Boxcar Acne Scars
A 17-year-old Asian adolescent was concerned about unsightly lesions on his face, especially on the temples and cheeks. He had severe acne vulgaris starting at the age of 13, but he ignored the lesions for almost 2 years. He then avoided spicy foods and tried many over-the-counter products without much improvement, despite counseling from his pharmacist. Ten months ago, he had been seen by a dermatologist who started him on isotretinoin, which led to subsidence of the acne lesions. However, he had numerous residual depressions on the facial areas. He was socially withdrawn as a result of these scars. His past health was unremarkable.
Physical examination revealed numerous, U-shaped, punched-out depressions with sharply demarcated vertical edges and wide bases on the face, especially on the temples and cheeks. Physical examination findings were otherwise unremarkable.
A diagnosis of atrophic boxcar scars was made. His dermatologist treated him with a combination of fractionated laser resurfacing, microneedling, and medium-depth chemical peels, with very good results.
Acne vulgaris is a disorder of the pilosebaceous unit caused primarily by increased sebum production, hyperkeratinization of the follicle, bacterial colonization by Propionibacterium acnes, and inflammation. The prevalence of acne in boys increases from 40% at age 12 years to 95% at age 16 years.1 In girls, the prevalence increases similarly from 61% to 83%.1 Predisposing factors include genetic predisposition, stress, premenstruation, topically applied occlusive preparations, and medications (eg, anabolic steroids, lithium, hydantoin).2 Although generally considered to be a benign, self-limited condition, acne may cause disfiguring scars and severe psychological problems. Acne scars usually are atrophic in nature and, based on their distinctive physical characteristics, can be divided into three basic types: boxcar scars, icepick scars, and rolling scars.3 Conversely, acne scars also can be thick, such as hypertrophic and keloid scars.
Approximately 11% of the male population and 14% of the female population with acne end up with residual scars.4 Scarring is more common and severe if acne treatment is delayed.4,5 Scarring is particularly common in susceptible individuals, especially with the severe variants such as nodulocystic acne, acne conglobata, and acne fulminans. In general, the deeper the inflammatory process, the more likely it will result in permanent scarring.1 However, even comedonal acne can result in scarring. Boxcar scars are caused by destruction and loss of collagen in the dermis; subsequent contraction results in the indented appearance.6
Boxcar scars are punched-out, U-shaped angular scars with sharply demarcated vertical edges.3 As such, they do not taper to a point at the base.3 Typically, they present as round to oval depressions most often 1.5 to 4 mm in diameter.3 Boxcar scars can be shallow (0.1-0.5 mm) or deep (> 0.5 mm).3,6 They often are found on the cheeks and temples.
The diagnosis mainly is a clinical one, based on the distinctive physical characteristic of the scars. Boxcar scars should be differentiated from other atrophic scars such as icepick scars and rolling scars, as well as from keloids and hypertrophic scars, since treatment varies with scar type.7
Icepick scars are narrow (< 2 mm across), deep, punctiform, and V-shaped. Characteristically, they are wider at the epithelial surface and taper as they go deeper.6 They can extend into the deep dermis or subcutaneous tissue, giving the skin an appearance of having been punctured by an icepick.
Rolling scars occur from dermal tethering of the dermis to the subcutis.3 They are wider (usually > 4 mm across) and shallower than icepick scars. They have rounded, sloping edges and produce a wavelike or undulating appearance. The combination of several of these scars in a region of skin gives it a rolling appearance.
Keloids are elevated fibrous scars that usually develop within several months after the initial scars. Characteristically, keloids outgrow the boundaries of the original scars, invading surrounding normal tissue.7 They typically grow with time and then stabilize. Keloids rarely regress. Clinically, keloids present as firm and rubbery nodules that can be skin-colored, hypopigmented or reddish brown (most common). The lesions are often pruritic and/or painful and most commonly are found on the jawline, neck, chest, shoulders, and upper back.
Hypertrophic scars remain within the confines of the original scar borders and generally arise within 4 weeks after the dermal insult, grow intensely for several months, and then regress.7 Hypertrophic scars are less likely to be symptomatic.
The disfiguring boxcar scars and their common occurrence on the face are apt to be embarrassing and psychologically traumatic, and they may result in depression, anxiety, and low self-esteem.7 Self-consciousness related to the scars can have an adverse effect on dating, participation in social activities, and quality of life.7
Boxcar scarring is a permanent condition; treatment may improve the condition, but it rarely removes it completely. Treatment should be individualized, taking into consideration the number, size, depth, and location of the boxcar scars; the available downtime; the impact on quality of life; the cost, side effects, and availability of the treatment options; the response to previous treatment; the skin phototype; the preference of the patient; and the experience and preference of the physician.
For some patients, treatment might not be necessary apart from reassurance and self-acceptance of the condition. For those patients with boxcar scars in whom treatment is desired mainly for esthetic reasons, the most common treatment options include laser skin resurfacing, dermabrasion, chemical reconstruction of skin scars (CROSS) technique for icepick scars, and punch excision and elevation.3,5,6,8,9 Punch excision and elevation is especially suitable for deep boxcar scars.3 Other treatment options include chemical peels, skin needling, injection of subcutaneous or dermal fillers, and subcutaneous incisions (subcision).3,4,6,10 Patients prone to acne scarring should have any ongoing acne managed more aggressively. Referral to a dermatologist should be considered for treating acne scarring.
1. Leung AKC. Acne. In: Leung AKC, ed. Common Problems in Ambulatory Pediatrics: Specific Clinical Problems. Vol 2. New York, NY: Nova Science Publishers; 2011:275-282.
2. Basak SA, Zaenglein AL. Acne and its management. Pediatr Rev. 2013;34 (11):479-497.
3. Jacob CI, Dover JS, Kaminer MS. Acne scarring: a classification system and review of treatment options. J Am Acad Dermatol. 2001;45(1):109-117.
4. Basta-Juzbašić A. Current therapeutic approach to acne scars. Acta Derematovenerol Croat. 2010;18(3):171-175.
5. Sardana K, Manjhi M, Garg VK, Sagar V. Which type of atrophic scar (ice-pick, boxcar, or rolling) responds to nonablative fractional laser therapy? Dermatol Surg. 2014;40(3):288-300.
6. Saedi N, Uebelhoer N. Management of acne scars. UpToDate. http://www.uptodate.com/contents/management-of-acne-scars. Updated March 17, 2015. Accessed September 11, 2015.
7. Leung AKC, Barankin B. An adolescent’s acne-related lesions: hypertrophic scars or keloids? Consultant Pediatrician. 2015;14(3):108-112.
8. Agarwal N, Gupta LK, Khare AK, Kuldeep CM, Mittal A. Therapeutic response of 70% trichloroacetic acid CROSS in atrophic acne scars. Dermatol Surg. 2015;41(5):597-604.
9. Woo SH, Park JH, Kye YC. Resurfacing of different types of facial acne scar with short-pulsed, variable-pulsed, and dual-mode Er:YAG laser. Dermatol Surg. 2004;30(4 pt 1):488-493.
10. Aalami Harandi S, Balighi K, Lajevardi V, Akbari E. Subcision-suction method: a new successful combination therapy in treatment of atrophic acne scars and other depressed scars. J Eur Acad Dermatol Venereol. 2011;25(1):92-99.