for dermatologists and insurers on documentation and performance standards for each phototherapy service is needed.

Existing coding guidance for phototherapy indicates that actinotherapy (96900) defines the basic service of treating a patient with a UV light unit.⁵ Actinotherapy does not involve application of topical medications while the patient is in the office.

In contrast, photochemotherapy (96910) implies addition of a chemo agent to phototherapy. Despite the somewhat nonspecific nature of the code descriptor, it is apparent that application of photoenhancing agents such as tar, petrolatum, or distillates of petrolatum meet the requirements of 96910. The Coder's Desk Reference for Procedures 2017 describes 96910 as "the physician uses photosensitizing chemicals and light rays to treat skin ailments."⁶ Application of light-enhancing topical products should occur within the office by either staff or the patient. In fact, examination of practice expense data from the Centers for Medicare & Medicaid Services indicated that the 96910 code includes payment for clinical staff time to apply topical products as well as the cost of the topical agent(s).⁷ 

The PUVA code 96912 is defined by the use of photosensitizing psoralen medication, which can be administered topically or orally, followed by UVA treatment. In my experience, PUVA has similar performance standards with in-office application of psoralen, if applicable. If application of topical photoenhancing products occurs outside the office, the requirements of photochemotherapy are not met, and 96900 should be reported. 

The 96913 code defines prolonged phototherapy service with intensive topical therapy requirements and multiple phototherapy sessions per day.³ This code is rarely reported (average of fewer than 100 times in the Medicare population per year), and most insurers do not reimburse this service. 

Protecting Yourself From an Audit

In my experience, review of private insurer audits of phototherapy services has yielded important lessons. First, having a written standard operating procedure in place regarding the performance of phototherapy services and how application of topicals will be handled has been helpful in audit defense. The other key to beating audits for phototherapy services is to have detailed documentation or a flowchart in the medical record regarding the topical agent and the light administration. The medical record should include what topical agent was applied, if any; whether the topical agent was applied in the office; where the topical product was applied; and who applied the topical product. Sometimes topical product application by a physician or staff is not feasible because of patient preference or the site of application. If the patient applied the topical, document that assistance was offered and refused, along with what type of UV light was used and the dosage. Inclusion of these elements in the medical record provides a clear picture of the delivery of the phototherapy service and will aid in responding to medical record audit.

Final Thoughts

Phototherapy is a critical treatment modality that continues to be utilized frequently in the expanding armamentarium of treatments for dermatoses. Phototherapy is performed almost exclusively by dermatologists and allows dermatologists to offer a unique level of care and value in the treatment of skin disease. Careful documentation, a written standard operating procedure, and adherence to proper performance standards will allow dermatologists to be compensated fairly for this important treatment modality and pass audits that are likely to occur.

In this era of biologics for psoriasis with ever-increasing effectiveness and safety as well as patients who have less and less time to visit the physician's office, it would seem that the days of in-office UV treatments would be numbered. However, rumors of the demise of phototherapy may be greatly exaggerated. Phototherapy is still one of the safest and most cost-effective treatments for psoriasis and other dermatoses.1 Its use often is a prerequisite for biologic therapy, and it may be the only therapeutic option for certain subsets of patients, such as children, pregnant women, and immunosuppressed patients. Moreover, narrowband UVB technology has breathed new life into phototherapy, with better efficacy and less long-term risk. Although the utilization of psoralen plus UVA (PUVA) light therapy has indeed decreased over the last 2 decades, the use of UVB therapies continues to increase dramatically.²

Phototherapy Codes

There are 4 chief Current Procedural Terminology (CPT) codes for reporting phototherapy services: (1) 96900: actinotherapy (UV light treatment); (2) 96910: photochemotherapy, tar, and UVB (Goeckerman treatment) or petrolatum and UVB; (3) 96912: photochemotherapy and PUVA; and (4) 96913: photochemotherapy (Goeckerman and/or PUVA) for severe photoresponsive dermatoses requiring at least 4 to 8 hours of care under direct supervision of the physician.³

There is lack of specificity of the CPT code descriptions for phototherapy. Moreover, insurer guidance for documentation for phototherapy is vague to nonexistent, and of course whenever the use of any medical service increases, insurer scrutiny is sure to follow. Therefore, it is not surprising that dermatology practices have reported that private insurers as well as Medicare are auditing medical records for phototherapy treatments.⁴ In fact, recently we have seen a Midwest private insurer demand payment from dermatologists for hundreds of 96910 phototherapy services, which the insurer asserted should have been coded as 96900 because topical therapies were not applied by the dermatology staff. The insurer did not just evaluate medical records but also contacted patients directly and asked how services had been provided. Clearly, more detailed guidance for dermatologists and insurers on documentation and performance standards for each phototherapy service is needed.

Existing coding guidance for phototherapy indicates that actinotherapy (96900) defines the basic service of treating a patient with a UV light unit.⁵ Actinotherapy does not involve application of topical medications while the patient is in the office.

In contrast, photochemotherapy (96910) implies addition of a chemo agent to phototherapy. Despite the somewhat nonspecific nature of the code descriptor, it is apparent that application of photoenhancing agents such as tar, petrolatum, or distillates of petrolatum meet the requirements of 96910. The Coder's Desk Reference for Procedures 2017 describes 96910 as "the physician uses photosensitizing chemicals and light rays to treat skin ailments."⁶ Application of light-enhancing topical products should occur within the office by either staff or the patient. In fact, examination of practice expense data from the Centers for Medicare & Medicaid Services indicated that the 96910 code includes payment for clinical staff time to apply topical products as well as the cost of the topical agent(s).⁷ 

The PUVA code 96912 is defined by the use of photosensitizing psoralen medication, which can be administered topically or orally, followed by UVA treatment. In my experience, PUVA has similar performance standards with in-office application of psoralen, if applicable. If application of topical photoenhancing products occurs outside the office, the requirements of photochemotherapy are not met, and 96900 should be reported. 

The 96913 code defines prolonged phototherapy service with intensive topical therapy requirements and multiple phototherapy sessions per day.³ This code is rarely reported (average of fewer than 100 times in the Medicare population per year), and most insurers do not reimburse this service. 

Protecting Yourself From an Audit

In my experience, review of private insurer audits of phototherapy services has yielded important lessons. First, having a written standard operating procedure in place regarding the performance of phototherapy services and how application of topicals will be handled has been helpful in audit defense. The other key to beating audits for phototherapy services is to have detailed documentation or a flowchart in the medical record regarding the topical agent and the light administration. The medical record should include what topical agent was applied, if any; whether the topical agent was applied in the office; where the topical product was applied; and who applied the topical product. Sometimes topical product application by a physician or staff is not feasible because of patient preference or the site of application. If the patient applied the topical, document that assistance was offered and refused, along with what type of UV light was used and the dosage. Inclusion of these elements in the medical record provides a clear picture of the delivery of the phototherapy service and will aid in responding to medical record audit.

Final Thoughts

Phototherapy is a critical treatment modality that continues to be utilized frequently in the expanding armamentarium of treatments for dermatoses. Phototherapy is performed almost exclusively by dermatologists and allows dermatologists to offer a unique level of care and value in the treatment of skin disease. Careful documentation, a written standard operating procedure, and adherence to proper performance standards will allow dermatologists to be compensated fairly for this important treatment modality and pass audits that are likely to occur.

In this era of biologics for psoriasis with ever-increasing effectiveness and safety as well as patients who have less and less time to visit the physician's office, it would seem that the days of in-office UV treatments would be numbered. However, rumors of the demise of phototherapy may be greatly exaggerated. Phototherapy is still one of the safest and most cost-effective treatments for psoriasis and other dermatoses.1 Its use often is a prerequisite for biologic therapy, and it may be the only therapeutic option for certain subsets of patients, such as children, pregnant women, and immunosuppressed patients. Moreover, narrowband UVB technology has breathed new life into phototherapy, with better efficacy and less long-term risk. Although the utilization of psoralen plus UVA (PUVA) light therapy has indeed decreased over the last 2 decades, the use of UVB therapies continues to increase dramatically.²

Phototherapy Codes

There are 4 chief Current Procedural Terminology (CPT) codes for reporting phototherapy services: (1) 96900: actinotherapy (UV light treatment); (2) 96910: photochemotherapy, tar, and UVB (Goeckerman treatment) or petrolatum and UVB; (3) 96912: photochemotherapy and PUVA; and (4) 96913: photochemotherapy (Goeckerman and/or PUVA) for severe photoresponsive dermatoses requiring at least 4 to 8 hours of care under direct supervision of the physician.³

There is lack of specificity of the CPT code descriptions for phototherapy. Moreover, insurer guidance for documentation for phototherapy is vague to nonexistent, and of course whenever the use of any medical service increases, insurer scrutiny is sure to follow. Therefore, it is not surprising that dermatology practices have reported that private insurers as well as Medicare are auditing medical records for phototherapy treatments.⁴ In fact, recently we have seen a Midwest private insurer demand payment from dermatologists for hundreds of 96910 phototherapy services, which the insurer asserted should have been coded as 96900 because topical therapies were not applied by the dermatology staff. The insurer did not just evaluate medical records but also contacted patients directly and asked how services had been provided. Clearly, more detailed guidance for dermatologists and insurers on documentation and performance standards for each phototherapy service is needed.

Existing coding guidance for phototherapy indicates that actinotherapy (96900) defines the basic service of treating a patient with a UV light unit.⁵ Actinotherapy does not involve application of topical medications while the patient is in the office.

In contrast, photochemotherapy (96910) implies addition of a chemo agent to phototherapy. Despite the somewhat nonspecific nature of the code descriptor, it is apparent that application of photoenhancing agents such as tar, petrolatum, or distillates of petrolatum meet the requirements of 96910. The Coder's Desk Reference for Procedures 2017 describes 96910 as "the physician uses photosensitizing chemicals and light rays to treat skin ailments."⁶ Application of light-enhancing topical products should occur within the office by either staff or the patient. In fact, examination of practice expense data from the Centers for Medicare & Medicaid Services indicated that the 96910 code includes payment for clinical staff time to apply topical products as well as the cost of the topical agent(s).⁷ 

The PUVA code 96912 is defined by the use of photosensitizing psoralen medication, which can be administered topically or orally, followed by UVA treatment. In my experience, PUVA has similar performance standards with in-office application of psoralen, if applicable. If application of topical photoenhancing products occurs outside the office, the requirements of photochemotherapy are not met, and 96900 should be reported. 

The 96913 code defines prolonged phototherapy service with intensive topical therapy requirements and multiple phototherapy sessions per day.³ This code is rarely reported (average of fewer than 100 times in the Medicare population per year), and most insurers do not reimburse this service. 

Protecting Yourself From an Audit

In my experience, review of private insurer audits of phototherapy services has yielded important lessons. First, having a written standard operating procedure in place regarding the performance of phototherapy services and how application of topicals will be handled has been helpful in audit defense. The other key to beating audits for phototherapy services is to have detailed documentation or a flowchart in the medical record regarding the topical agent and the light administration. The medical record should include what topical agent was applied, if any; whether the topical agent was applied in the office; where the topical product was applied; and who applied the topical product. Sometimes topical product application by a physician or staff is not feasible because of patient preference or the site of application. If the patient applied the topical, document that assistance was offered and refused, along with what type of UV light was used and the dosage. Inclusion of these elements in the medical record provides a clear picture of the delivery of the phototherapy service and will aid in responding to medical record audit.

Final Thoughts

Phototherapy is a critical treatment modality that continues to be utilized frequently in the expanding armamentarium of treatments for dermatoses. Phototherapy is performed almost exclusively by dermatologists and allows dermatologists to offer a unique level of care and value in the treatment of skin disease. Careful documentation, a written standard operating procedure, and adherence to proper performance standards will allow dermatologists to be compensated fairly for this important treatment modality and pass audits that are likely to occur.

Rosacea is a chronic inflammatory skin disease characterized by central facial erythema with or without intermittent papules and pustules (described as the inflammatory lesions of rosacea). Although twice-daily clindamycin 1% solution or gel has been used in the treatment of acne, few studies have investigated the use of clindamycin in rosacea.^1,2 In one study comparing twice-daily clindamycin lotion 1% with oral tetracycline in 43 rosacea patients, clindamycin was found to be superior in the eradication of pustules.³ A combination therapy of clindamycin 1% and benzoyl peroxide 5% was found to be more effective than the vehicle in inflammatory lesions and erythema of rosacea in a 12-week randomized controlled trial; however, a definitive advantage over US Food and Drug Administration-approved topical agents used to treat papulopustular rosacea was not established.^4,5 Two further studies evaluated clindamycin phosphate 1.2%-tretinoin 0.025% combination gel in the treatment of rosacea, but only 1 showed any effect on papulopustular lesions.^6-8 The objective of the studies reported here was to evaluate the efficacy and safety of clindamycin in the treatment of patients with moderate to severe rosacea.

Methods

Study Design

Two multicenter (study A, 20 centers; study B, 10 centers), randomized, investigator-blinded, vehicle-controlled studies were conducted in the United States between 1999 and 2002 in accordance with the Declaration of Helsinki, International Conference on Harmonisation Good Clinical Practice guidelines, and local regulatory requirements. The studies were reviewed and approved by the respective institutional review boards, and all participants provided written informed consent.

In study A, moderate to severe rosacea patients with erythema, telangiectasia, and at least 8 inflammatory lesions were randomized to receive clindamycin cream 1% or vehicle cream once (in the evening) or twice daily (in the morning and evening) or clindamycin cream 0.3% once daily (in the evening) for 12 weeks (1:1:1:1:1 ratio). All study treatments were supplied in identical tubes with blinded labels.

In study B, patients with moderate to severe rosacea and at least 8 inflammatory lesions were randomized in a 1:1 ratio with instructions to apply clindamycin gel 1% or vehicle gel to the affected areas twice daily (morning and evening) for 12 weeks.

Efficacy Evaluation

Evaluations were performed at baseline and weeks 2, 4, 8, and 12 on the intention-to-treat population with the last observation carried forward.

Efficacy assessments in both studies included inflammatory lesion counts (papules and pustules) of 5 facial regions--forehead, chin, nose, right cheek, left cheek--counted separately and then combined to give the total inflammatory lesion count (both studies), as well as improvement in the investigator global rosacea severity score (0=none/clear; 1=mild, detectable erythema with ≤7 papules/pustules; 2=moderate, prominent erythema with ≥8 papules/pustules; 3=severe, intense erythema with ≥10 to <50 papules/pustules; 3.5 [study A] or 4 [study B]=very severe, intense erythema with >50 papules/pustules). In study B, the proportion of participants dichotomized to success (a score of 0 [none/clear] or 1 [mild/almost clear]) or failure (a score of ≥2) on the 5-point investigator global rosacea severity scale at week 12 was evaluated. In study A, investigator global improvement assessment at week 12, based on photographs taken at baseline, was graded on a 7-point scale (from -1 [worse], 0 [no change], and 1 [minimal improvement] to 5 [clear]). In both studies, erythema severity was graded on a 7-point scale in increments of 0.5 (from 0=no erythema to 3.5=very severe redness, very intense redness). Skin irritation also was graded as none, mild, moderate, or severe. 

Safety Evaluation

Safety was assessed by the incidence of adverse events (AEs).

Statistical Analysis

Studies were powered assuming 60% reduction in inflammatory lesion counts with active and 40% with vehicle, based on historical data from a prior study with metronidazole cream 0.75% versus vehicle; 64 participants were required in each treatment group to detect this effect using a 2-sided t test (&#945;=.017). Pairwise comparisons (clindamycin vs respective vehicle) were performed using the Cochran-Mantel-Haenszel test for combined lesion count percentage change.

Results

Participant Disposition and Baseline Characteristics

Overall, a total of 629 participants were randomized across both studies. In study A, a total of 416 participants were randomized into 5 treatment arms, with 369 participants (88.7%) completing the study; 47 (11.3%) participants discontinued study A, mainly due to participant request (19/47 [40.4%]) or lost to follow-up (11/47 [23.4%]). In study B, a total of 213 participants were randomized to receive either clindamycin gel 1% (n=109 [51.2%]) twice daily or vehicle gel (n=104 [48.8%]) twice daily, with 193 participants (90.6%) completing the study; 20 (9.4%) participants discontinued study B, mainly due to participant request (6/20 [30%]) or lost to follow-up (4/20 [20%]). Participants in studies A and B were similar in demographics and baseline disease characteristics (Table). The majority of participants were white females. 

Efficacy

No statistically significant difference was observed in all pairwise comparisons (clindamycin cream twice daily vs vehicle twice daily, clindamycin cream once daily vs vehicle once daily, clindamycin gel vs vehicle gel) for the primary end point of mean percentage change from baseline in inflammatory lesion counts at week 12 (Figure 1; P>.5 for all pairwise comparisons). 

At week 12, the proportion of participants in study B deemed as a success (none/clear or mild/almost clear [investigator global rosacea severity score of 0 or 1]) in the clindamycin gel 1% and vehicle gel groups were 45% versus 38%, respectively (P=.347) (Figure 2). 

For the secondary end point of mean investigator global rosacea severity assessment at week 12 (study A), there were no significant differences between the active and vehicle control groups (P>.5 for all pairwise comparisons)(Figure 3). Also, the proportion of participants with at least a moderate investigator global improvement assessment from baseline to week 12 ranged from 45% for clindamycin cream 1% twice daily to 56% for clindamycin cream 0.3% cream once daily and from 45% for vehicle cream once daily to 51% for vehicle cream twice daily (P>.5 for all pairwise comparisons).

There were no significant differences in the mean total erythema severity scores at week 12 for clindamycin cream 1% twice daily versus vehicle cream twice daily (6.3 vs 6.0; P>.5), clindamycin cream 1% once daily versus vehicle cream once daily (6.2 vs 6.0; P>.5), clindamycin cream 0.3% once daily versus vehicle cream once daily (5.9 vs 6.0; P>.5), and clindamycin gel 1% twice daily versus vehicle gel twice daily (6.7 vs 6.2; P>.5). 

There were no relevant differences between any of the clindamycin cream groups and their respective vehicle group at week 12 for skin irritation, including desquamation, edema, dryness, pruritus, and stinging/burning.

Safety

In study A, the majority of AEs in all 5 treatment arms were nondermatologic, mild in intensity, and not considered to be related to the study treatment by the investigator. Overall, 12 participants had AEs considered by the investigator as possibly or probably related to the study treatment: 4.9% in the clindamycin cream 1% twice daily group, 4.6% in the clindamycin cream 1% once daily group, 3.7% in the vehicle cream twice daily group, 1.2% in the clindamycin cream 0.3% once daily group, and 0% in the vehicle cream once daily group. Two treatment-related AEs led to treatment discontinuation, including dermatitis in 1 participant from the clindamycin cream 1% once daily group and contact dermatitis in 1 participant from the clindamycin cream 1% twice daily group.

Comment

No evidence of increased efficacy over the respective vehicles was observed with clindamycin cream or gel, whatever the regimen, in the treatment of rosacea patients in either of these well-designed and well-powered, blinded studies. Slight improvements in the various efficacy criteria were observed, even in the vehicle groups, highlighting the importance of using a good basic skin care regimen in the management of rosacea.⁹ In contrast to our observations of lack of efficacy in the treatment of rosacea, clinical efficacy of clindamycin has been demonstrated in acne,^10-12 albeit with low efficacy for clindamycin monotherapy.¹³ It is noteworthy that oral or topical antibiotics are no longer recommended as monotherapy for acne to prevent and minimize antibiotic resistance and to preserve the therapeutic value of antibiotics.¹⁴

Acne and rosacea are both chronic inflammatory disorders of the skin associated with papules and pustules, and they share some common inflammatory patterns.^15-19 Furthermore, the intrinsic anti-inflammatory activity of clindamycin in addition to its antibiotic effects has been suggested by some authors as the main reason for treating acne with clindamycin.²⁰ However, the relative contributions of antibacterial and/or anti-inflammatory properties remain to be fully elucidated, and evidence for direct anti-inflammatory effects of clindamycin remains heterogeneous.^21,22 Several pathophysiological factors have been implicated in acne, including hormonal effects, abnormal keratinocyte function, increased sebum production, and microbial components (eg, hypercolonization of the skin follicles by Propionibacterium acnes).^23,24 The antibiotic activity of clindamycin against P acnes may be the key factor responsible for the clinical effects in acne.^25,26 Although clindamycin may have anti-inflammatory effects in acne via a different inflammatory pathway not shared by rosacea, a purely antibiotic mechanism of action of clindamycin also could explain why we observed no evidence of efficacy in the treatment of rosacea, as no causative bacterial component has been clearly demonstrated in rosacea.²⁷

Conclusion

In these studies, clindamycin cream 0.3% once daily, clindamycin cream 1% once or twice daily, and clindamycin gel 1% twice daily were all well tolerated; however, they were no more effective than the vehicles in the treatment of moderate to severe rosacea.  

Acknowledgment

The authors would like to thank Helen Simpson, PhD, of Galderma R&D (Sophia Antipolis, France), for editorial and medical writing assistance.

Rosacea is a chronic inflammatory skin disease characterized by central facial erythema with or without intermittent papules and pustules (described as the inflammatory lesions of rosacea). Although twice-daily clindamycin 1% solution or gel has been used in the treatment of acne, few studies have investigated the use of clindamycin in rosacea.^1,2 In one study comparing twice-daily clindamycin lotion 1% with oral tetracycline in 43 rosacea patients, clindamycin was found to be superior in the eradication of pustules.³ A combination therapy of clindamycin 1% and benzoyl peroxide 5% was found to be more effective than the vehicle in inflammatory lesions and erythema of rosacea in a 12-week randomized controlled trial; however, a definitive advantage over US Food and Drug Administration-approved topical agents used to treat papulopustular rosacea was not established.^4,5 Two further studies evaluated clindamycin phosphate 1.2%-tretinoin 0.025% combination gel in the treatment of rosacea, but only 1 showed any effect on papulopustular lesions.^6-8 The objective of the studies reported here was to evaluate the efficacy and safety of clindamycin in the treatment of patients with moderate to severe rosacea.

Methods

Study Design

Two multicenter (study A, 20 centers; study B, 10 centers), randomized, investigator-blinded, vehicle-controlled studies were conducted in the United States between 1999 and 2002 in accordance with the Declaration of Helsinki, International Conference on Harmonisation Good Clinical Practice guidelines, and local regulatory requirements. The studies were reviewed and approved by the respective institutional review boards, and all participants provided written informed consent.

In study A, moderate to severe rosacea patients with erythema, telangiectasia, and at least 8 inflammatory lesions were randomized to receive clindamycin cream 1% or vehicle cream once (in the evening) or twice daily (in the morning and evening) or clindamycin cream 0.3% once daily (in the evening) for 12 weeks (1:1:1:1:1 ratio). All study treatments were supplied in identical tubes with blinded labels.

In study B, patients with moderate to severe rosacea and at least 8 inflammatory lesions were randomized in a 1:1 ratio with instructions to apply clindamycin gel 1% or vehicle gel to the affected areas twice daily (morning and evening) for 12 weeks.

Efficacy Evaluation

Evaluations were performed at baseline and weeks 2, 4, 8, and 12 on the intention-to-treat population with the last observation carried forward.

Efficacy assessments in both studies included inflammatory lesion counts (papules and pustules) of 5 facial regions--forehead, chin, nose, right cheek, left cheek--counted separately and then combined to give the total inflammatory lesion count (both studies), as well as improvement in the investigator global rosacea severity score (0=none/clear; 1=mild, detectable erythema with ≤7 papules/pustules; 2=moderate, prominent erythema with ≥8 papules/pustules; 3=severe, intense erythema with ≥10 to <50 papules/pustules; 3.5 [study A] or 4 [study B]=very severe, intense erythema with >50 papules/pustules). In study B, the proportion of participants dichotomized to success (a score of 0 [none/clear] or 1 [mild/almost clear]) or failure (a score of ≥2) on the 5-point investigator global rosacea severity scale at week 12 was evaluated. In study A, investigator global improvement assessment at week 12, based on photographs taken at baseline, was graded on a 7-point scale (from -1 [worse], 0 [no change], and 1 [minimal improvement] to 5 [clear]). In both studies, erythema severity was graded on a 7-point scale in increments of 0.5 (from 0=no erythema to 3.5=very severe redness, very intense redness). Skin irritation also was graded as none, mild, moderate, or severe. 

Safety Evaluation

Safety was assessed by the incidence of adverse events (AEs).

Statistical Analysis

Studies were powered assuming 60% reduction in inflammatory lesion counts with active and 40% with vehicle, based on historical data from a prior study with metronidazole cream 0.75% versus vehicle; 64 participants were required in each treatment group to detect this effect using a 2-sided t test (&#945;=.017). Pairwise comparisons (clindamycin vs respective vehicle) were performed using the Cochran-Mantel-Haenszel test for combined lesion count percentage change.

Results

Participant Disposition and Baseline Characteristics

Overall, a total of 629 participants were randomized across both studies. In study A, a total of 416 participants were randomized into 5 treatment arms, with 369 participants (88.7%) completing the study; 47 (11.3%) participants discontinued study A, mainly due to participant request (19/47 [40.4%]) or lost to follow-up (11/47 [23.4%]). In study B, a total of 213 participants were randomized to receive either clindamycin gel 1% (n=109 [51.2%]) twice daily or vehicle gel (n=104 [48.8%]) twice daily, with 193 participants (90.6%) completing the study; 20 (9.4%) participants discontinued study B, mainly due to participant request (6/20 [30%]) or lost to follow-up (4/20 [20%]). Participants in studies A and B were similar in demographics and baseline disease characteristics (Table). The majority of participants were white females. 

Efficacy

No statistically significant difference was observed in all pairwise comparisons (clindamycin cream twice daily vs vehicle twice daily, clindamycin cream once daily vs vehicle once daily, clindamycin gel vs vehicle gel) for the primary end point of mean percentage change from baseline in inflammatory lesion counts at week 12 (Figure 1; P>.5 for all pairwise comparisons). 

At week 12, the proportion of participants in study B deemed as a success (none/clear or mild/almost clear [investigator global rosacea severity score of 0 or 1]) in the clindamycin gel 1% and vehicle gel groups were 45% versus 38%, respectively (P=.347) (Figure 2). 

For the secondary end point of mean investigator global rosacea severity assessment at week 12 (study A), there were no significant differences between the active and vehicle control groups (P>.5 for all pairwise comparisons)(Figure 3). Also, the proportion of participants with at least a moderate investigator global improvement assessment from baseline to week 12 ranged from 45% for clindamycin cream 1% twice daily to 56% for clindamycin cream 0.3% cream once daily and from 45% for vehicle cream once daily to 51% for vehicle cream twice daily (P>.5 for all pairwise comparisons).

There were no significant differences in the mean total erythema severity scores at week 12 for clindamycin cream 1% twice daily versus vehicle cream twice daily (6.3 vs 6.0; P>.5), clindamycin cream 1% once daily versus vehicle cream once daily (6.2 vs 6.0; P>.5), clindamycin cream 0.3% once daily versus vehicle cream once daily (5.9 vs 6.0; P>.5), and clindamycin gel 1% twice daily versus vehicle gel twice daily (6.7 vs 6.2; P>.5). 

There were no relevant differences between any of the clindamycin cream groups and their respective vehicle group at week 12 for skin irritation, including desquamation, edema, dryness, pruritus, and stinging/burning.

Safety

In study A, the majority of AEs in all 5 treatment arms were nondermatologic, mild in intensity, and not considered to be related to the study treatment by the investigator. Overall, 12 participants had AEs considered by the investigator as possibly or probably related to the study treatment: 4.9% in the clindamycin cream 1% twice daily group, 4.6% in the clindamycin cream 1% once daily group, 3.7% in the vehicle cream twice daily group, 1.2% in the clindamycin cream 0.3% once daily group, and 0% in the vehicle cream once daily group. Two treatment-related AEs led to treatment discontinuation, including dermatitis in 1 participant from the clindamycin cream 1% once daily group and contact dermatitis in 1 participant from the clindamycin cream 1% twice daily group.

Comment

No evidence of increased efficacy over the respective vehicles was observed with clindamycin cream or gel, whatever the regimen, in the treatment of rosacea patients in either of these well-designed and well-powered, blinded studies. Slight improvements in the various efficacy criteria were observed, even in the vehicle groups, highlighting the importance of using a good basic skin care regimen in the management of rosacea.⁹ In contrast to our observations of lack of efficacy in the treatment of rosacea, clinical efficacy of clindamycin has been demonstrated in acne,^10-12 albeit with low efficacy for clindamycin monotherapy.¹³ It is noteworthy that oral or topical antibiotics are no longer recommended as monotherapy for acne to prevent and minimize antibiotic resistance and to preserve the therapeutic value of antibiotics.¹⁴

Acne and rosacea are both chronic inflammatory disorders of the skin associated with papules and pustules, and they share some common inflammatory patterns.^15-19 Furthermore, the intrinsic anti-inflammatory activity of clindamycin in addition to its antibiotic effects has been suggested by some authors as the main reason for treating acne with clindamycin.²⁰ However, the relative contributions of antibacterial and/or anti-inflammatory properties remain to be fully elucidated, and evidence for direct anti-inflammatory effects of clindamycin remains heterogeneous.^21,22 Several pathophysiological factors have been implicated in acne, including hormonal effects, abnormal keratinocyte function, increased sebum production, and microbial components (eg, hypercolonization of the skin follicles by Propionibacterium acnes).^23,24 The antibiotic activity of clindamycin against P acnes may be the key factor responsible for the clinical effects in acne.^25,26 Although clindamycin may have anti-inflammatory effects in acne via a different inflammatory pathway not shared by rosacea, a purely antibiotic mechanism of action of clindamycin also could explain why we observed no evidence of efficacy in the treatment of rosacea, as no causative bacterial component has been clearly demonstrated in rosacea.²⁷

Conclusion

In these studies, clindamycin cream 0.3% once daily, clindamycin cream 1% once or twice daily, and clindamycin gel 1% twice daily were all well tolerated; however, they were no more effective than the vehicles in the treatment of moderate to severe rosacea.  

Acknowledgment

The authors would like to thank Helen Simpson, PhD, of Galderma R&D (Sophia Antipolis, France), for editorial and medical writing assistance.

Rosacea is a chronic inflammatory skin disease characterized by central facial erythema with or without intermittent papules and pustules (described as the inflammatory lesions of rosacea). Although twice-daily clindamycin 1% solution or gel has been used in the treatment of acne, few studies have investigated the use of clindamycin in rosacea.^1,2 In one study comparing twice-daily clindamycin lotion 1% with oral tetracycline in 43 rosacea patients, clindamycin was found to be superior in the eradication of pustules.³ A combination therapy of clindamycin 1% and benzoyl peroxide 5% was found to be more effective than the vehicle in inflammatory lesions and erythema of rosacea in a 12-week randomized controlled trial; however, a definitive advantage over US Food and Drug Administration-approved topical agents used to treat papulopustular rosacea was not established.^4,5 Two further studies evaluated clindamycin phosphate 1.2%-tretinoin 0.025% combination gel in the treatment of rosacea, but only 1 showed any effect on papulopustular lesions.^6-8 The objective of the studies reported here was to evaluate the efficacy and safety of clindamycin in the treatment of patients with moderate to severe rosacea.

Methods

Study Design

Two multicenter (study A, 20 centers; study B, 10 centers), randomized, investigator-blinded, vehicle-controlled studies were conducted in the United States between 1999 and 2002 in accordance with the Declaration of Helsinki, International Conference on Harmonisation Good Clinical Practice guidelines, and local regulatory requirements. The studies were reviewed and approved by the respective institutional review boards, and all participants provided written informed consent.

In study A, moderate to severe rosacea patients with erythema, telangiectasia, and at least 8 inflammatory lesions were randomized to receive clindamycin cream 1% or vehicle cream once (in the evening) or twice daily (in the morning and evening) or clindamycin cream 0.3% once daily (in the evening) for 12 weeks (1:1:1:1:1 ratio). All study treatments were supplied in identical tubes with blinded labels.

In study B, patients with moderate to severe rosacea and at least 8 inflammatory lesions were randomized in a 1:1 ratio with instructions to apply clindamycin gel 1% or vehicle gel to the affected areas twice daily (morning and evening) for 12 weeks.

Efficacy Evaluation

Evaluations were performed at baseline and weeks 2, 4, 8, and 12 on the intention-to-treat population with the last observation carried forward.

Efficacy assessments in both studies included inflammatory lesion counts (papules and pustules) of 5 facial regions--forehead, chin, nose, right cheek, left cheek--counted separately and then combined to give the total inflammatory lesion count (both studies), as well as improvement in the investigator global rosacea severity score (0=none/clear; 1=mild, detectable erythema with ≤7 papules/pustules; 2=moderate, prominent erythema with ≥8 papules/pustules; 3=severe, intense erythema with ≥10 to <50 papules/pustules; 3.5 [study A] or 4 [study B]=very severe, intense erythema with >50 papules/pustules). In study B, the proportion of participants dichotomized to success (a score of 0 [none/clear] or 1 [mild/almost clear]) or failure (a score of ≥2) on the 5-point investigator global rosacea severity scale at week 12 was evaluated. In study A, investigator global improvement assessment at week 12, based on photographs taken at baseline, was graded on a 7-point scale (from -1 [worse], 0 [no change], and 1 [minimal improvement] to 5 [clear]). In both studies, erythema severity was graded on a 7-point scale in increments of 0.5 (from 0=no erythema to 3.5=very severe redness, very intense redness). Skin irritation also was graded as none, mild, moderate, or severe. 

Safety Evaluation

Safety was assessed by the incidence of adverse events (AEs).

Statistical Analysis

Studies were powered assuming 60% reduction in inflammatory lesion counts with active and 40% with vehicle, based on historical data from a prior study with metronidazole cream 0.75% versus vehicle; 64 participants were required in each treatment group to detect this effect using a 2-sided t test (&#945;=.017). Pairwise comparisons (clindamycin vs respective vehicle) were performed using the Cochran-Mantel-Haenszel test for combined lesion count percentage change.

Results

Participant Disposition and Baseline Characteristics

Overall, a total of 629 participants were randomized across both studies. In study A, a total of 416 participants were randomized into 5 treatment arms, with 369 participants (88.7%) completing the study; 47 (11.3%) participants discontinued study A, mainly due to participant request (19/47 [40.4%]) or lost to follow-up (11/47 [23.4%]). In study B, a total of 213 participants were randomized to receive either clindamycin gel 1% (n=109 [51.2%]) twice daily or vehicle gel (n=104 [48.8%]) twice daily, with 193 participants (90.6%) completing the study; 20 (9.4%) participants discontinued study B, mainly due to participant request (6/20 [30%]) or lost to follow-up (4/20 [20%]). Participants in studies A and B were similar in demographics and baseline disease characteristics (Table). The majority of participants were white females. 

Efficacy

No statistically significant difference was observed in all pairwise comparisons (clindamycin cream twice daily vs vehicle twice daily, clindamycin cream once daily vs vehicle once daily, clindamycin gel vs vehicle gel) for the primary end point of mean percentage change from baseline in inflammatory lesion counts at week 12 (Figure 1; P>.5 for all pairwise comparisons). 

At week 12, the proportion of participants in study B deemed as a success (none/clear or mild/almost clear [investigator global rosacea severity score of 0 or 1]) in the clindamycin gel 1% and vehicle gel groups were 45% versus 38%, respectively (P=.347) (Figure 2). 

For the secondary end point of mean investigator global rosacea severity assessment at week 12 (study A), there were no significant differences between the active and vehicle control groups (P>.5 for all pairwise comparisons)(Figure 3). Also, the proportion of participants with at least a moderate investigator global improvement assessment from baseline to week 12 ranged from 45% for clindamycin cream 1% twice daily to 56% for clindamycin cream 0.3% cream once daily and from 45% for vehicle cream once daily to 51% for vehicle cream twice daily (P>.5 for all pairwise comparisons).

There were no significant differences in the mean total erythema severity scores at week 12 for clindamycin cream 1% twice daily versus vehicle cream twice daily (6.3 vs 6.0; P>.5), clindamycin cream 1% once daily versus vehicle cream once daily (6.2 vs 6.0; P>.5), clindamycin cream 0.3% once daily versus vehicle cream once daily (5.9 vs 6.0; P>.5), and clindamycin gel 1% twice daily versus vehicle gel twice daily (6.7 vs 6.2; P>.5). 

There were no relevant differences between any of the clindamycin cream groups and their respective vehicle group at week 12 for skin irritation, including desquamation, edema, dryness, pruritus, and stinging/burning.

Safety

In study A, the majority of AEs in all 5 treatment arms were nondermatologic, mild in intensity, and not considered to be related to the study treatment by the investigator. Overall, 12 participants had AEs considered by the investigator as possibly or probably related to the study treatment: 4.9% in the clindamycin cream 1% twice daily group, 4.6% in the clindamycin cream 1% once daily group, 3.7% in the vehicle cream twice daily group, 1.2% in the clindamycin cream 0.3% once daily group, and 0% in the vehicle cream once daily group. Two treatment-related AEs led to treatment discontinuation, including dermatitis in 1 participant from the clindamycin cream 1% once daily group and contact dermatitis in 1 participant from the clindamycin cream 1% twice daily group.

Comment

No evidence of increased efficacy over the respective vehicles was observed with clindamycin cream or gel, whatever the regimen, in the treatment of rosacea patients in either of these well-designed and well-powered, blinded studies. Slight improvements in the various efficacy criteria were observed, even in the vehicle groups, highlighting the importance of using a good basic skin care regimen in the management of rosacea.⁹ In contrast to our observations of lack of efficacy in the treatment of rosacea, clinical efficacy of clindamycin has been demonstrated in acne,^10-12 albeit with low efficacy for clindamycin monotherapy.¹³ It is noteworthy that oral or topical antibiotics are no longer recommended as monotherapy for acne to prevent and minimize antibiotic resistance and to preserve the therapeutic value of antibiotics.¹⁴

Acne and rosacea are both chronic inflammatory disorders of the skin associated with papules and pustules, and they share some common inflammatory patterns.^15-19 Furthermore, the intrinsic anti-inflammatory activity of clindamycin in addition to its antibiotic effects has been suggested by some authors as the main reason for treating acne with clindamycin.²⁰ However, the relative contributions of antibacterial and/or anti-inflammatory properties remain to be fully elucidated, and evidence for direct anti-inflammatory effects of clindamycin remains heterogeneous.^21,22 Several pathophysiological factors have been implicated in acne, including hormonal effects, abnormal keratinocyte function, increased sebum production, and microbial components (eg, hypercolonization of the skin follicles by Propionibacterium acnes).^23,24 The antibiotic activity of clindamycin against P acnes may be the key factor responsible for the clinical effects in acne.^25,26 Although clindamycin may have anti-inflammatory effects in acne via a different inflammatory pathway not shared by rosacea, a purely antibiotic mechanism of action of clindamycin also could explain why we observed no evidence of efficacy in the treatment of rosacea, as no causative bacterial component has been clearly demonstrated in rosacea.²⁷

Conclusion

In these studies, clindamycin cream 0.3% once daily, clindamycin cream 1% once or twice daily, and clindamycin gel 1% twice daily were all well tolerated; however, they were no more effective than the vehicles in the treatment of moderate to severe rosacea.  

Acknowledgment

The authors would like to thank Helen Simpson, PhD, of Galderma R&D (Sophia Antipolis, France), for editorial and medical writing assistance.

To improve patient care and outcomes, leading dermatologists offered their recommendations on redness-reducing products. Consideration must be given to:

• Avène Antirougeurs FORT Relief Concentrate
  Pierre Fabre Dermo-Cosmetique USA
  “This formula has medical-grade ruscus extract to support microcirculation and soothe skin reactivity and redness, as well as soothing Avène Thermal Spring Water.” — Jeannette Graf, MD, New York, New York
   
• Eucerin Redness Relief
  Beiersdorf Inc
  “Eucerin’s Redness Relief product line has worked well for some of my patients.” — Gary Goldenberg, MD, New York, New York
   
• Redness Solutions Daily Protective Base Broad Spectrum SPF 15
  Clinique Laboratories, LLC
  “This oil-free makeup primer has a sheer green tint that camouflages redness while also protecting from UV rays.” — Shari Lipner, MD, PhD, New York, New York

Cutis invites readers to send us their recommendations. Athlete’s foot treatments, cleansing devices, and men’s products will be featured in upcoming editions of Cosmetic Corner. Please email your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

To improve patient care and outcomes, leading dermatologists offered their recommendations on redness-reducing products. Consideration must be given to:

• Avène Antirougeurs FORT Relief Concentrate
  Pierre Fabre Dermo-Cosmetique USA
  “This formula has medical-grade ruscus extract to support microcirculation and soothe skin reactivity and redness, as well as soothing Avène Thermal Spring Water.” — Jeannette Graf, MD, New York, New York
   
• Eucerin Redness Relief
  Beiersdorf Inc
  “Eucerin’s Redness Relief product line has worked well for some of my patients.” — Gary Goldenberg, MD, New York, New York
   
• Redness Solutions Daily Protective Base Broad Spectrum SPF 15
  Clinique Laboratories, LLC
  “This oil-free makeup primer has a sheer green tint that camouflages redness while also protecting from UV rays.” — Shari Lipner, MD, PhD, New York, New York

Cutis invites readers to send us their recommendations. Athlete’s foot treatments, cleansing devices, and men’s products will be featured in upcoming editions of Cosmetic Corner. Please email your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

To improve patient care and outcomes, leading dermatologists offered their recommendations on redness-reducing products. Consideration must be given to:

• Avène Antirougeurs FORT Relief Concentrate
  Pierre Fabre Dermo-Cosmetique USA
  “This formula has medical-grade ruscus extract to support microcirculation and soothe skin reactivity and redness, as well as soothing Avène Thermal Spring Water.” — Jeannette Graf, MD, New York, New York
   
• Eucerin Redness Relief
  Beiersdorf Inc
  “Eucerin’s Redness Relief product line has worked well for some of my patients.” — Gary Goldenberg, MD, New York, New York
   
• Redness Solutions Daily Protective Base Broad Spectrum SPF 15
  Clinique Laboratories, LLC
  “This oil-free makeup primer has a sheer green tint that camouflages redness while also protecting from UV rays.” — Shari Lipner, MD, PhD, New York, New York

Cutis invites readers to send us their recommendations. Athlete’s foot treatments, cleansing devices, and men’s products will be featured in upcoming editions of Cosmetic Corner. Please email your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

Glytone Sunscreen Lotion Broad Spectrum SPF 40

Pierre Fabre Dermo-Cosmetique USA introduces Glytone Sunscreen Lotion Broad Spectrum SPF 40, a mineral-based formula for face and body with micronized zinc oxide, octinoxate, and octisalate. The lightweight formula is water resistant for up to 40 minutes and contains hyaluronic acid to nourish the skin and help boost natural moisture levels to visibly reduce the appearance of fine lines and wrinkles. For more information, visit www.glytone-usa.com.

proactivMD

The Proactiv Company launches the proactivMD Essentials System, a 3-step acne regimen that has been reformulated to include the topical retinoid adapalene. Step 1 is the Deep Cleansing Face Wash formulated to help clear dirt and debris from deep within the pores. Step 2 is the Balancing Toner, an alcohol-free formula that contains a light astringent to sweep away impurities leaving the skin feeling fresh and balanced. Step 3 consists of the Daily Oil Control Moisturizer (morning), which protects the skin and controls shine, and Adapalene Gel 0.1% (evening) to speed acne healing and prevent new acne from forming. For more information, visit www.proactiv.com.

If you would like your product included in Product News, please email a press release to the Editorial Office at [email protected].

Glytone Sunscreen Lotion Broad Spectrum SPF 40

Pierre Fabre Dermo-Cosmetique USA introduces Glytone Sunscreen Lotion Broad Spectrum SPF 40, a mineral-based formula for face and body with micronized zinc oxide, octinoxate, and octisalate. The lightweight formula is water resistant for up to 40 minutes and contains hyaluronic acid to nourish the skin and help boost natural moisture levels to visibly reduce the appearance of fine lines and wrinkles. For more information, visit www.glytone-usa.com.

proactivMD

The Proactiv Company launches the proactivMD Essentials System, a 3-step acne regimen that has been reformulated to include the topical retinoid adapalene. Step 1 is the Deep Cleansing Face Wash formulated to help clear dirt and debris from deep within the pores. Step 2 is the Balancing Toner, an alcohol-free formula that contains a light astringent to sweep away impurities leaving the skin feeling fresh and balanced. Step 3 consists of the Daily Oil Control Moisturizer (morning), which protects the skin and controls shine, and Adapalene Gel 0.1% (evening) to speed acne healing and prevent new acne from forming. For more information, visit www.proactiv.com.

If you would like your product included in Product News, please email a press release to the Editorial Office at [email protected].

Glytone Sunscreen Lotion Broad Spectrum SPF 40

Pierre Fabre Dermo-Cosmetique USA introduces Glytone Sunscreen Lotion Broad Spectrum SPF 40, a mineral-based formula for face and body with micronized zinc oxide, octinoxate, and octisalate. The lightweight formula is water resistant for up to 40 minutes and contains hyaluronic acid to nourish the skin and help boost natural moisture levels to visibly reduce the appearance of fine lines and wrinkles. For more information, visit www.glytone-usa.com.

proactivMD

The Proactiv Company launches the proactivMD Essentials System, a 3-step acne regimen that has been reformulated to include the topical retinoid adapalene. Step 1 is the Deep Cleansing Face Wash formulated to help clear dirt and debris from deep within the pores. Step 2 is the Balancing Toner, an alcohol-free formula that contains a light astringent to sweep away impurities leaving the skin feeling fresh and balanced. Step 3 consists of the Daily Oil Control Moisturizer (morning), which protects the skin and controls shine, and Adapalene Gel 0.1% (evening) to speed acne healing and prevent new acne from forming. For more information, visit www.proactiv.com.

If you would like your product included in Product News, please email a press release to the Editorial Office at [email protected].

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

Seborrheic Dermatitis

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

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

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

Acquired Trichorrhexis Nodosa

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

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

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

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

Acne Keloidalis Nuchae

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

Pseudofolliculitis Barbae

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

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

Alopecia

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

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

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

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

Tinea Capitis in Black Pediatric Patients

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

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

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

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

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

Hair Growth

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

Conclusion

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

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

Seborrheic Dermatitis

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

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

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

Acquired Trichorrhexis Nodosa

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

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

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

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

Acne Keloidalis Nuchae

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

Pseudofolliculitis Barbae

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

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

Alopecia

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

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

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

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

Tinea Capitis in Black Pediatric Patients

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

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

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

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

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

Hair Growth

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

Conclusion

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

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

Seborrheic Dermatitis

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

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

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

Acquired Trichorrhexis Nodosa

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

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

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

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

Acne Keloidalis Nuchae

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

Pseudofolliculitis Barbae

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

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

Alopecia

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

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

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

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

Tinea Capitis in Black Pediatric Patients

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

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

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

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

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

Hair Growth

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

Conclusion

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

Hypertrophic scarring secondary to trauma, burns, and surgical interventions is a major source of morbidity worldwide and often is mechanically, aesthetically, and symptomatically debilitating. Modern advances in acute trauma care protocols have resulted in survival rates greater than 90% in both civilian and military populations.^1,2 Patients with wounds that have historically proven fatal are now surviving and are confronted with the long-term sequelae of their injuries. With more than 52,000 service members injured in military engagements from 2001 to 2015 and 8.5 million civilians presenting annually with injury patterns at risk for hypertrophic scarring, it is paramount that we ensure access to safe and effective long-term scar care.^2,3

At its simplest level, hypertrophic scarring is believed to result from a disequilibrium between collagen production and degradation. This failure to properly transition through the stages of wound healing results in bothersome symptoms, a disfigured appearance, and mechanical dysfunction of the skin (Figure, A). Decreased elasticity and extensibility, increased dermal thickness, and scar contractures impair patient range of motion and functional mobility. Those affected commonly experience varying degrees of pruritus and dysesthesia along the scar. Combined with aesthetic variations in pigmentation, erythema, texture, and thickness, hypertrophic scarring often leads to long-term psychosocial impairment and decreased health-related quality of life.⁴

Treatment Approach

Treatment of hypertrophic scars requires a multimodal approach due to the spectrum of associated concerns and the natural recalcitrance of the scar to therapy. Protocols should be tailored to the individual but generally begin with tissue-conserving surgical interventions followed by selective photothermolysis of the scar vasculature. Subsequently, deep and superficial ablative fractional laser (AFL) treatment and local pharmacotherapy also are employed. Treatment can be accomplished in the outpatient setting under local anesthesia in a serial fashion. In the authors’ experience, these therapies behave in a synergistic fashion, achieving outcomes that far exceed the sum of their parts, often obviating the need for scar excision in the majority of cases (Figure, B).

Tissue-Conserving Surgical Intervention

Z-plasty is an indispensable surgical tool due to its ability to lengthen scars and reduce wound tension. Treatment is easily customizable to the patient and can be performed using the individual or multiple Z-plasty techniques. Undermining and step-off correction while suturing allow the physician to lower raised scars, elevate depressed scars, and obscure scar presence by minimizing the straight lines that draw the eye to the scar. Z-plasties rely on the creation and transposition of 2 triangular flaps and permit a 75% increase in length along the desired tension vector. As such, Z-plasties decrease wound tension and facilitate scar maturation.

Selective Photothermolysis of the Vasculature

Although there are several devices available to treat vascular and immature hypertrophic scars, the majority of studies have been conducted with the 595-nm pulsed dye laser. By preferentially heating oxyhemoglobin within the dermal microvasculature, the pulsed dye laser irreparably injures the vascular endothelium. The subsequent tissue hypoxia and collagen fiber heating results in collagen fiber realignment, normalization of collagen subtypes, and neocollagenesis.⁵ Pulsed dye laser therapy most effectively reduces erythema and pruritus; however, improvements in scar volume, pliability, and elasticity also have been reported.⁵ When targeting the fine vasculature of the scar, thermal confinement is critical to prevent injury to the surrounding dermis. As such, pulse widths of 0.45 to 1.5 milliseconds are routinely utilized with a fluence just sufficient to elicit transient purpura lasting 3 to 5 seconds. Employing a spot size of 7 to 10 mm, typical fluences range from 4.5 to 6.5 J/cm². Engagement of the dynamic cooling device reduces the risk for complications, allowing the patient to proceed to the next step in their therapy regimen: the AFL.

Ablative Fractional Laser

The AFL creates a pixilated pattern of injury throughout the epidermis and dermis of the treatment area. Ablative fractional laser platforms include the 10,600-nm CO₂ and 2940-nm erbium-doped YAG lasers, both targeting intracellular water. The AFL vaporizes columns of tissue, leaving minute vertical channels with narrow rims of protein coagulation referred to as microscopic treatment zones (MTZs).⁶ Scar collagen analysis after AFL treatment has shown a profile resembling unaffected skin.⁷ Consistently, patients report improvements in stiffness, range of motion, pain, pruritus, pigmentation, and erythema.Physician observers also have reported similar improvements in these end points.^8,9 Recently, interim data from a prospective controlled trial were presented showing objective improvements in dermal thickness, elasticity, and extensibility after 3 treatments with the CO₂ AFL.⁶ The UltraPulse CO₂ laser (Lumenis) is the most well-studied and widely available AFL for scar therapy and as such we will outline common treatment parameters with this device. Of note, treatment end points may be generalized to any AFL.

The DeepFX UltraPulse configuration is utilized to achieve deep AFL therapy and has a fixed pulse width of 0.8 milliseconds, slightly less than the thermal relaxation time of the skin. The diameter of the MTZs is 120 µm, and MTZ density for scar treatment ranges from 1% to 10% with a goal depth of at least 80% of scar thickness. Maximal penetration of the AFL is 4 mm, which is directly proportional to fluence. The goal of deep AFL is the removal of scar tissue to facilitate remodeling and neocollagenesis. Superficial fractional ablation can then be achieved utilizing the ActiveFX UltraPulse configuration generating a 1.3-mm MTZ spot size. We commonly use a treatment level of 3 (82% density). Typical treatment energy ranges from 80 to 125 mJ, which correlates with depths of approximately 50 to 115 µm. With both configurations, the size and shape of the treatment area can be customized to the scar. In addition, frequency may be adjusted to control the speed of treatment while balancing the risk of bulk heating. The goal of superficial AFL is to minimize scar surface irregularities and ensure blending of deep AFL treatment. Once AFL treatment is complete, local pharmacotherapy can then be employed.

Pharmacotherapy

Intralesional corticosteroids have long represented the standard of care for hypertrophic scars, with concentrations between 2.5 and 40 mg/mL that are titrated to scar thickness and location to avoid unwanted atrophy. Visual blanching of the scar represents the clinical end point for treatment. Corticosteroids act by inhibiting fibroblast proliferation and enhancing collagen degradation.¹⁰ 5-Fluorouracil (5-FU) also is used in scar management. In addition to inhibiting fibroblast proliferation and inducing fibroblast apoptosis, 5-FU inhibits myofibroblast proliferation, which is helpful in the prevention and treatment of scar contracture.¹¹ As monotherapy, weekly injections with 1 to 3 mL of 50 mg/mL 5-FU has been safe and effective. Combination intralesional corticosteroid and 5-FU therapy has been reported and is associated with improved scar regression, reduced reoccurrence, and fewer side effects.¹¹ In our experience, a 1:1 suspension is effective with appropriate titration of the corticosteroid component. Although less well defined, topical application of pharmacotherapy and massage to the newly created MTZs appears beneficial and offers another option for delivery of corticosteroids and 5-FU, in addition to a number of promising medications such as bimatoprost, poly-L-lactic acid, timolol, and rapamycin.¹²

Conclusion

Advances in laser surgery and our understanding of wound healing have created a paradigm shift in the treatment approach to trauma and burn scars. In lieu of extensive scar excisions, the summarized multimodal regimen emphasizing tissue conservation and autologous remodeling is gaining favor in the military, academic medical centers, and scar centers of excellence, but patients are finding local access to care difficult. Dermatologists are uniquely positioned to cost-effectively deliver this care in the outpatient setting utilizing devices and techniques they already possess. With the end goal of optimization of functional, symptomatic, and aesthetic state of the patient, it is critical that dermatologists seize this opportunity to truly make a difference for the military and civilian patients that need it most.

Hypertrophic scarring secondary to trauma, burns, and surgical interventions is a major source of morbidity worldwide and often is mechanically, aesthetically, and symptomatically debilitating. Modern advances in acute trauma care protocols have resulted in survival rates greater than 90% in both civilian and military populations.^1,2 Patients with wounds that have historically proven fatal are now surviving and are confronted with the long-term sequelae of their injuries. With more than 52,000 service members injured in military engagements from 2001 to 2015 and 8.5 million civilians presenting annually with injury patterns at risk for hypertrophic scarring, it is paramount that we ensure access to safe and effective long-term scar care.^2,3

At its simplest level, hypertrophic scarring is believed to result from a disequilibrium between collagen production and degradation. This failure to properly transition through the stages of wound healing results in bothersome symptoms, a disfigured appearance, and mechanical dysfunction of the skin (Figure, A). Decreased elasticity and extensibility, increased dermal thickness, and scar contractures impair patient range of motion and functional mobility. Those affected commonly experience varying degrees of pruritus and dysesthesia along the scar. Combined with aesthetic variations in pigmentation, erythema, texture, and thickness, hypertrophic scarring often leads to long-term psychosocial impairment and decreased health-related quality of life.⁴

Treatment Approach

Treatment of hypertrophic scars requires a multimodal approach due to the spectrum of associated concerns and the natural recalcitrance of the scar to therapy. Protocols should be tailored to the individual but generally begin with tissue-conserving surgical interventions followed by selective photothermolysis of the scar vasculature. Subsequently, deep and superficial ablative fractional laser (AFL) treatment and local pharmacotherapy also are employed. Treatment can be accomplished in the outpatient setting under local anesthesia in a serial fashion. In the authors’ experience, these therapies behave in a synergistic fashion, achieving outcomes that far exceed the sum of their parts, often obviating the need for scar excision in the majority of cases (Figure, B).

Tissue-Conserving Surgical Intervention

Z-plasty is an indispensable surgical tool due to its ability to lengthen scars and reduce wound tension. Treatment is easily customizable to the patient and can be performed using the individual or multiple Z-plasty techniques. Undermining and step-off correction while suturing allow the physician to lower raised scars, elevate depressed scars, and obscure scar presence by minimizing the straight lines that draw the eye to the scar. Z-plasties rely on the creation and transposition of 2 triangular flaps and permit a 75% increase in length along the desired tension vector. As such, Z-plasties decrease wound tension and facilitate scar maturation.

Selective Photothermolysis of the Vasculature

Although there are several devices available to treat vascular and immature hypertrophic scars, the majority of studies have been conducted with the 595-nm pulsed dye laser. By preferentially heating oxyhemoglobin within the dermal microvasculature, the pulsed dye laser irreparably injures the vascular endothelium. The subsequent tissue hypoxia and collagen fiber heating results in collagen fiber realignment, normalization of collagen subtypes, and neocollagenesis.⁵ Pulsed dye laser therapy most effectively reduces erythema and pruritus; however, improvements in scar volume, pliability, and elasticity also have been reported.⁵ When targeting the fine vasculature of the scar, thermal confinement is critical to prevent injury to the surrounding dermis. As such, pulse widths of 0.45 to 1.5 milliseconds are routinely utilized with a fluence just sufficient to elicit transient purpura lasting 3 to 5 seconds. Employing a spot size of 7 to 10 mm, typical fluences range from 4.5 to 6.5 J/cm². Engagement of the dynamic cooling device reduces the risk for complications, allowing the patient to proceed to the next step in their therapy regimen: the AFL.

Ablative Fractional Laser

The AFL creates a pixilated pattern of injury throughout the epidermis and dermis of the treatment area. Ablative fractional laser platforms include the 10,600-nm CO₂ and 2940-nm erbium-doped YAG lasers, both targeting intracellular water. The AFL vaporizes columns of tissue, leaving minute vertical channels with narrow rims of protein coagulation referred to as microscopic treatment zones (MTZs).⁶ Scar collagen analysis after AFL treatment has shown a profile resembling unaffected skin.⁷ Consistently, patients report improvements in stiffness, range of motion, pain, pruritus, pigmentation, and erythema.Physician observers also have reported similar improvements in these end points.^8,9 Recently, interim data from a prospective controlled trial were presented showing objective improvements in dermal thickness, elasticity, and extensibility after 3 treatments with the CO₂ AFL.⁶ The UltraPulse CO₂ laser (Lumenis) is the most well-studied and widely available AFL for scar therapy and as such we will outline common treatment parameters with this device. Of note, treatment end points may be generalized to any AFL.

The DeepFX UltraPulse configuration is utilized to achieve deep AFL therapy and has a fixed pulse width of 0.8 milliseconds, slightly less than the thermal relaxation time of the skin. The diameter of the MTZs is 120 µm, and MTZ density for scar treatment ranges from 1% to 10% with a goal depth of at least 80% of scar thickness. Maximal penetration of the AFL is 4 mm, which is directly proportional to fluence. The goal of deep AFL is the removal of scar tissue to facilitate remodeling and neocollagenesis. Superficial fractional ablation can then be achieved utilizing the ActiveFX UltraPulse configuration generating a 1.3-mm MTZ spot size. We commonly use a treatment level of 3 (82% density). Typical treatment energy ranges from 80 to 125 mJ, which correlates with depths of approximately 50 to 115 µm. With both configurations, the size and shape of the treatment area can be customized to the scar. In addition, frequency may be adjusted to control the speed of treatment while balancing the risk of bulk heating. The goal of superficial AFL is to minimize scar surface irregularities and ensure blending of deep AFL treatment. Once AFL treatment is complete, local pharmacotherapy can then be employed.

Pharmacotherapy

Intralesional corticosteroids have long represented the standard of care for hypertrophic scars, with concentrations between 2.5 and 40 mg/mL that are titrated to scar thickness and location to avoid unwanted atrophy. Visual blanching of the scar represents the clinical end point for treatment. Corticosteroids act by inhibiting fibroblast proliferation and enhancing collagen degradation.¹⁰ 5-Fluorouracil (5-FU) also is used in scar management. In addition to inhibiting fibroblast proliferation and inducing fibroblast apoptosis, 5-FU inhibits myofibroblast proliferation, which is helpful in the prevention and treatment of scar contracture.¹¹ As monotherapy, weekly injections with 1 to 3 mL of 50 mg/mL 5-FU has been safe and effective. Combination intralesional corticosteroid and 5-FU therapy has been reported and is associated with improved scar regression, reduced reoccurrence, and fewer side effects.¹¹ In our experience, a 1:1 suspension is effective with appropriate titration of the corticosteroid component. Although less well defined, topical application of pharmacotherapy and massage to the newly created MTZs appears beneficial and offers another option for delivery of corticosteroids and 5-FU, in addition to a number of promising medications such as bimatoprost, poly-L-lactic acid, timolol, and rapamycin.¹²

Conclusion

Advances in laser surgery and our understanding of wound healing have created a paradigm shift in the treatment approach to trauma and burn scars. In lieu of extensive scar excisions, the summarized multimodal regimen emphasizing tissue conservation and autologous remodeling is gaining favor in the military, academic medical centers, and scar centers of excellence, but patients are finding local access to care difficult. Dermatologists are uniquely positioned to cost-effectively deliver this care in the outpatient setting utilizing devices and techniques they already possess. With the end goal of optimization of functional, symptomatic, and aesthetic state of the patient, it is critical that dermatologists seize this opportunity to truly make a difference for the military and civilian patients that need it most.

Hypertrophic scarring secondary to trauma, burns, and surgical interventions is a major source of morbidity worldwide and often is mechanically, aesthetically, and symptomatically debilitating. Modern advances in acute trauma care protocols have resulted in survival rates greater than 90% in both civilian and military populations.^1,2 Patients with wounds that have historically proven fatal are now surviving and are confronted with the long-term sequelae of their injuries. With more than 52,000 service members injured in military engagements from 2001 to 2015 and 8.5 million civilians presenting annually with injury patterns at risk for hypertrophic scarring, it is paramount that we ensure access to safe and effective long-term scar care.^2,3

At its simplest level, hypertrophic scarring is believed to result from a disequilibrium between collagen production and degradation. This failure to properly transition through the stages of wound healing results in bothersome symptoms, a disfigured appearance, and mechanical dysfunction of the skin (Figure, A). Decreased elasticity and extensibility, increased dermal thickness, and scar contractures impair patient range of motion and functional mobility. Those affected commonly experience varying degrees of pruritus and dysesthesia along the scar. Combined with aesthetic variations in pigmentation, erythema, texture, and thickness, hypertrophic scarring often leads to long-term psychosocial impairment and decreased health-related quality of life.⁴

Treatment Approach

Treatment of hypertrophic scars requires a multimodal approach due to the spectrum of associated concerns and the natural recalcitrance of the scar to therapy. Protocols should be tailored to the individual but generally begin with tissue-conserving surgical interventions followed by selective photothermolysis of the scar vasculature. Subsequently, deep and superficial ablative fractional laser (AFL) treatment and local pharmacotherapy also are employed. Treatment can be accomplished in the outpatient setting under local anesthesia in a serial fashion. In the authors’ experience, these therapies behave in a synergistic fashion, achieving outcomes that far exceed the sum of their parts, often obviating the need for scar excision in the majority of cases (Figure, B).

Tissue-Conserving Surgical Intervention

Z-plasty is an indispensable surgical tool due to its ability to lengthen scars and reduce wound tension. Treatment is easily customizable to the patient and can be performed using the individual or multiple Z-plasty techniques. Undermining and step-off correction while suturing allow the physician to lower raised scars, elevate depressed scars, and obscure scar presence by minimizing the straight lines that draw the eye to the scar. Z-plasties rely on the creation and transposition of 2 triangular flaps and permit a 75% increase in length along the desired tension vector. As such, Z-plasties decrease wound tension and facilitate scar maturation.

Selective Photothermolysis of the Vasculature

Although there are several devices available to treat vascular and immature hypertrophic scars, the majority of studies have been conducted with the 595-nm pulsed dye laser. By preferentially heating oxyhemoglobin within the dermal microvasculature, the pulsed dye laser irreparably injures the vascular endothelium. The subsequent tissue hypoxia and collagen fiber heating results in collagen fiber realignment, normalization of collagen subtypes, and neocollagenesis.⁵ Pulsed dye laser therapy most effectively reduces erythema and pruritus; however, improvements in scar volume, pliability, and elasticity also have been reported.⁵ When targeting the fine vasculature of the scar, thermal confinement is critical to prevent injury to the surrounding dermis. As such, pulse widths of 0.45 to 1.5 milliseconds are routinely utilized with a fluence just sufficient to elicit transient purpura lasting 3 to 5 seconds. Employing a spot size of 7 to 10 mm, typical fluences range from 4.5 to 6.5 J/cm². Engagement of the dynamic cooling device reduces the risk for complications, allowing the patient to proceed to the next step in their therapy regimen: the AFL.

Ablative Fractional Laser

The AFL creates a pixilated pattern of injury throughout the epidermis and dermis of the treatment area. Ablative fractional laser platforms include the 10,600-nm CO₂ and 2940-nm erbium-doped YAG lasers, both targeting intracellular water. The AFL vaporizes columns of tissue, leaving minute vertical channels with narrow rims of protein coagulation referred to as microscopic treatment zones (MTZs).⁶ Scar collagen analysis after AFL treatment has shown a profile resembling unaffected skin.⁷ Consistently, patients report improvements in stiffness, range of motion, pain, pruritus, pigmentation, and erythema.Physician observers also have reported similar improvements in these end points.^8,9 Recently, interim data from a prospective controlled trial were presented showing objective improvements in dermal thickness, elasticity, and extensibility after 3 treatments with the CO₂ AFL.⁶ The UltraPulse CO₂ laser (Lumenis) is the most well-studied and widely available AFL for scar therapy and as such we will outline common treatment parameters with this device. Of note, treatment end points may be generalized to any AFL.

The DeepFX UltraPulse configuration is utilized to achieve deep AFL therapy and has a fixed pulse width of 0.8 milliseconds, slightly less than the thermal relaxation time of the skin. The diameter of the MTZs is 120 µm, and MTZ density for scar treatment ranges from 1% to 10% with a goal depth of at least 80% of scar thickness. Maximal penetration of the AFL is 4 mm, which is directly proportional to fluence. The goal of deep AFL is the removal of scar tissue to facilitate remodeling and neocollagenesis. Superficial fractional ablation can then be achieved utilizing the ActiveFX UltraPulse configuration generating a 1.3-mm MTZ spot size. We commonly use a treatment level of 3 (82% density). Typical treatment energy ranges from 80 to 125 mJ, which correlates with depths of approximately 50 to 115 µm. With both configurations, the size and shape of the treatment area can be customized to the scar. In addition, frequency may be adjusted to control the speed of treatment while balancing the risk of bulk heating. The goal of superficial AFL is to minimize scar surface irregularities and ensure blending of deep AFL treatment. Once AFL treatment is complete, local pharmacotherapy can then be employed.

Pharmacotherapy

Intralesional corticosteroids have long represented the standard of care for hypertrophic scars, with concentrations between 2.5 and 40 mg/mL that are titrated to scar thickness and location to avoid unwanted atrophy. Visual blanching of the scar represents the clinical end point for treatment. Corticosteroids act by inhibiting fibroblast proliferation and enhancing collagen degradation.¹⁰ 5-Fluorouracil (5-FU) also is used in scar management. In addition to inhibiting fibroblast proliferation and inducing fibroblast apoptosis, 5-FU inhibits myofibroblast proliferation, which is helpful in the prevention and treatment of scar contracture.¹¹ As monotherapy, weekly injections with 1 to 3 mL of 50 mg/mL 5-FU has been safe and effective. Combination intralesional corticosteroid and 5-FU therapy has been reported and is associated with improved scar regression, reduced reoccurrence, and fewer side effects.¹¹ In our experience, a 1:1 suspension is effective with appropriate titration of the corticosteroid component. Although less well defined, topical application of pharmacotherapy and massage to the newly created MTZs appears beneficial and offers another option for delivery of corticosteroids and 5-FU, in addition to a number of promising medications such as bimatoprost, poly-L-lactic acid, timolol, and rapamycin.¹²

Conclusion

Advances in laser surgery and our understanding of wound healing have created a paradigm shift in the treatment approach to trauma and burn scars. In lieu of extensive scar excisions, the summarized multimodal regimen emphasizing tissue conservation and autologous remodeling is gaining favor in the military, academic medical centers, and scar centers of excellence, but patients are finding local access to care difficult. Dermatologists are uniquely positioned to cost-effectively deliver this care in the outpatient setting utilizing devices and techniques they already possess. With the end goal of optimization of functional, symptomatic, and aesthetic state of the patient, it is critical that dermatologists seize this opportunity to truly make a difference for the military and civilian patients that need it most.

When tasked with outlining updated therapy regimens for rosacea, specific patient vignettes come to mind.

A 53-year-old male golfer presents with years of central facial flushing, prominent telangiectases, erythema, and scattered pink papules. He attempted various over-the-counter topical products indicated for acne, such as salicylic acid scrub and benzoyl peroxide cream, with no improvement and much irritation. Recently, his wife has been helping him apply redness-concealing makeup in the morning and over-the-counter hydrocortisone cream in the evening, which has been slightly helpful.

This patient’s rosacea could conceivably be labeled under the papulopustular rosacea subtype; however, the conventional categories are fluid with subtype overlap and imprecise diagnostic criteria. He also seemed to display features of the erythematotelangiectatic subtype, perhaps with underlying photodamage as well as steroid rebound erythema and/or atrophy.¹ Nevertheless, it is a common presentation, and certain baseline tenets should be applied. First, all steroid products and irritants (eg, benzoyl peroxide and salicylic acid ingredients, any scrub vehicle) should be discontinued. Education about avoidance of triggers (ie, sun, heat, spicy food, alcohol, stress is paramount. Because barrier inadequacy is a recent insight into rosacea pathogenesis, mild syndet- or lipid-free cleansers, daily sunscreen, and evening emollients dictate baseline skin care, as does meticulous situation-specific sun protection.^2,3 The papular component and immediate erythema in and around the papules can be managed topically (prior to sunscreen or emollient application) with metronidazole gel or cream up to twice daily, ivermectin cream once daily, or azelaic acid gel or foam up to twice daily. Oral doxycycline 40 mg (delayed release) on an empty stomach or 50 mg (immediate release) with food to avert antimicrobial dosing and antibiotic resistance also could be considered if topical therapy is inadequate or irritating, though gastrointestinal comorbidities with rosacea also should be delineated before initiating oral antibiotics.^4-6 (Management of this patient’s nonlesional fixed erythema, telangiectases, and flushing is discussed after the next vignette.)

What if a woman presented in a similar fashion as above, only without papules? Her family physician prescribed metronidazole gel twice daily for years with no improvement in flushing, redness, or telangiectases.

Background erythema in rosacea often is persistent with trigger-specific intensification, with or without episodic facial flushing; undoubtedly, these symptoms can be difficult to compartmentalize depending on the clarity of the patient’s history and frequency of clinic visits. The aforementioned baseline skin care and sun-protection regimen applies, and newer topical agents such as α-adrenergics (daily oxymetazoline cream or brimonidine gel) may be considered for persistent erythema; however, irritant potential and rebound erythema are common.^7-9 Topical therapies such as metronidazole gel, as in this case, are inadequate for persistent background erythema or flushing. Persistent erythema and telangiectases can be reduced with pulsed dye laser or intense pulsed light modalities, particularly following conservative management of acute inflammation.⁵ Episodic flushing is poorly controlled with the above tactics, but anecdotally, topical or oral α-adrenergics or oral nonselective beta-blockers could be considered; the latter is also applicable to migraine therapy, which is perhaps comorbid with rosacea.^5,10

A 35-year-old Hispanic woman states that the scalp, forehead, and cheeks have been flaky, pink, and pruritic for years. She saw several aestheticians for it and the admixed “acne” on the face, receiving salicylic acid chemical peels with no improvement and much dyspigmentation.

Although underreported, the commingling of rosacea with seborrheic dermatitis is common, perhaps with mutual Demodex mite overpopulation, assigning topical therapies to its management such as daily ivermectin cream or steroid-sparing pimecrolimus cream for inflammatory papules and scaly regions of the face and scalp.^11-13 Further, this case exemplifies the increasing incidence and awareness of rosacea in darker skin types, along with its postinflammatory pigmentary perturbations, which necessitate repeated education about barrier control and sun protection.¹⁴

A 72-year-old male farmer presents with his wife whoinsists that his nose has been increasing in size for years; she procures a prior driver’s license photograph as proof. She also notes that he has been snoring at night and having more trouble breathing while working outdoors. The patient had not noticed.

Phymatous rosacea may exist as an additional feature of any rosacea subtype or as a singular finding, presenting as actively inflamed, fibrotic/noninflamed, or both. Management, particularly if inflamed, involves baseline gentle skin care and sun protection, avoidance of rosacea triggers, and implementation of oral therapy such as doxycycline or isotretinoin. Many cases, particularly those with a fibrotic component, warrant surgical methods such as fractionated CO₂ laser or Shaw scalpel surgical sculpting. These cases frequently demonstrate varying degrees of airway compromise, validating surgery as a legitimate medical, not merely cosmetic, presentation.^5,15

Final Thoughts

The Table, constructed as a concise therapy compendium by the ROSacea COnsensus (ROSCO) international panel of dermatologists and ophthalmologists, outlines data-driven and expert experience-based therapies for rosacea.⁵ This panel asserts that phenotypical features, not rigid subtypes, oblige patient-specific treatment schema. Also, as these cases outline, an evolving understanding of rosacea’s multifaceted pathogenesis, assorted presentations, and frequent pitfalls in daily skin care and initial management require individualized care.

When tasked with outlining updated therapy regimens for rosacea, specific patient vignettes come to mind.

A 53-year-old male golfer presents with years of central facial flushing, prominent telangiectases, erythema, and scattered pink papules. He attempted various over-the-counter topical products indicated for acne, such as salicylic acid scrub and benzoyl peroxide cream, with no improvement and much irritation. Recently, his wife has been helping him apply redness-concealing makeup in the morning and over-the-counter hydrocortisone cream in the evening, which has been slightly helpful.

This patient’s rosacea could conceivably be labeled under the papulopustular rosacea subtype; however, the conventional categories are fluid with subtype overlap and imprecise diagnostic criteria. He also seemed to display features of the erythematotelangiectatic subtype, perhaps with underlying photodamage as well as steroid rebound erythema and/or atrophy.¹ Nevertheless, it is a common presentation, and certain baseline tenets should be applied. First, all steroid products and irritants (eg, benzoyl peroxide and salicylic acid ingredients, any scrub vehicle) should be discontinued. Education about avoidance of triggers (ie, sun, heat, spicy food, alcohol, stress is paramount. Because barrier inadequacy is a recent insight into rosacea pathogenesis, mild syndet- or lipid-free cleansers, daily sunscreen, and evening emollients dictate baseline skin care, as does meticulous situation-specific sun protection.^2,3 The papular component and immediate erythema in and around the papules can be managed topically (prior to sunscreen or emollient application) with metronidazole gel or cream up to twice daily, ivermectin cream once daily, or azelaic acid gel or foam up to twice daily. Oral doxycycline 40 mg (delayed release) on an empty stomach or 50 mg (immediate release) with food to avert antimicrobial dosing and antibiotic resistance also could be considered if topical therapy is inadequate or irritating, though gastrointestinal comorbidities with rosacea also should be delineated before initiating oral antibiotics.^4-6 (Management of this patient’s nonlesional fixed erythema, telangiectases, and flushing is discussed after the next vignette.)

What if a woman presented in a similar fashion as above, only without papules? Her family physician prescribed metronidazole gel twice daily for years with no improvement in flushing, redness, or telangiectases.

Background erythema in rosacea often is persistent with trigger-specific intensification, with or without episodic facial flushing; undoubtedly, these symptoms can be difficult to compartmentalize depending on the clarity of the patient’s history and frequency of clinic visits. The aforementioned baseline skin care and sun-protection regimen applies, and newer topical agents such as α-adrenergics (daily oxymetazoline cream or brimonidine gel) may be considered for persistent erythema; however, irritant potential and rebound erythema are common.^7-9 Topical therapies such as metronidazole gel, as in this case, are inadequate for persistent background erythema or flushing. Persistent erythema and telangiectases can be reduced with pulsed dye laser or intense pulsed light modalities, particularly following conservative management of acute inflammation.⁵ Episodic flushing is poorly controlled with the above tactics, but anecdotally, topical or oral α-adrenergics or oral nonselective beta-blockers could be considered; the latter is also applicable to migraine therapy, which is perhaps comorbid with rosacea.^5,10

A 35-year-old Hispanic woman states that the scalp, forehead, and cheeks have been flaky, pink, and pruritic for years. She saw several aestheticians for it and the admixed “acne” on the face, receiving salicylic acid chemical peels with no improvement and much dyspigmentation.

Although underreported, the commingling of rosacea with seborrheic dermatitis is common, perhaps with mutual Demodex mite overpopulation, assigning topical therapies to its management such as daily ivermectin cream or steroid-sparing pimecrolimus cream for inflammatory papules and scaly regions of the face and scalp.^11-13 Further, this case exemplifies the increasing incidence and awareness of rosacea in darker skin types, along with its postinflammatory pigmentary perturbations, which necessitate repeated education about barrier control and sun protection.¹⁴

A 72-year-old male farmer presents with his wife whoinsists that his nose has been increasing in size for years; she procures a prior driver’s license photograph as proof. She also notes that he has been snoring at night and having more trouble breathing while working outdoors. The patient had not noticed.

Phymatous rosacea may exist as an additional feature of any rosacea subtype or as a singular finding, presenting as actively inflamed, fibrotic/noninflamed, or both. Management, particularly if inflamed, involves baseline gentle skin care and sun protection, avoidance of rosacea triggers, and implementation of oral therapy such as doxycycline or isotretinoin. Many cases, particularly those with a fibrotic component, warrant surgical methods such as fractionated CO₂ laser or Shaw scalpel surgical sculpting. These cases frequently demonstrate varying degrees of airway compromise, validating surgery as a legitimate medical, not merely cosmetic, presentation.^5,15

Final Thoughts

The Table, constructed as a concise therapy compendium by the ROSacea COnsensus (ROSCO) international panel of dermatologists and ophthalmologists, outlines data-driven and expert experience-based therapies for rosacea.⁵ This panel asserts that phenotypical features, not rigid subtypes, oblige patient-specific treatment schema. Also, as these cases outline, an evolving understanding of rosacea’s multifaceted pathogenesis, assorted presentations, and frequent pitfalls in daily skin care and initial management require individualized care.

When tasked with outlining updated therapy regimens for rosacea, specific patient vignettes come to mind.

A 53-year-old male golfer presents with years of central facial flushing, prominent telangiectases, erythema, and scattered pink papules. He attempted various over-the-counter topical products indicated for acne, such as salicylic acid scrub and benzoyl peroxide cream, with no improvement and much irritation. Recently, his wife has been helping him apply redness-concealing makeup in the morning and over-the-counter hydrocortisone cream in the evening, which has been slightly helpful.

This patient’s rosacea could conceivably be labeled under the papulopustular rosacea subtype; however, the conventional categories are fluid with subtype overlap and imprecise diagnostic criteria. He also seemed to display features of the erythematotelangiectatic subtype, perhaps with underlying photodamage as well as steroid rebound erythema and/or atrophy.¹ Nevertheless, it is a common presentation, and certain baseline tenets should be applied. First, all steroid products and irritants (eg, benzoyl peroxide and salicylic acid ingredients, any scrub vehicle) should be discontinued. Education about avoidance of triggers (ie, sun, heat, spicy food, alcohol, stress is paramount. Because barrier inadequacy is a recent insight into rosacea pathogenesis, mild syndet- or lipid-free cleansers, daily sunscreen, and evening emollients dictate baseline skin care, as does meticulous situation-specific sun protection.^2,3 The papular component and immediate erythema in and around the papules can be managed topically (prior to sunscreen or emollient application) with metronidazole gel or cream up to twice daily, ivermectin cream once daily, or azelaic acid gel or foam up to twice daily. Oral doxycycline 40 mg (delayed release) on an empty stomach or 50 mg (immediate release) with food to avert antimicrobial dosing and antibiotic resistance also could be considered if topical therapy is inadequate or irritating, though gastrointestinal comorbidities with rosacea also should be delineated before initiating oral antibiotics.^4-6 (Management of this patient’s nonlesional fixed erythema, telangiectases, and flushing is discussed after the next vignette.)

What if a woman presented in a similar fashion as above, only without papules? Her family physician prescribed metronidazole gel twice daily for years with no improvement in flushing, redness, or telangiectases.

Background erythema in rosacea often is persistent with trigger-specific intensification, with or without episodic facial flushing; undoubtedly, these symptoms can be difficult to compartmentalize depending on the clarity of the patient’s history and frequency of clinic visits. The aforementioned baseline skin care and sun-protection regimen applies, and newer topical agents such as α-adrenergics (daily oxymetazoline cream or brimonidine gel) may be considered for persistent erythema; however, irritant potential and rebound erythema are common.^7-9 Topical therapies such as metronidazole gel, as in this case, are inadequate for persistent background erythema or flushing. Persistent erythema and telangiectases can be reduced with pulsed dye laser or intense pulsed light modalities, particularly following conservative management of acute inflammation.⁵ Episodic flushing is poorly controlled with the above tactics, but anecdotally, topical or oral α-adrenergics or oral nonselective beta-blockers could be considered; the latter is also applicable to migraine therapy, which is perhaps comorbid with rosacea.^5,10

A 35-year-old Hispanic woman states that the scalp, forehead, and cheeks have been flaky, pink, and pruritic for years. She saw several aestheticians for it and the admixed “acne” on the face, receiving salicylic acid chemical peels with no improvement and much dyspigmentation.

Although underreported, the commingling of rosacea with seborrheic dermatitis is common, perhaps with mutual Demodex mite overpopulation, assigning topical therapies to its management such as daily ivermectin cream or steroid-sparing pimecrolimus cream for inflammatory papules and scaly regions of the face and scalp.^11-13 Further, this case exemplifies the increasing incidence and awareness of rosacea in darker skin types, along with its postinflammatory pigmentary perturbations, which necessitate repeated education about barrier control and sun protection.¹⁴

A 72-year-old male farmer presents with his wife whoinsists that his nose has been increasing in size for years; she procures a prior driver’s license photograph as proof. She also notes that he has been snoring at night and having more trouble breathing while working outdoors. The patient had not noticed.

Phymatous rosacea may exist as an additional feature of any rosacea subtype or as a singular finding, presenting as actively inflamed, fibrotic/noninflamed, or both. Management, particularly if inflamed, involves baseline gentle skin care and sun protection, avoidance of rosacea triggers, and implementation of oral therapy such as doxycycline or isotretinoin. Many cases, particularly those with a fibrotic component, warrant surgical methods such as fractionated CO₂ laser or Shaw scalpel surgical sculpting. These cases frequently demonstrate varying degrees of airway compromise, validating surgery as a legitimate medical, not merely cosmetic, presentation.^5,15

Final Thoughts

The Table, constructed as a concise therapy compendium by the ROSacea COnsensus (ROSCO) international panel of dermatologists and ophthalmologists, outlines data-driven and expert experience-based therapies for rosacea.⁵ This panel asserts that phenotypical features, not rigid subtypes, oblige patient-specific treatment schema. Also, as these cases outline, an evolving understanding of rosacea’s multifaceted pathogenesis, assorted presentations, and frequent pitfalls in daily skin care and initial management require individualized care.

The prevalence of topical cannabinoids has risen sharply in recent years. Commercial advertisers promote their usage as a safe means to treat a multitude of skin disorders, including atopic dermatitis (AD), psoriasis, and acne. Topical compounds have garnered interest in laboratory studies, but the purchase of commercial formulations is limited to over-the-counter products from unregulated suppliers. In this article, we review the scientific evidence behind topical cannabinoids and evaluate their role in clinical dermatology.

Background

Cannabis is designated as a Schedule I drug, according to the Controlled Substances Act of 1970. This listing is given to substances with no therapeutic value and a high potential for abuse. However, as of 2017, 29 states and the District of Columbia have laws legalizing cannabis in some capacity. These regulations typically apply to medicinal use, though several states have now legalized recreational use.

Cannabinoids represent a broad class of chemical compounds derived from the cannabis plant. Originally, this class only comprised phytocannabinoids, cannabinoids produced by the cannabis plant. Tetrahydrocannabinol (THC) is the most well-known phytocannabinoid and leads to the psychoactive effects typically associated with cannabis use. Later investigation led to the discovery of endocannabinoids, cannabinoids that are naturally produced by human and animal bodies, as well as synthetic cannabinoids.¹ Cannabidiol is a phytocannabinoid that has been investigated in neurologic and anti-inflammatory conditions.^2-4

Cannabinoids act as agonists on 2 principal receptors— cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2)—which are both G protein–coupled receptors (Figure).⁵ Both have distinct distributions throughout different organ systems, to which cannabinoids (eg, THC, cannabidiol, endocannabinoids) show differential binding.^6,7 Importantly, the expression of CB1 and CB2 has been identified on sensory nerve fibers, inflammatory cells, and adnexal structures of human skin.⁸ Based on these associations, topical application of cannabinoids has become a modality of interest for dermatological disorders. These formulations aim to influence cutaneous morphology without producing psychoactive effects.

Topical Cannabinoids in Inflammatory Disorders

Atopic dermatitis has emerged as an active area of investigation for cannabinoid receptors and topical agonists (Table 1). In an animal model, Kim et al⁹ examined the effects of CB1 agonism on skin inflammation. Mice treated with topical CB1 agonists showed greater recovery of epidermal barrier function in acutely abrogated skin relative to those treated with a vehicle preparation. In addition, agonism of CB1 led to significant (P<.001) decreases in skin fold thickness among models of acute and chronic skin inflammation.⁹

Nam et al¹⁰ also examined the role of topical CB1 agonists in mice with induced AD-like symptoms. Relative to treatment with vehicle, CB1 agonists significantly reduced the recruitment of mast cells (P<.01) and lowered the blood concentration of histamine (P<.05). Given the noted decrease in the release of inflammatory mediators, the authors speculated that topical agonsim of CB1 may prove useful in several conditions related to mast cell activation, such as AD, contact dermatitis, and psoriasis.¹⁰

The anti-inflammatory properties of topical THC were evaluated by Gaffal et al.¹¹ In a mouse model of allergic contact dermatitis, mice treated with topical THC showed decreases in myeloid immune cell infiltration, with these beneficial effects existing even in mice with deficient CB1 and CB2 receptors. These results support a potentially wide anti-inflammatory activity of topical THC.¹¹

Topical Cannabinoids in Pain Management

The effects of smoked cannabis in treating pain have undergone thorough investigation over recent years. Benefits have been noted in treating neuropathic pain, particularly in human immunodeficiency virus–associated sensory neuropathy.^12-15 Smoked cannabis also may provide value as a synergistic therapy with opioids, thereby allowing for lower opioid doses.¹⁶

In contrast, research into the relationship between topical application of cannabinoids and nociception remains in preliminary stages (Table 2). In a mouse model, Dogrul et al¹⁷ assessed the topical antinociceptive potential of a mixed CB1-CB2 agonist. Results showed significant (P<.01) and dose-dependent antinociceptive effects relative to treatment with a vehicle.¹⁷ In a related study, Yesilyurt et al¹⁸ evaluated whether a mixed CB1-CB2 agonist could enhance the antinociceptive effects of topical opioids. Among mice treated with the combination of a cannabinoid agonist and topical morphine, a significantly (P<.05) greater analgesic effect was demonstrated relative to topical morphine alone.¹⁸

Studies in humans have been far more limited. Phan et al¹⁹ conducted a small, nonrandomized, open-label trial of a topical cannabinoid cream in patients with facial postherpetic neuralgia. Of 8 patients treated, 5 noted a mean pain reduction of 87.8%. No comparison vehicle was used. Based on this narrow study design, it is difficult to extrapolate these positive results to a broader patient population.¹⁹

Commercial Products

Although preliminary models with topical cannabinoids have shown potential, large-scale clinical trials in humans have yet to be performed. Despite this lack of investigation, commercial formulations of topical cannabinoids are available to dermatology patients. These formulations are nonstandardized, and no safety data exists regarding their use. Topical cannabinoids on the market may contain various amounts of active ingredient and may be combined with a range of other compounds.

In dermatology offices, it is not uncommon for patients to express an intention to use topical cannabinoid products following their planned treatment or procedure. Patients also have been known to use topical cannabinoid products prior to dermatologic procedures, sometimes in place of an approved topical anesthetic, without consulting the physician performing the procedure. With interventions that lead to active areas of wound healing, the application of such products may increase the risk for contamination and infection. Therefore, patients should be counseled that the use of commercial topical cannabinoids could jeopardize the success of their planned procedure, put them at risk for infection, and possibly lead to systemic absorption and/or changes in wound-healing capacities.

Conclusion

Based on the results from recent animal models, cannabinoids may have a role in future treatment algorithms for several inflammatory conditions. However, current efficacy and safety data are almost entirely limited to preliminary animal studies in rodents. In addition, the formulation of topical cannabinoid products is nonstandardized and poorly regulated. As such, the present evidence does not support the use of topical cannabinoids in dermatology practices. Dermatologists should ask patients about the use of any cannabinoid products as part of a treatment program, especially given the unsubstantiated claims often made by unscrupulous advertisers. This issue highlights the need for further research and regulation.

The prevalence of topical cannabinoids has risen sharply in recent years. Commercial advertisers promote their usage as a safe means to treat a multitude of skin disorders, including atopic dermatitis (AD), psoriasis, and acne. Topical compounds have garnered interest in laboratory studies, but the purchase of commercial formulations is limited to over-the-counter products from unregulated suppliers. In this article, we review the scientific evidence behind topical cannabinoids and evaluate their role in clinical dermatology.

Background

Cannabis is designated as a Schedule I drug, according to the Controlled Substances Act of 1970. This listing is given to substances with no therapeutic value and a high potential for abuse. However, as of 2017, 29 states and the District of Columbia have laws legalizing cannabis in some capacity. These regulations typically apply to medicinal use, though several states have now legalized recreational use.

Cannabinoids represent a broad class of chemical compounds derived from the cannabis plant. Originally, this class only comprised phytocannabinoids, cannabinoids produced by the cannabis plant. Tetrahydrocannabinol (THC) is the most well-known phytocannabinoid and leads to the psychoactive effects typically associated with cannabis use. Later investigation led to the discovery of endocannabinoids, cannabinoids that are naturally produced by human and animal bodies, as well as synthetic cannabinoids.¹ Cannabidiol is a phytocannabinoid that has been investigated in neurologic and anti-inflammatory conditions.^2-4

Cannabinoids act as agonists on 2 principal receptors— cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2)—which are both G protein–coupled receptors (Figure).⁵ Both have distinct distributions throughout different organ systems, to which cannabinoids (eg, THC, cannabidiol, endocannabinoids) show differential binding.^6,7 Importantly, the expression of CB1 and CB2 has been identified on sensory nerve fibers, inflammatory cells, and adnexal structures of human skin.⁸ Based on these associations, topical application of cannabinoids has become a modality of interest for dermatological disorders. These formulations aim to influence cutaneous morphology without producing psychoactive effects.

Topical Cannabinoids in Inflammatory Disorders

Atopic dermatitis has emerged as an active area of investigation for cannabinoid receptors and topical agonists (Table 1). In an animal model, Kim et al⁹ examined the effects of CB1 agonism on skin inflammation. Mice treated with topical CB1 agonists showed greater recovery of epidermal barrier function in acutely abrogated skin relative to those treated with a vehicle preparation. In addition, agonism of CB1 led to significant (P<.001) decreases in skin fold thickness among models of acute and chronic skin inflammation.⁹

Nam et al¹⁰ also examined the role of topical CB1 agonists in mice with induced AD-like symptoms. Relative to treatment with vehicle, CB1 agonists significantly reduced the recruitment of mast cells (P<.01) and lowered the blood concentration of histamine (P<.05). Given the noted decrease in the release of inflammatory mediators, the authors speculated that topical agonsim of CB1 may prove useful in several conditions related to mast cell activation, such as AD, contact dermatitis, and psoriasis.¹⁰

The anti-inflammatory properties of topical THC were evaluated by Gaffal et al.¹¹ In a mouse model of allergic contact dermatitis, mice treated with topical THC showed decreases in myeloid immune cell infiltration, with these beneficial effects existing even in mice with deficient CB1 and CB2 receptors. These results support a potentially wide anti-inflammatory activity of topical THC.¹¹

Topical Cannabinoids in Pain Management

The effects of smoked cannabis in treating pain have undergone thorough investigation over recent years. Benefits have been noted in treating neuropathic pain, particularly in human immunodeficiency virus–associated sensory neuropathy.^12-15 Smoked cannabis also may provide value as a synergistic therapy with opioids, thereby allowing for lower opioid doses.¹⁶

In contrast, research into the relationship between topical application of cannabinoids and nociception remains in preliminary stages (Table 2). In a mouse model, Dogrul et al¹⁷ assessed the topical antinociceptive potential of a mixed CB1-CB2 agonist. Results showed significant (P<.01) and dose-dependent antinociceptive effects relative to treatment with a vehicle.¹⁷ In a related study, Yesilyurt et al¹⁸ evaluated whether a mixed CB1-CB2 agonist could enhance the antinociceptive effects of topical opioids. Among mice treated with the combination of a cannabinoid agonist and topical morphine, a significantly (P<.05) greater analgesic effect was demonstrated relative to topical morphine alone.¹⁸

Studies in humans have been far more limited. Phan et al¹⁹ conducted a small, nonrandomized, open-label trial of a topical cannabinoid cream in patients with facial postherpetic neuralgia. Of 8 patients treated, 5 noted a mean pain reduction of 87.8%. No comparison vehicle was used. Based on this narrow study design, it is difficult to extrapolate these positive results to a broader patient population.¹⁹

Commercial Products

Although preliminary models with topical cannabinoids have shown potential, large-scale clinical trials in humans have yet to be performed. Despite this lack of investigation, commercial formulations of topical cannabinoids are available to dermatology patients. These formulations are nonstandardized, and no safety data exists regarding their use. Topical cannabinoids on the market may contain various amounts of active ingredient and may be combined with a range of other compounds.

In dermatology offices, it is not uncommon for patients to express an intention to use topical cannabinoid products following their planned treatment or procedure. Patients also have been known to use topical cannabinoid products prior to dermatologic procedures, sometimes in place of an approved topical anesthetic, without consulting the physician performing the procedure. With interventions that lead to active areas of wound healing, the application of such products may increase the risk for contamination and infection. Therefore, patients should be counseled that the use of commercial topical cannabinoids could jeopardize the success of their planned procedure, put them at risk for infection, and possibly lead to systemic absorption and/or changes in wound-healing capacities.

Conclusion

Based on the results from recent animal models, cannabinoids may have a role in future treatment algorithms for several inflammatory conditions. However, current efficacy and safety data are almost entirely limited to preliminary animal studies in rodents. In addition, the formulation of topical cannabinoid products is nonstandardized and poorly regulated. As such, the present evidence does not support the use of topical cannabinoids in dermatology practices. Dermatologists should ask patients about the use of any cannabinoid products as part of a treatment program, especially given the unsubstantiated claims often made by unscrupulous advertisers. This issue highlights the need for further research and regulation.

The prevalence of topical cannabinoids has risen sharply in recent years. Commercial advertisers promote their usage as a safe means to treat a multitude of skin disorders, including atopic dermatitis (AD), psoriasis, and acne. Topical compounds have garnered interest in laboratory studies, but the purchase of commercial formulations is limited to over-the-counter products from unregulated suppliers. In this article, we review the scientific evidence behind topical cannabinoids and evaluate their role in clinical dermatology.

Background

Cannabis is designated as a Schedule I drug, according to the Controlled Substances Act of 1970. This listing is given to substances with no therapeutic value and a high potential for abuse. However, as of 2017, 29 states and the District of Columbia have laws legalizing cannabis in some capacity. These regulations typically apply to medicinal use, though several states have now legalized recreational use.

Cannabinoids represent a broad class of chemical compounds derived from the cannabis plant. Originally, this class only comprised phytocannabinoids, cannabinoids produced by the cannabis plant. Tetrahydrocannabinol (THC) is the most well-known phytocannabinoid and leads to the psychoactive effects typically associated with cannabis use. Later investigation led to the discovery of endocannabinoids, cannabinoids that are naturally produced by human and animal bodies, as well as synthetic cannabinoids.¹ Cannabidiol is a phytocannabinoid that has been investigated in neurologic and anti-inflammatory conditions.^2-4

Cannabinoids act as agonists on 2 principal receptors— cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2)—which are both G protein–coupled receptors (Figure).⁵ Both have distinct distributions throughout different organ systems, to which cannabinoids (eg, THC, cannabidiol, endocannabinoids) show differential binding.^6,7 Importantly, the expression of CB1 and CB2 has been identified on sensory nerve fibers, inflammatory cells, and adnexal structures of human skin.⁸ Based on these associations, topical application of cannabinoids has become a modality of interest for dermatological disorders. These formulations aim to influence cutaneous morphology without producing psychoactive effects.

Topical Cannabinoids in Inflammatory Disorders

Atopic dermatitis has emerged as an active area of investigation for cannabinoid receptors and topical agonists (Table 1). In an animal model, Kim et al⁹ examined the effects of CB1 agonism on skin inflammation. Mice treated with topical CB1 agonists showed greater recovery of epidermal barrier function in acutely abrogated skin relative to those treated with a vehicle preparation. In addition, agonism of CB1 led to significant (P<.001) decreases in skin fold thickness among models of acute and chronic skin inflammation.⁹

Nam et al¹⁰ also examined the role of topical CB1 agonists in mice with induced AD-like symptoms. Relative to treatment with vehicle, CB1 agonists significantly reduced the recruitment of mast cells (P<.01) and lowered the blood concentration of histamine (P<.05). Given the noted decrease in the release of inflammatory mediators, the authors speculated that topical agonsim of CB1 may prove useful in several conditions related to mast cell activation, such as AD, contact dermatitis, and psoriasis.¹⁰

The anti-inflammatory properties of topical THC were evaluated by Gaffal et al.¹¹ In a mouse model of allergic contact dermatitis, mice treated with topical THC showed decreases in myeloid immune cell infiltration, with these beneficial effects existing even in mice with deficient CB1 and CB2 receptors. These results support a potentially wide anti-inflammatory activity of topical THC.¹¹

Topical Cannabinoids in Pain Management

The effects of smoked cannabis in treating pain have undergone thorough investigation over recent years. Benefits have been noted in treating neuropathic pain, particularly in human immunodeficiency virus–associated sensory neuropathy.^12-15 Smoked cannabis also may provide value as a synergistic therapy with opioids, thereby allowing for lower opioid doses.¹⁶

In contrast, research into the relationship between topical application of cannabinoids and nociception remains in preliminary stages (Table 2). In a mouse model, Dogrul et al¹⁷ assessed the topical antinociceptive potential of a mixed CB1-CB2 agonist. Results showed significant (P<.01) and dose-dependent antinociceptive effects relative to treatment with a vehicle.¹⁷ In a related study, Yesilyurt et al¹⁸ evaluated whether a mixed CB1-CB2 agonist could enhance the antinociceptive effects of topical opioids. Among mice treated with the combination of a cannabinoid agonist and topical morphine, a significantly (P<.05) greater analgesic effect was demonstrated relative to topical morphine alone.¹⁸

Studies in humans have been far more limited. Phan et al¹⁹ conducted a small, nonrandomized, open-label trial of a topical cannabinoid cream in patients with facial postherpetic neuralgia. Of 8 patients treated, 5 noted a mean pain reduction of 87.8%. No comparison vehicle was used. Based on this narrow study design, it is difficult to extrapolate these positive results to a broader patient population.¹⁹

Commercial Products

Although preliminary models with topical cannabinoids have shown potential, large-scale clinical trials in humans have yet to be performed. Despite this lack of investigation, commercial formulations of topical cannabinoids are available to dermatology patients. These formulations are nonstandardized, and no safety data exists regarding their use. Topical cannabinoids on the market may contain various amounts of active ingredient and may be combined with a range of other compounds.

In dermatology offices, it is not uncommon for patients to express an intention to use topical cannabinoid products following their planned treatment or procedure. Patients also have been known to use topical cannabinoid products prior to dermatologic procedures, sometimes in place of an approved topical anesthetic, without consulting the physician performing the procedure. With interventions that lead to active areas of wound healing, the application of such products may increase the risk for contamination and infection. Therefore, patients should be counseled that the use of commercial topical cannabinoids could jeopardize the success of their planned procedure, put them at risk for infection, and possibly lead to systemic absorption and/or changes in wound-healing capacities.

Conclusion

Based on the results from recent animal models, cannabinoids may have a role in future treatment algorithms for several inflammatory conditions. However, current efficacy and safety data are almost entirely limited to preliminary animal studies in rodents. In addition, the formulation of topical cannabinoid products is nonstandardized and poorly regulated. As such, the present evidence does not support the use of topical cannabinoids in dermatology practices. Dermatologists should ask patients about the use of any cannabinoid products as part of a treatment program, especially given the unsubstantiated claims often made by unscrupulous advertisers. This issue highlights the need for further research and regulation.

Facial acne vulgaris is a common skin disease among teenagers and adolescents that may negatively affect self-esteem, perceived facial attractiveness, and social participation.¹ Treatments for acne often are multimodal and require the utmost adherence. For these reasons, acne treatments have been challenging to clinicians and patients alike, as patient compliance in maintaining the use of prescribed topical and oral medications remains essential to attain improvement in quality of life (QOL).

Salicylic acid is a popular medicament for acne treatment that frequently is used as monotherapy or as an adjuvant for other acne treatments, especially in patients with oily skin.² Salicylic acid has a keratolytic effect, causing corneocyte discohesion in clogged pores or congested follicles,² and it is effective in treating both inflammatory and noninflammatory acne.^3,4

Light therapy, particularly with visible light, has been demonstrated to improve acne outcomes.⁵ Pneumatic broadband light (PBBL) is a therapeutic light treatment in the broadband range (400–1200 nm) that is combined with vacuum suction, which creates a mechanical lysis of thin-walled pustules and dislodges pore impaction. Additionally, the blue light portion of the PBBL spectrum targets endogenous porphyrins in Propionibacterium acnes, resulting in bacterial destruction.^6-8

The purpose of this study was to compare the efficacy, tolerability, and safety of salicylic acid 30% peel versus PBBL in the treatment of mild to moderately severe facial acne vulgaris.

METHODS

Study Design

This single-blind, randomized, split-face pilot study was approved by the institutional review board of the University of Pennsylvania (Philadelphia, Pennsylvania). All patients provided informed consent before entering the study. The single-blind evaluation was performed by one dermatologist (C.T.) who examined the participants on every visit prior to PBBL treatment.

Before the study started, participants were randomized for which side of the face was to be treated with PBBL using a number assigned to each participant. Participants received both treatments—salicylic acid 30% peel on one side of the face and PBBL treatment on the other side of the face—once weekly for a total of 6 treatments. They were then asked to return for 2 follow-up evaluations at weeks 3 and 6 following the last treatment session and were instructed not to use any topical or oral acne medications during these follow-up periods.

Inclusion and Exclusion Criteria

Patients aged 18 years and older of any race and sex with noninflammatory papules, some inflammatory papules, and no more than 1 nodule (considered as mild to moderately severe facial acne) were included in the study. Participants had not been on any topical acne medications for at least 1 month and/or oral retinoids for at least 1 year prior to the study period. All women completed urine pregnancy tests prior to the study and were advised to utilize birth control during the study period.

Study Treatments

Salicylic Acid 30% Peel

The participant’s face was cleansed thoroughly before application of salicylic acid 30% (1.5 g/2.5 mL) to half of the face and left on for 5 minutes before being carefully rinsed off by spraying with spring water. Prior to initiating PBBL therapy, the peeled side of the participant’s face was covered with a towel.

Pneumatic Broadband Light

On the other side of the face, PBBL was performed to deliver broadband light within the spectrum range of 400 to 1200 nm at a setting approximately equivalent to a fluence of 4 to 6 J/cm² and a vacuum setting approximately equivalent to a negative pressure of 3 lb/in². The power setting was increased on each subsequent visit depending on each participant’s tolerability.

Participants were required to apply a moisturizer and sunscreen to the face and avoid excessive sun exposure between study visits.

Efficacy Evaluation

A comparison of the efficacy of the treatments was determined by clinical evaluation and examining the results of the outcome measurements with the modified Global Acne Grading Score (mGAGS) and Acne QOL Scale during each treatment visit. Facial photographs were taken at each visit.

Modified Global Acne Grading Score

The mGAGS is a modification of the Global Acne Grading Scale (GAGS) that has been used to evaluate acne severity in many studies.^9-11 The GAGS considers 6 locations on the face with a grading factor for each location. The local score is obtained by multiplying the factor rated by location with the factor of clinical assessment: local score = factor rated by location × factor rated by clinical assessment. The total score is the sum of the individual local scores (Table 1).

Although the original GAGS incorporated the type and location of the lesions in its calculation, we felt that the number of lesions also was important to add to our grading score. Therefore, we modified the GAGS by adding a factor rated by the number of lesions to improve the accuracy of the test. Accordingly, the local mGAGS scores were calculated by multiplying the location factor by the lesion type and number of lesions factors: local score = location factor × lesion type factor × number of lesions factor.

Acne QOL Questionnaire

Acne QOL was assessed during each visit to demonstrate if the treatment results affected participants’ socialization due to appearance.¹² Participants were asked to complete the questionnaire, which consisted of 9 questions with 4 rating answers (0=not affected; 1=mildly affected; 2=moderately affected; 3=markedly affected). A total score of 9 or higher (high score) indicated that acne had a substantial negative impact on the participant, while a total score below 9 (low score) meant acne scarcely impacted social aspects and daily activities of the patient.

Safety Evaluation

The safety of the treatments was evaluated by clinical inspection and by comparing the results of the Wong-Baker FACES Pain Rating Scale (WBPRS)¹³ after treatment. The WBPRS is used worldwide among researchers to assess pain, particularly in children.^14,15 It is composed of 6 faces expressing pain with word descriptions with a corresponding number range reflecting pain severity from 0 to 5 (0=no hurt; 1=hurts little bit; 2=hurts little more; 3=hurts even more; 4=hurts whole lot; 5=hurts worst).¹³

Statistical Analysis

All variables were presented as the median (range). A Wilcoxon signed rank test was used to compare clinical responses between the salicylic acid 30% peel and PBBL therapies. SPSS software version 12.0 was used for all statistical analysis. A 2-tailed P value of ≤.05 was considered statistically significant.

RESULTS

Study Population

Twelve participants (2 males, 10 females) aged 17 to 36 years (median age, 22 years; mean age [SD], 23.33 [1.65] years) with both comedonal and inflammatory acne were enrolled into this study for 6 split-face treatments of salicylic acid 30% peel and PBBL at 1-week intervals for 6 weeks, with 2 subsequent follow-up sessions at weeks 3 and 6 posttreatment. Of the 12 participants, 11 were white and 1 was Asian American, with Fitzpatrick skin types II to IV. Nine participants (75%) completed the study. One participant dropped out of the study after the fourth treatment due to a scheduling conflict, and the other 2 participants did not return for follow-up. No participants withdrew from the study because of adverse therapeutic events.

Efficacy Evaluation

Comparisons between the salicylic acid 30% peel and PBBL procedures for mGAGS at each visit are shown in Table 2. There was no significant difference in treatment efficacy between the salicylic acid 30% peel and PBBL therapies during the study’s treatment and follow-up events; however, both procedures contributed to a major improvement in acne symptoms by the third treatment session and through to the last follow-up session (P≤.05). Clinical photographs at baseline, at last treatment visit (week 6), and at last follow-up (week 12) are shown in Figures 1 and 2.

The results of the acne QOL questionnaire are shown in Table 2. Lower scores reflect a higher QOL. Median QOL scores at each visit ranged from 0.5 to 4.5. There was no significant difference found between the peel agent or PBBL based on the baseline QOL and subsequent visit assessments; however, the differences between the 2 treatments were significant at weeks 3 (P=.05) and 5 (P=.03) of treatment as well as at the last follow-up visit (P=.05).

According to the QOL scores, by the third treatment session participants were more satisfied with their improved acne condition from the PBBL procedure than the salicylic acid 30% peel as demonstrated by a positive range of the QOL assessments between PBBL and salicylic acid 30% peel (as shown in the difference in QOL in Table 2: week 3, 0–6; week 4, 0–3; week 5, 0–7). On the other hand, participants saw more improvement from the salicylic acid 30% peel than from PBBL by the last follow-up evaluation, as the differences in QOL scores between the 2 treatments resulted in a negative range (−5–0).

Safety

Pain assessment by the WBPRS at every visit showed a low pain rating associated with both salicylic acid 30% peel (range, 0–0.5) and PBBL (range, 1.0–1.5) treatments. The median pain score of the salicylic acid 30% peel appeared higher compared to the PBBL treatment, yet a significant difference between both treatments was seen only at weeks 1, 3, and 6 of treatment (P≤.05).

There were no unexpected therapeutic reactions reported in our study, and no participants withdrew from the study due to adverse events. Most participants experienced only mild adverse reactions, including redness, stinging, and a burning sensation on the salicylic acid 30% peel side, which were transient and disappeared in minutes; only redness occurred on the PBBL-treated side.

Comment

Facial acne treatment is challenging, as prolonged and/or severe acne contributes to scarring, declining self-confidence, and undesirable financial consequences. Even though salicylic acid peel is a commonly used acne treatment choice, the PBBL methodology was approved by the US Food and Drug Administration⁶ and has become an alternative procedure for acne treatment.

The pharmacological effects of salicylic acid are related to its corneocyte desquamation and exfoliative actions, thereby reducing corneocyte cohesion and unclogging follicular pores.¹⁶ Salicylic acid has been demonstrated to ameliorate inflammatory acne by its effects on the arachidonic acid cascade.^2,4,17 In our study, salicylic acid 30% peel met participants’ satisfaction in acne improvement similar to a study showing a 50% improvement in acne scores after just 2 treatments.¹⁸ Our data support and corroborate that salicylic acid 30% peel renders an improvement in acne sequelae reported in several other studies.^2,17,18

Pneumatic broadband light has been known to treat acne by the mechanism of pneumatic suction combined with photodynamic therapy using broadband-pulsed light (400–1200 nm).^6-8 By applying the pneumatic device, a vacuum is created on the skin to remove sebum contents from follicles, whereas broadband light is emitted simultaneously to destroy bacteria and decrease the inflammatory process.⁷ During the vacuum process, the skin is stretched to reduce pain and avoid competitive chromophores (eg, hemoglobin), while the broadband light is administered.⁷ Broadband light encompasses 2 main light spectrums: blue light (415 nm) activates coproporphyrin III, which induces reactive free radicals and singlet oxygen species and has been reported to be the cause of bacterial cell death,¹⁹ and red light (633 nm), which renders an increase of fibroblast growth factors to work against the inflammatory processes.²⁰ There are numerous studies showing a reduction of acne lesions after photopneumatic therapy with minimal side effects.^6-8

In our study, we compared the efficacy of salicylic acid 30% peel with PBBL in the treatment of acne. Both treatments showed significant reduction of mGAGS compared to baseline starting from week 3 and lasting until week 12. Remarkably, although there were some participants who reported acne recurrence after completing all treatments at week 6, which could have happened when the treatments were ended, the final acne score at week 12 was still significantly lower than baseline. It is clear that the participants continued their acne improvement up to the 6-week follow-up period without any topical or oral medication. We do not propose that either salicylic acid peel or PBBL treatment is a solitary option but speculate that the combination of both treatments may initiate a faster resolution in the disappearance of acne.

Although there was no statistically significant difference in efficacy between salicylic acid 30% peel and PBBL procedures at each visit, QOL assessments related to treatment satisfaction did yield significant differences between baseline and the end of treatment. We noticed that participants had more positive attitudes toward the PBBL side at week 3 and week 5 but only mild satisfaction at week 4, as the differences in QOL scores between both treatments showed positive ranging values. This finding is most likely related to the immediate reduction of acne pustules by the PBBL vacuum lysis of these lesions. The differences in the QOL scores between both treatments at week 12 (the last follow-up evaluation) provided opposite findings, which meant patients had nearly even improvement in both PBBL method and salicylic acid 30% peel. Therefore, according to QOL data, acne disappeared quickly with the application of PBBL therapy but reappeared on the PBBL-treated side by the follow-up evaluations, though the acne score between both sides showed no statistically significant difference.

We reason that the PBBL therapy works better than salicylic acid 30% peel because the pneumatic system may help to unclog the pores through mechanical debridement via suctioning versus desquamation from salicylic acid 30% peel. Nonetheless, salicylic acid 30% peel sustained improvement when compared to PBBL through the follow-up periods. Both salicylic acid 30% peel and PBBL treatments are well tolerated and may initiate a faster resolution in the improvement of acne when incorporated with a medical program.

Because of the recurrence of acne after treatments were stopped, additional medical therapies are advised to be used along with this study’s clinical treatments to help mitigate the acne symptoms. These treatments should be considered in patients concerned about antibiotic resistance or those who cannot take oral antibiotics or retinoids. Salicylic acid peel is more accessible and affordable than PBBL, whereas PBBL is slightly more tolerable and less irritating than salicylic acid peel. Nevertheless, the cost of investment in PBBL is quite high—as much as $70,000—and does not include disposable, single-use tips, which cost $30 each. The machine is easy to set up, weighs about 40 lb, and requires little space to store. The average cost per visit of PBBL treatment in office is $150.00 and $75.00 for salicylic acid peel (unpublished data, Hospital of the University of Pennsylvania, 2010). Most patients may select salicylic acid peel over PBBL due to the cost and convenience of the treatment. Neither procedure should be considered as a solitary treatment option but rather as adjunctive procedures combined with oral and/or topical acne medications. After this study’s treatments were stopped and without other medications to maintain treatment effectiveness, the lesions reappeared, trending back toward baseline.

Conclusion

Both salicylic acid 30% peel and PBBL procedures are effective, safe, and well tolerated in treating acne. Although there was no significant difference in the efficacy between both treatments in this study, the small sample size and short follow-up intervals warrant further studies to support the observed outstanding outcomes and should be considered in combination with other medical treatment options. These procedures may be beneficial in holding the patient compliant until their medical therapies have an opportunity to work.

Acknowledgment

The authors would like to thank Joyce Okawa, RN (Philadelphia, Pennsylvania), for her assistance in the submission to the institutional review board of the University of Pennsylvania.

Facial acne vulgaris is a common skin disease among teenagers and adolescents that may negatively affect self-esteem, perceived facial attractiveness, and social participation.¹ Treatments for acne often are multimodal and require the utmost adherence. For these reasons, acne treatments have been challenging to clinicians and patients alike, as patient compliance in maintaining the use of prescribed topical and oral medications remains essential to attain improvement in quality of life (QOL).

Salicylic acid is a popular medicament for acne treatment that frequently is used as monotherapy or as an adjuvant for other acne treatments, especially in patients with oily skin.² Salicylic acid has a keratolytic effect, causing corneocyte discohesion in clogged pores or congested follicles,² and it is effective in treating both inflammatory and noninflammatory acne.^3,4

Light therapy, particularly with visible light, has been demonstrated to improve acne outcomes.⁵ Pneumatic broadband light (PBBL) is a therapeutic light treatment in the broadband range (400–1200 nm) that is combined with vacuum suction, which creates a mechanical lysis of thin-walled pustules and dislodges pore impaction. Additionally, the blue light portion of the PBBL spectrum targets endogenous porphyrins in Propionibacterium acnes, resulting in bacterial destruction.^6-8

The purpose of this study was to compare the efficacy, tolerability, and safety of salicylic acid 30% peel versus PBBL in the treatment of mild to moderately severe facial acne vulgaris.

METHODS

Study Design

This single-blind, randomized, split-face pilot study was approved by the institutional review board of the University of Pennsylvania (Philadelphia, Pennsylvania). All patients provided informed consent before entering the study. The single-blind evaluation was performed by one dermatologist (C.T.) who examined the participants on every visit prior to PBBL treatment.

Before the study started, participants were randomized for which side of the face was to be treated with PBBL using a number assigned to each participant. Participants received both treatments—salicylic acid 30% peel on one side of the face and PBBL treatment on the other side of the face—once weekly for a total of 6 treatments. They were then asked to return for 2 follow-up evaluations at weeks 3 and 6 following the last treatment session and were instructed not to use any topical or oral acne medications during these follow-up periods.

Inclusion and Exclusion Criteria

Patients aged 18 years and older of any race and sex with noninflammatory papules, some inflammatory papules, and no more than 1 nodule (considered as mild to moderately severe facial acne) were included in the study. Participants had not been on any topical acne medications for at least 1 month and/or oral retinoids for at least 1 year prior to the study period. All women completed urine pregnancy tests prior to the study and were advised to utilize birth control during the study period.

Study Treatments

Salicylic Acid 30% Peel

The participant’s face was cleansed thoroughly before application of salicylic acid 30% (1.5 g/2.5 mL) to half of the face and left on for 5 minutes before being carefully rinsed off by spraying with spring water. Prior to initiating PBBL therapy, the peeled side of the participant’s face was covered with a towel.

Pneumatic Broadband Light

On the other side of the face, PBBL was performed to deliver broadband light within the spectrum range of 400 to 1200 nm at a setting approximately equivalent to a fluence of 4 to 6 J/cm² and a vacuum setting approximately equivalent to a negative pressure of 3 lb/in². The power setting was increased on each subsequent visit depending on each participant’s tolerability.

Participants were required to apply a moisturizer and sunscreen to the face and avoid excessive sun exposure between study visits.

Efficacy Evaluation

A comparison of the efficacy of the treatments was determined by clinical evaluation and examining the results of the outcome measurements with the modified Global Acne Grading Score (mGAGS) and Acne QOL Scale during each treatment visit. Facial photographs were taken at each visit.

Modified Global Acne Grading Score

The mGAGS is a modification of the Global Acne Grading Scale (GAGS) that has been used to evaluate acne severity in many studies.^9-11 The GAGS considers 6 locations on the face with a grading factor for each location. The local score is obtained by multiplying the factor rated by location with the factor of clinical assessment: local score = factor rated by location × factor rated by clinical assessment. The total score is the sum of the individual local scores (Table 1).

Although the original GAGS incorporated the type and location of the lesions in its calculation, we felt that the number of lesions also was important to add to our grading score. Therefore, we modified the GAGS by adding a factor rated by the number of lesions to improve the accuracy of the test. Accordingly, the local mGAGS scores were calculated by multiplying the location factor by the lesion type and number of lesions factors: local score = location factor × lesion type factor × number of lesions factor.

Acne QOL Questionnaire

Acne QOL was assessed during each visit to demonstrate if the treatment results affected participants’ socialization due to appearance.¹² Participants were asked to complete the questionnaire, which consisted of 9 questions with 4 rating answers (0=not affected; 1=mildly affected; 2=moderately affected; 3=markedly affected). A total score of 9 or higher (high score) indicated that acne had a substantial negative impact on the participant, while a total score below 9 (low score) meant acne scarcely impacted social aspects and daily activities of the patient.

Safety Evaluation

The safety of the treatments was evaluated by clinical inspection and by comparing the results of the Wong-Baker FACES Pain Rating Scale (WBPRS)¹³ after treatment. The WBPRS is used worldwide among researchers to assess pain, particularly in children.^14,15 It is composed of 6 faces expressing pain with word descriptions with a corresponding number range reflecting pain severity from 0 to 5 (0=no hurt; 1=hurts little bit; 2=hurts little more; 3=hurts even more; 4=hurts whole lot; 5=hurts worst).¹³

Statistical Analysis

All variables were presented as the median (range). A Wilcoxon signed rank test was used to compare clinical responses between the salicylic acid 30% peel and PBBL therapies. SPSS software version 12.0 was used for all statistical analysis. A 2-tailed P value of ≤.05 was considered statistically significant.

RESULTS

Study Population

Twelve participants (2 males, 10 females) aged 17 to 36 years (median age, 22 years; mean age [SD], 23.33 [1.65] years) with both comedonal and inflammatory acne were enrolled into this study for 6 split-face treatments of salicylic acid 30% peel and PBBL at 1-week intervals for 6 weeks, with 2 subsequent follow-up sessions at weeks 3 and 6 posttreatment. Of the 12 participants, 11 were white and 1 was Asian American, with Fitzpatrick skin types II to IV. Nine participants (75%) completed the study. One participant dropped out of the study after the fourth treatment due to a scheduling conflict, and the other 2 participants did not return for follow-up. No participants withdrew from the study because of adverse therapeutic events.

Efficacy Evaluation

Comparisons between the salicylic acid 30% peel and PBBL procedures for mGAGS at each visit are shown in Table 2. There was no significant difference in treatment efficacy between the salicylic acid 30% peel and PBBL therapies during the study’s treatment and follow-up events; however, both procedures contributed to a major improvement in acne symptoms by the third treatment session and through to the last follow-up session (P≤.05). Clinical photographs at baseline, at last treatment visit (week 6), and at last follow-up (week 12) are shown in Figures 1 and 2.

The results of the acne QOL questionnaire are shown in Table 2. Lower scores reflect a higher QOL. Median QOL scores at each visit ranged from 0.5 to 4.5. There was no significant difference found between the peel agent or PBBL based on the baseline QOL and subsequent visit assessments; however, the differences between the 2 treatments were significant at weeks 3 (P=.05) and 5 (P=.03) of treatment as well as at the last follow-up visit (P=.05).

According to the QOL scores, by the third treatment session participants were more satisfied with their improved acne condition from the PBBL procedure than the salicylic acid 30% peel as demonstrated by a positive range of the QOL assessments between PBBL and salicylic acid 30% peel (as shown in the difference in QOL in Table 2: week 3, 0–6; week 4, 0–3; week 5, 0–7). On the other hand, participants saw more improvement from the salicylic acid 30% peel than from PBBL by the last follow-up evaluation, as the differences in QOL scores between the 2 treatments resulted in a negative range (−5–0).

Safety

Pain assessment by the WBPRS at every visit showed a low pain rating associated with both salicylic acid 30% peel (range, 0–0.5) and PBBL (range, 1.0–1.5) treatments. The median pain score of the salicylic acid 30% peel appeared higher compared to the PBBL treatment, yet a significant difference between both treatments was seen only at weeks 1, 3, and 6 of treatment (P≤.05).

There were no unexpected therapeutic reactions reported in our study, and no participants withdrew from the study due to adverse events. Most participants experienced only mild adverse reactions, including redness, stinging, and a burning sensation on the salicylic acid 30% peel side, which were transient and disappeared in minutes; only redness occurred on the PBBL-treated side.

Comment

Facial acne treatment is challenging, as prolonged and/or severe acne contributes to scarring, declining self-confidence, and undesirable financial consequences. Even though salicylic acid peel is a commonly used acne treatment choice, the PBBL methodology was approved by the US Food and Drug Administration⁶ and has become an alternative procedure for acne treatment.

The pharmacological effects of salicylic acid are related to its corneocyte desquamation and exfoliative actions, thereby reducing corneocyte cohesion and unclogging follicular pores.¹⁶ Salicylic acid has been demonstrated to ameliorate inflammatory acne by its effects on the arachidonic acid cascade.^2,4,17 In our study, salicylic acid 30% peel met participants’ satisfaction in acne improvement similar to a study showing a 50% improvement in acne scores after just 2 treatments.¹⁸ Our data support and corroborate that salicylic acid 30% peel renders an improvement in acne sequelae reported in several other studies.^2,17,18

Pneumatic broadband light has been known to treat acne by the mechanism of pneumatic suction combined with photodynamic therapy using broadband-pulsed light (400–1200 nm).^6-8 By applying the pneumatic device, a vacuum is created on the skin to remove sebum contents from follicles, whereas broadband light is emitted simultaneously to destroy bacteria and decrease the inflammatory process.⁷ During the vacuum process, the skin is stretched to reduce pain and avoid competitive chromophores (eg, hemoglobin), while the broadband light is administered.⁷ Broadband light encompasses 2 main light spectrums: blue light (415 nm) activates coproporphyrin III, which induces reactive free radicals and singlet oxygen species and has been reported to be the cause of bacterial cell death,¹⁹ and red light (633 nm), which renders an increase of fibroblast growth factors to work against the inflammatory processes.²⁰ There are numerous studies showing a reduction of acne lesions after photopneumatic therapy with minimal side effects.^6-8

In our study, we compared the efficacy of salicylic acid 30% peel with PBBL in the treatment of acne. Both treatments showed significant reduction of mGAGS compared to baseline starting from week 3 and lasting until week 12. Remarkably, although there were some participants who reported acne recurrence after completing all treatments at week 6, which could have happened when the treatments were ended, the final acne score at week 12 was still significantly lower than baseline. It is clear that the participants continued their acne improvement up to the 6-week follow-up period without any topical or oral medication. We do not propose that either salicylic acid peel or PBBL treatment is a solitary option but speculate that the combination of both treatments may initiate a faster resolution in the disappearance of acne.

Although there was no statistically significant difference in efficacy between salicylic acid 30% peel and PBBL procedures at each visit, QOL assessments related to treatment satisfaction did yield significant differences between baseline and the end of treatment. We noticed that participants had more positive attitudes toward the PBBL side at week 3 and week 5 but only mild satisfaction at week 4, as the differences in QOL scores between both treatments showed positive ranging values. This finding is most likely related to the immediate reduction of acne pustules by the PBBL vacuum lysis of these lesions. The differences in the QOL scores between both treatments at week 12 (the last follow-up evaluation) provided opposite findings, which meant patients had nearly even improvement in both PBBL method and salicylic acid 30% peel. Therefore, according to QOL data, acne disappeared quickly with the application of PBBL therapy but reappeared on the PBBL-treated side by the follow-up evaluations, though the acne score between both sides showed no statistically significant difference.

We reason that the PBBL therapy works better than salicylic acid 30% peel because the pneumatic system may help to unclog the pores through mechanical debridement via suctioning versus desquamation from salicylic acid 30% peel. Nonetheless, salicylic acid 30% peel sustained improvement when compared to PBBL through the follow-up periods. Both salicylic acid 30% peel and PBBL treatments are well tolerated and may initiate a faster resolution in the improvement of acne when incorporated with a medical program.

Because of the recurrence of acne after treatments were stopped, additional medical therapies are advised to be used along with this study’s clinical treatments to help mitigate the acne symptoms. These treatments should be considered in patients concerned about antibiotic resistance or those who cannot take oral antibiotics or retinoids. Salicylic acid peel is more accessible and affordable than PBBL, whereas PBBL is slightly more tolerable and less irritating than salicylic acid peel. Nevertheless, the cost of investment in PBBL is quite high—as much as $70,000—and does not include disposable, single-use tips, which cost $30 each. The machine is easy to set up, weighs about 40 lb, and requires little space to store. The average cost per visit of PBBL treatment in office is $150.00 and $75.00 for salicylic acid peel (unpublished data, Hospital of the University of Pennsylvania, 2010). Most patients may select salicylic acid peel over PBBL due to the cost and convenience of the treatment. Neither procedure should be considered as a solitary treatment option but rather as adjunctive procedures combined with oral and/or topical acne medications. After this study’s treatments were stopped and without other medications to maintain treatment effectiveness, the lesions reappeared, trending back toward baseline.

Conclusion

Both salicylic acid 30% peel and PBBL procedures are effective, safe, and well tolerated in treating acne. Although there was no significant difference in the efficacy between both treatments in this study, the small sample size and short follow-up intervals warrant further studies to support the observed outstanding outcomes and should be considered in combination with other medical treatment options. These procedures may be beneficial in holding the patient compliant until their medical therapies have an opportunity to work.

Acknowledgment

The authors would like to thank Joyce Okawa, RN (Philadelphia, Pennsylvania), for her assistance in the submission to the institutional review board of the University of Pennsylvania.

Facial acne vulgaris is a common skin disease among teenagers and adolescents that may negatively affect self-esteem, perceived facial attractiveness, and social participation.¹ Treatments for acne often are multimodal and require the utmost adherence. For these reasons, acne treatments have been challenging to clinicians and patients alike, as patient compliance in maintaining the use of prescribed topical and oral medications remains essential to attain improvement in quality of life (QOL).

Salicylic acid is a popular medicament for acne treatment that frequently is used as monotherapy or as an adjuvant for other acne treatments, especially in patients with oily skin.² Salicylic acid has a keratolytic effect, causing corneocyte discohesion in clogged pores or congested follicles,² and it is effective in treating both inflammatory and noninflammatory acne.^3,4

Light therapy, particularly with visible light, has been demonstrated to improve acne outcomes.⁵ Pneumatic broadband light (PBBL) is a therapeutic light treatment in the broadband range (400–1200 nm) that is combined with vacuum suction, which creates a mechanical lysis of thin-walled pustules and dislodges pore impaction. Additionally, the blue light portion of the PBBL spectrum targets endogenous porphyrins in Propionibacterium acnes, resulting in bacterial destruction.^6-8

The purpose of this study was to compare the efficacy, tolerability, and safety of salicylic acid 30% peel versus PBBL in the treatment of mild to moderately severe facial acne vulgaris.

METHODS

Study Design

This single-blind, randomized, split-face pilot study was approved by the institutional review board of the University of Pennsylvania (Philadelphia, Pennsylvania). All patients provided informed consent before entering the study. The single-blind evaluation was performed by one dermatologist (C.T.) who examined the participants on every visit prior to PBBL treatment.

Before the study started, participants were randomized for which side of the face was to be treated with PBBL using a number assigned to each participant. Participants received both treatments—salicylic acid 30% peel on one side of the face and PBBL treatment on the other side of the face—once weekly for a total of 6 treatments. They were then asked to return for 2 follow-up evaluations at weeks 3 and 6 following the last treatment session and were instructed not to use any topical or oral acne medications during these follow-up periods.

Inclusion and Exclusion Criteria

Patients aged 18 years and older of any race and sex with noninflammatory papules, some inflammatory papules, and no more than 1 nodule (considered as mild to moderately severe facial acne) were included in the study. Participants had not been on any topical acne medications for at least 1 month and/or oral retinoids for at least 1 year prior to the study period. All women completed urine pregnancy tests prior to the study and were advised to utilize birth control during the study period.

Study Treatments

Salicylic Acid 30% Peel

The participant’s face was cleansed thoroughly before application of salicylic acid 30% (1.5 g/2.5 mL) to half of the face and left on for 5 minutes before being carefully rinsed off by spraying with spring water. Prior to initiating PBBL therapy, the peeled side of the participant’s face was covered with a towel.

Pneumatic Broadband Light

On the other side of the face, PBBL was performed to deliver broadband light within the spectrum range of 400 to 1200 nm at a setting approximately equivalent to a fluence of 4 to 6 J/cm² and a vacuum setting approximately equivalent to a negative pressure of 3 lb/in². The power setting was increased on each subsequent visit depending on each participant’s tolerability.

Participants were required to apply a moisturizer and sunscreen to the face and avoid excessive sun exposure between study visits.

Efficacy Evaluation

A comparison of the efficacy of the treatments was determined by clinical evaluation and examining the results of the outcome measurements with the modified Global Acne Grading Score (mGAGS) and Acne QOL Scale during each treatment visit. Facial photographs were taken at each visit.

Modified Global Acne Grading Score

The mGAGS is a modification of the Global Acne Grading Scale (GAGS) that has been used to evaluate acne severity in many studies.^9-11 The GAGS considers 6 locations on the face with a grading factor for each location. The local score is obtained by multiplying the factor rated by location with the factor of clinical assessment: local score = factor rated by location × factor rated by clinical assessment. The total score is the sum of the individual local scores (Table 1).

Although the original GAGS incorporated the type and location of the lesions in its calculation, we felt that the number of lesions also was important to add to our grading score. Therefore, we modified the GAGS by adding a factor rated by the number of lesions to improve the accuracy of the test. Accordingly, the local mGAGS scores were calculated by multiplying the location factor by the lesion type and number of lesions factors: local score = location factor × lesion type factor × number of lesions factor.

Acne QOL Questionnaire

Acne QOL was assessed during each visit to demonstrate if the treatment results affected participants’ socialization due to appearance.¹² Participants were asked to complete the questionnaire, which consisted of 9 questions with 4 rating answers (0=not affected; 1=mildly affected; 2=moderately affected; 3=markedly affected). A total score of 9 or higher (high score) indicated that acne had a substantial negative impact on the participant, while a total score below 9 (low score) meant acne scarcely impacted social aspects and daily activities of the patient.

Safety Evaluation

The safety of the treatments was evaluated by clinical inspection and by comparing the results of the Wong-Baker FACES Pain Rating Scale (WBPRS)¹³ after treatment. The WBPRS is used worldwide among researchers to assess pain, particularly in children.^14,15 It is composed of 6 faces expressing pain with word descriptions with a corresponding number range reflecting pain severity from 0 to 5 (0=no hurt; 1=hurts little bit; 2=hurts little more; 3=hurts even more; 4=hurts whole lot; 5=hurts worst).¹³

Statistical Analysis

All variables were presented as the median (range). A Wilcoxon signed rank test was used to compare clinical responses between the salicylic acid 30% peel and PBBL therapies. SPSS software version 12.0 was used for all statistical analysis. A 2-tailed P value of ≤.05 was considered statistically significant.

RESULTS

Study Population

Twelve participants (2 males, 10 females) aged 17 to 36 years (median age, 22 years; mean age [SD], 23.33 [1.65] years) with both comedonal and inflammatory acne were enrolled into this study for 6 split-face treatments of salicylic acid 30% peel and PBBL at 1-week intervals for 6 weeks, with 2 subsequent follow-up sessions at weeks 3 and 6 posttreatment. Of the 12 participants, 11 were white and 1 was Asian American, with Fitzpatrick skin types II to IV. Nine participants (75%) completed the study. One participant dropped out of the study after the fourth treatment due to a scheduling conflict, and the other 2 participants did not return for follow-up. No participants withdrew from the study because of adverse therapeutic events.

Efficacy Evaluation

Comparisons between the salicylic acid 30% peel and PBBL procedures for mGAGS at each visit are shown in Table 2. There was no significant difference in treatment efficacy between the salicylic acid 30% peel and PBBL therapies during the study’s treatment and follow-up events; however, both procedures contributed to a major improvement in acne symptoms by the third treatment session and through to the last follow-up session (P≤.05). Clinical photographs at baseline, at last treatment visit (week 6), and at last follow-up (week 12) are shown in Figures 1 and 2.

The results of the acne QOL questionnaire are shown in Table 2. Lower scores reflect a higher QOL. Median QOL scores at each visit ranged from 0.5 to 4.5. There was no significant difference found between the peel agent or PBBL based on the baseline QOL and subsequent visit assessments; however, the differences between the 2 treatments were significant at weeks 3 (P=.05) and 5 (P=.03) of treatment as well as at the last follow-up visit (P=.05).

According to the QOL scores, by the third treatment session participants were more satisfied with their improved acne condition from the PBBL procedure than the salicylic acid 30% peel as demonstrated by a positive range of the QOL assessments between PBBL and salicylic acid 30% peel (as shown in the difference in QOL in Table 2: week 3, 0–6; week 4, 0–3; week 5, 0–7). On the other hand, participants saw more improvement from the salicylic acid 30% peel than from PBBL by the last follow-up evaluation, as the differences in QOL scores between the 2 treatments resulted in a negative range (−5–0).

Safety

Pain assessment by the WBPRS at every visit showed a low pain rating associated with both salicylic acid 30% peel (range, 0–0.5) and PBBL (range, 1.0–1.5) treatments. The median pain score of the salicylic acid 30% peel appeared higher compared to the PBBL treatment, yet a significant difference between both treatments was seen only at weeks 1, 3, and 6 of treatment (P≤.05).

There were no unexpected therapeutic reactions reported in our study, and no participants withdrew from the study due to adverse events. Most participants experienced only mild adverse reactions, including redness, stinging, and a burning sensation on the salicylic acid 30% peel side, which were transient and disappeared in minutes; only redness occurred on the PBBL-treated side.

Comment

Facial acne treatment is challenging, as prolonged and/or severe acne contributes to scarring, declining self-confidence, and undesirable financial consequences. Even though salicylic acid peel is a commonly used acne treatment choice, the PBBL methodology was approved by the US Food and Drug Administration⁶ and has become an alternative procedure for acne treatment.

The pharmacological effects of salicylic acid are related to its corneocyte desquamation and exfoliative actions, thereby reducing corneocyte cohesion and unclogging follicular pores.¹⁶ Salicylic acid has been demonstrated to ameliorate inflammatory acne by its effects on the arachidonic acid cascade.^2,4,17 In our study, salicylic acid 30% peel met participants’ satisfaction in acne improvement similar to a study showing a 50% improvement in acne scores after just 2 treatments.¹⁸ Our data support and corroborate that salicylic acid 30% peel renders an improvement in acne sequelae reported in several other studies.^2,17,18

Pneumatic broadband light has been known to treat acne by the mechanism of pneumatic suction combined with photodynamic therapy using broadband-pulsed light (400–1200 nm).^6-8 By applying the pneumatic device, a vacuum is created on the skin to remove sebum contents from follicles, whereas broadband light is emitted simultaneously to destroy bacteria and decrease the inflammatory process.⁷ During the vacuum process, the skin is stretched to reduce pain and avoid competitive chromophores (eg, hemoglobin), while the broadband light is administered.⁷ Broadband light encompasses 2 main light spectrums: blue light (415 nm) activates coproporphyrin III, which induces reactive free radicals and singlet oxygen species and has been reported to be the cause of bacterial cell death,¹⁹ and red light (633 nm), which renders an increase of fibroblast growth factors to work against the inflammatory processes.²⁰ There are numerous studies showing a reduction of acne lesions after photopneumatic therapy with minimal side effects.^6-8

In our study, we compared the efficacy of salicylic acid 30% peel with PBBL in the treatment of acne. Both treatments showed significant reduction of mGAGS compared to baseline starting from week 3 and lasting until week 12. Remarkably, although there were some participants who reported acne recurrence after completing all treatments at week 6, which could have happened when the treatments were ended, the final acne score at week 12 was still significantly lower than baseline. It is clear that the participants continued their acne improvement up to the 6-week follow-up period without any topical or oral medication. We do not propose that either salicylic acid peel or PBBL treatment is a solitary option but speculate that the combination of both treatments may initiate a faster resolution in the disappearance of acne.

Although there was no statistically significant difference in efficacy between salicylic acid 30% peel and PBBL procedures at each visit, QOL assessments related to treatment satisfaction did yield significant differences between baseline and the end of treatment. We noticed that participants had more positive attitudes toward the PBBL side at week 3 and week 5 but only mild satisfaction at week 4, as the differences in QOL scores between both treatments showed positive ranging values. This finding is most likely related to the immediate reduction of acne pustules by the PBBL vacuum lysis of these lesions. The differences in the QOL scores between both treatments at week 12 (the last follow-up evaluation) provided opposite findings, which meant patients had nearly even improvement in both PBBL method and salicylic acid 30% peel. Therefore, according to QOL data, acne disappeared quickly with the application of PBBL therapy but reappeared on the PBBL-treated side by the follow-up evaluations, though the acne score between both sides showed no statistically significant difference.

We reason that the PBBL therapy works better than salicylic acid 30% peel because the pneumatic system may help to unclog the pores through mechanical debridement via suctioning versus desquamation from salicylic acid 30% peel. Nonetheless, salicylic acid 30% peel sustained improvement when compared to PBBL through the follow-up periods. Both salicylic acid 30% peel and PBBL treatments are well tolerated and may initiate a faster resolution in the improvement of acne when incorporated with a medical program.

Because of the recurrence of acne after treatments were stopped, additional medical therapies are advised to be used along with this study’s clinical treatments to help mitigate the acne symptoms. These treatments should be considered in patients concerned about antibiotic resistance or those who cannot take oral antibiotics or retinoids. Salicylic acid peel is more accessible and affordable than PBBL, whereas PBBL is slightly more tolerable and less irritating than salicylic acid peel. Nevertheless, the cost of investment in PBBL is quite high—as much as $70,000—and does not include disposable, single-use tips, which cost $30 each. The machine is easy to set up, weighs about 40 lb, and requires little space to store. The average cost per visit of PBBL treatment in office is $150.00 and $75.00 for salicylic acid peel (unpublished data, Hospital of the University of Pennsylvania, 2010). Most patients may select salicylic acid peel over PBBL due to the cost and convenience of the treatment. Neither procedure should be considered as a solitary treatment option but rather as adjunctive procedures combined with oral and/or topical acne medications. After this study’s treatments were stopped and without other medications to maintain treatment effectiveness, the lesions reappeared, trending back toward baseline.

Conclusion

Both salicylic acid 30% peel and PBBL procedures are effective, safe, and well tolerated in treating acne. Although there was no significant difference in the efficacy between both treatments in this study, the small sample size and short follow-up intervals warrant further studies to support the observed outstanding outcomes and should be considered in combination with other medical treatment options. These procedures may be beneficial in holding the patient compliant until their medical therapies have an opportunity to work.

Acknowledgment

The authors would like to thank Joyce Okawa, RN (Philadelphia, Pennsylvania), for her assistance in the submission to the institutional review board of the University of Pennsylvania.