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There are many options when treating acne scarring on the back and chest.
Truncal acne is an extremely common, but often undertreated entity. It has been reported that only 25% of patients with truncal acne voluntarily provide this information to their dermatologist, but most (78%) do want treatment.1 Truncal acne often goes untreated because patients are embarrassed to show their doctor, physicians do not inquire about it, and truncal acne often covers a large area that is difficult to treat with topical medications.2 However, it is extremely important for health care practitioners to recognize and treat this entity, due to the potential for scarring. Prevention of scarring through early detection and treatment of truncal acne is necessary, as treatment of truncal scars is difficult.
Scarring occurs in 95% of acne patients and the degree of scarring is correlated with the time delay to starting treatment.3 Severe scarring is associated with significant psychological distress, so it is paramount that practitioners evaluate for truncal acne and treat accordingly.
An important part of truncal acne is dealing with the wound healing that needs to occur as a result of the inflammatory lesions. The wound healing process progresses through three stages: (1) inflammation, (2) granulation tissue formation, and (3) matrix remodeling.4
Blanching followed by erythema results from vasoconstriction for hemostasis followed by vasodilation. Melanogenesis may also be stimulated. Both play a role in the development of postacne erythema and hyperpigmentation. Many inflammatory cells also enter the wound to prepare the site for granulation tissue formation. Holland et al. determined that lesions were less likely to scar if the inflammatory reaction peaked within 48 hours of the acne lesion developing. In patients more prone to scarring, the inflammatory response was slow to develop and slower to resolve.5
In this stage, damaged tissues are repaired, and new vessels are formed. Growth factors are released that promote the proliferation of fibroblasts. Collagen formation by fibroblasts begins 3-5 days after the wound is created. Type III collagen dominates within the wound first, with a shift in the composition to 80% type I collagen in more mature scars.4
Fibroblasts and keratinocytes produce enzymes that determine the architecture of the extracellular matrix (ECM). These include matrix metalloproteinases (MMPs) and inhibitors of MMPs. MMPs degrade the ECM in order to promote remodeling. An imbalance between MMPs and MMP inhibitors is what results in atrophic and hypertrophic scars. An inadequate response and decreased deposition of collagen fibers will result in an atrophic scar, while an exuberant response can result in a raised, hypertrophic scar.4
When treating acne scars, it is important to determine the age of the scar as it will continue to evolve over 12 months and some treatments work better on newer scars.6 The distribution of scars is also important because your treatment modality will be different if there are a few individual scars versus scars that are widespread. Additionally, scar morphology is significant. Facial acne scars have three primary morphologies: icepick, boxcar, and rolling scars.3 These can be seen on the trunk, but acne scars on the chest and back are usually either raised (hypertrophic or keloidal) or depressed (atrophic).6 Lastly, it is essential to determine if isotretinoin has been used before, because recent isotretinoin treatment may alter the risk factors with a disease.6
These scars are characterized by excessive deposition of collage in the dermis and subcutaneous tissues at the site of traumatic or surgical injuries. These scars can result in disfigurement, contractures, itching, and pain.7 Hypertrophic scars are raised scars within the boundaries of the wound, whereas keloids grow beyond the confines of the original wound. There is a genetic predisposition to forming keloids, with approximately 15-20% of Blacks, Hispanics, and Asians developing these lesions within their lifetime. 7
Atrophic scars account for around 75% of all acne scars and are classified into three major types: 1) icepick, 2) rolled-over (or rolling), and 3) boxcar.8 It is common for patients to have more than one type of scar.
Scar Type | Shape | Additional Features 8 |
---|---|---|
Icepick |
V-shaped |
· <2 cm in diameter · Sharply marginated epithelial tracts · Extend into deep dermis or subcutaneous layer |
Boxcar |
U-shaped |
· Sharp vertical sides that extend 0.1-0.5mm into the dermis · May go deeper |
Rolled-over |
Irregular, undulating |
· May extend greater than 5mm in diameter · Fibrotic bands tether normal-looking dermis to subcutis |
The best treatment for truncal scarring is prevention. However, if scarring does occur, there are some therapeutic options, though less abundant than treatment options for facial scarring. These options depend on the number and type of scars.
Silicone Gel
Silicone gel has several advantages including: its transparency, quick drying and nonirritating nature, and usefulness in treatment of extensive scarring and on uneven areas of skin. The mechanism of action is poorly understood but may involve: (1) increased skin hydration, (2) increased skin temperature, (3) scar protection, (4) increased O2 tension, and (5) immune system activation. One study showed an average improvement in scar thickness by 40-50% compared to baseline. 4 This treatment is safe to use in patients of any age and in women of childbearing age.
Intralesional Corticosteroids
Intralesional (IL) corticosteroids can be beneficial for improving the appearance of hypertrophic and keloidal scars. It can be used alone or as part of multiple therapeutic approaches. The use of IL steroids may also improve the benefit seen with the pulsed dye laser if the two are used in conjunction.6 IL corticosteroids can reduce the volume, thickness, and texture of hypertrophic scars and keloids . They are also helpful with reducing symptoms, such as pain and itching. The mechanism of action is not completely understood but, in addition to steroids’ anti-inflammatory properties, they likely have vasoconstrictor and antimitotic activity.4 It is believes that steroids arrest pathological collagen production through (1) the reduction of oxygen and nutrients to the scar leading to inhibition of the proliferation of keratinocytes and fibroblasts and (2) by stimulating the digestion of collagen deposition through inhibition of a collagenase inhibitor (alpha-2-microglobulin).4 In terms of therapy, multiple treatments of IL triamcinolone acetonide in concentrations ranging from 2.5-20 mg/mL may be needed depending on the thickness of the scar.6
Intense Pulsed Light (IPL)
The mechanism of this therapy is not fully understood, but probably targets the vascular proliferation essential to the collagen overgrowth that results in scar development. One study showed that IPL resulted in significant clinical improvement of hypertrophic and keloidal scars, especially in textural smoothing.9
Other Treatments
Several other therapeutic methods have been tried including treatment with: interferon a-2b, bleomycin, hydrocolloid dressing, cryotherapy with liquid nitrogen, intralesional injection of verapamil, and intralesional cryosurgery.10 A combination therapeutic approach using several of the treatment methods listed above is recommended.10
Chemical Peels
This involves applying chemicals to the skin in order to damage the outer layer and accelerate the repair process. The best results are seen in macular scars. Deeper scars (icepick and rolling) do not do as well with standard chemical peels and may need more focused treatment such as 100% trichloracetic acid cross and multiple treatments. Some chemicals currently being used include: glycolic acid, Jessner’s solution, pyruvic acid, salicylic acid, and trichloracetic acid.4
Fillers
The appearance of individual atrophic scars may be improved by using fillers to elevate the depression. This approach cannot be utilized for patients with several confluent atrophic scars, but can be a good option for patients with a few well-demarcated atrophic scars. It is recommended to use a short-lived filler (like collagen) first to ensure a desirable cosmetic outcome before committing to a more permanent filler.6 Long term fillers include: liquid silicone, calcium hydroxyapatite, poly-L lactic acid, and polymethylmethacrylate.
Surgical excision
This can be used for a few scars on the trunk but should be avoided when scars are more widespread. Due to the high level of tension on truncal skin, however, it is likely that the scar from the excision will expand or even become hypertrophic or keloidal.6 Surgical excision should only be performed if the surgeon thinks that the new scar will be preferable to the old one. If a hypertrophic scar is removed, ionizing radiotherapy can be given within 24-48 hours to prevent recurrence of the hypertrophic scar by inhibiting fibroblast proliferation.6 Surgical excision should be carefully discussed with a dermatologist before proceeding due to the high risk for recurrence.
Microneedling
Microneedling is thought to break down collagen bundles in the superficial layer of the dermis that are responsible for the scar. This then induces the formation of more even collagen under the epidermis.11 Unlike ablative laser therapies, the needles penetrate the epidermis but do not add a burn injury component. Microneedling has been shown to provide a positive response for rolling and boxcar atrophic scars (moderate improvement in icepick scars).11 Hypertrophic scars and keloids may also respond to microneedling, but the failure rate is much higher (around 30%).12 Raised scars will also take several more months than atrophic scars to show visible improvement.
Pulsed Dye Laser
The pulsed dye laser can be used to decrease scar erythema (for both atrophic and hypertrophic scars) and help promote return of normal skin markings. These lasers act to damage the microvasculature, which gives scars their red color.13 Collagen is also broken down (either due to ischemia from microvasculature loss or via thermal damage), which can help to flatten scars. For atrophic scars, reformation of collagen after damage can help to elevate these depressed scars.13
Semiablative Lasers
Semiablative lasers are the preferred over ablative and non-ablative lasers for scar treatment off the face. Ablative skin resurfacing lasers, including CO2 and erbium lasers, remove superficial sun damage, pigmentation, and wrinkles by destroying the epidermis and superficial dermis. The laser enters the upper dermis, where thermal conduction denatures the collagen and causes tissue contraction.14 At least two weeks is required to allow for re-epithelization of the epidermis after its destruction. The use of these purely ablative lasers for truncal scarring is limited due to the lack of adnexal skin appendages required to re-epithelialize the skin after treatment.6
Semiablative therapies (such as the Fraxel laser) however, can be used safely off the face.14 These lasers work by producing fractional photothermolysis through the coagulation of multiple columns of tissue. These columns of coagulated tissue, called microthermal zones (MTZs), penetrate through the epidermis and into the deep dermis.14 Though the epidermis and stratum corneum are destroyed, greater portions of the epidermis and stratum corneum remains intact. This results in faster healing leading to less downtime and greater patient tolerance.14
To decrease the risk of skin irritation or scarring from the procedure, many practitioners will only perform the procedure once isotretinoin has been discontinued for 6-12 months after treatment. Some practitioners also like to stop the use of benzoyl peroxide at least one week and topical retinoids at least two weeks before treatment.14
Treatment type | Mechanism | Scar type the treatment is most effective for |
---|---|---|
Silicone Gel |
Poorly understood. May involve: (1) increased skin hydration (2) increased skin temperature (3) scar protection (4) increased O2 tension (5) immune system activation. |
Hypertrophic, keloid scars |
Intralesional Corticosteroids |
Not completely understood. Steroids likely arrest pathological collagen production through the reduction of oxygen and nutrients to the scar by inhibiting alpha-2-microglobulin (a collagenase inhibitor) |
Hypertrophic, keloid scars (few lesions) |
Intense Pulsed Light (IPL) |
Not completely understood. Likely targets the vascular proliferation essential to the collagen overgrowth. |
Hypertrophic, keloid scars |
Chemical Peels |
Damage the epidermis in order to accelerate repair and healing. |
Shallow boxcar atrophic scars |
Fillers |
Physically fills the scar to improve the appearance by the lesion. |
Atrophic scars (few lesions) |
Surgical excision |
Removal of a depressed or raised scar by cutting it out and closing to form a new, hopefully flatter, scar. |
Hypertrophic, keloidal, or atrophic scars (few lesions) |
Microneedling |
The needles break down collagen bundles in the superficial layer of the dermis that are responsible for the scar. This then induces the formation of more collagen under the epidermis. |
Hypertrophic, keloidal, or atrophic scars |
Pulsed Dye Laser |
Flattens scars through collagen breakdown (either due to ischemia from microvasculature loss or via thermal damage). Elevates depressed scars through reformation of collagen after its damage by the laser. |
Hypertrophic, keloidal, or atrophic scars |
Semiablative Laser |
Forms columns of coagulated tissue, called microthermal zones (MTZs) that penetrate through the epidermis and into the deep dermis. This stimulates new collagen formation and tissue contraction. |
Hypertrophic, keloidal, or atrophic scars |