Proper recognition and classification of scars is essential for selecting the optimal treatment modalities (see Chapter 5). Scars present with various morphologies and are generally classified into hypertrophic and atrophic subtypes. Keloids and hypertrophic scars result from excessive fibrotic tissue formation, and occur less frequently than atrophic scars on the face. Atrophic acne scars are further classified into ice-pick, rolling, shallow, and deep boxcar scars, and are the result of compromised collagen production and increased degradation during the natural wound-healing process following inflammation or injury, which leads to surface undulations4 (see Chapter 17) (Fig. 18-1).

Pathologic scars (hypertrophic scars and keloids) result from an aberrant wound-healing response and are seen in ethnic skin at rates ranging from 3- to 18-fold higher than in Caucasians. The incidence of keloids is 4.5% to 16% in skin of color, including African and Hispanic populations, especially in the second and third decades of life.³ Predisposing factors include location (particularly on jaw line, upper chest, sternal area, shoulder, upper back, and earlobe), race, family history, and past history of tendency to scar. Differences in scar characteristics between skin of color and Caucasian skin include an increased risk of hypertrophic scars and keloids with PIH. In addition, prolonged erythema, pigmentary alteration, hypertrophic scarring, and longer recovery period are more likely to occur in darker skin types (Fig. 18-2).

Hypertrophic scars differ from keloids in a number of ways. Hypertrophic scars are pink scars that are confined within the borders of the original wound, and they tend to improve over time. Keloids often form nodules and plaques of deep red color that extend beyond the original wound border with claw-like projections. The lesions may occur months or even years following injury, and they tend to enlarge and recur over time despite treatment. The lesions are disfiguring and are frequently associated with pain and pruritus. Histopathologically, keloids are composed of thick, disorganized collagen fibers with abundant mucoid matrix, whereas hypertrophic scars are comprised of more organized parallel collagen fibers within scanty mucoid matrix⁵ (see Chapter 5).

Atrophic facial scarring is a common long-term complication of moderate to severe acne, and patients with inflammatory acne should be counseled early that they have a significant risk of scar development. Every effort should be made to treat the inflammatory lesions and prevent this long-lasting complication. Acne scars can have substantial cosmetic and psychological effects, particularly in adolescence and young adulthood. Concerns about PIH and scarring are one of the main motivational factors that lead patients to seek treatment for acne.⁶ The precise prevalence of acne scarring is unknown. One community-based study reported the presence of acne scars in 14% of women and 11% of men aged 25 to 58 years.⁷ Most patients presented with macular atrophic or ice-pick scars. Other studies reported that between 30% and 95% of patients with acne developed some form of associated scarring, and a higher incidence of scarring on the trunk was observed in men.⁸

The exact mechanism of scar formation has not been fully elucidated (see Chapter 6). Inflammatory acne lesions often lead to atrophic scarring, and the formation of acne scars of various morphologies depends on the degree, depth, and duration of inflammation and on the extent of tissue damage.⁹ Acne scars are the result of a suboptimal wound-healing process that involves inflammation, granulation tissue formation with fibroplasia and new vessel formation during the proliferative phase, and wound contracture and tissue remodeling.¹⁰

Wound healing involves a stepwise process consisting of multiple overlapping phases including inflammation, proliferation, and remodeling. Tumor necrosis factor β and IL-6 appear to play a role in the scarring process.² Under normal circumstances, the immature scar passes into the final maturation phase, with degradation of the extracellular matrix and transformation of the immature type III collagen of early wound into mature type I collagen. The delicate balance of synthesis and degradation of different scar components is tightly regulated by a number of molecules, particularly epidermal growth factor, TGF-β, matrix metalloproteinases (MMPs), and basic fibroblast growth factor. The delay in regression of angiogenesis also contributes to persistent erythema in incipient pathologic scars.¹¹ Deep scars are more liable to occur when the destruction of subcutaneous fat is involved in the inflammatory process, because the enzymatic activity and inflammatory mediators also destroy the deeper tissue.

It is not clear why some wounds heal to become atrophic scars whereas others become hypertrophic. An abnormal healing response with persistent collagen production, unbalanced production of collagen type I relative to that of collagen type III, abnormal expression of a variety of growth factors, and dysregulation of the extracellular matrix have all been implicated in the formation of keloids, which tend to occur in families with a racial predisposition for dark skin. TGF-β is overproduced in keloids with a loss of feedback control during the production of collagen and the extracellular matrix.¹² Hypertrophic scars are primarily composed of well-organized bundles of type III collagen, whereas keloids contain disorganized type I and III collagen bundles. Fibroblasts in keloids have a greater number of growth factor receptors and thus an increased sensitivity to growth factor stimulation, particularly platelet-derived growth factor and TGF-β.¹³ The use of topical agents such as retinoids to treat acne may help to modulate the course of wound healing and prevent acne scar formation.¹⁴

For those patients with a family or personal history of pathologic scarring after surgery or injury, elective invasive procedures of the skin are best avoided. This is especially true over high-risk areas such as the chest, shoulders, beard area, and earlobes. The current trend is early intervention after surgery to modulate scar formation (Table 18-3) (see Chapters 8 and 9). Optimization of the wound-healing
response with early interventions such as a vascular-specific 595-nm PDL and the use of occlusive dressings may help minimize the development of hypertrophic scars or keloids. A reduction of the pigmentation and vascularity of newly revised surgical scars has been demonstrated by the application of silicone gel sheeting daily for 3 months after surgery in Asian patients.¹⁵ Topical silicone gel has also been shown to minimize the formation of hypertrophic scars in the early postoperative period after sternotomy in Asian patients.¹⁶ Intervention with laser treatment within the first weeks of the scar remodeling process after suture removal has been shown to ultimately reduce the amount of scar tissue formed.¹⁷ Early postoperative intralesional injection of 2 mg per mL triamcinolone acetonide combined with PDL treatment using subpurpuric settings has also been shown to minimize the development of hypertrophic scars after thyroidectomy in Asian patients.¹⁸ In the experience of the authors, scars earlier in the remodeling process seem to respond better and required fewer treatment sessions than more mature scars, indicating that proactive laser intervention may better modulate the wound-healing response. To prevent keloid or hypertrophic scar formation, scars should always be reevaluated 4 to 8 weeks after surgery to determine if further scar therapeutic interventions are needed. Intralesional injection of corticosteroid plus 5-fluorouracil (5-FU) should be considered once scar thickness increases, indicating the development of pathologic scars.

Patients who have nodulocystic acne with intense visible inflammation are more liable to develop scarring, particularly when there is a delay in the effective treatment of the problem. In contrast, scarring may occur early regardless of the severity of the acne. Thus, the early treatment of acne is of paramount importance to reduce the risk of scarring. Retinoids have been shown to reduce the inflammation in acne by the inhibition of leukocyte migration in the skin, and oral isotretinoin reduces the expression of MMP-9 and MMP-13 in the sebum of acne patients. This may prevent acne scar formation by normalizing the balance of MMPs and tissue inhibitors.¹⁹ In the practice of the authors, intervention with lasers can be considered 6 months after completion of isotretinoin therapy for acne.

Pathologic scars including hypertrophic scars and keloids are difficult to treat because of their persistent and recurrent nature. Hypertrophic scars are associated with a better prognosis and tend to improve somewhat with time. Treatments including intralesional corticosteroids and 5-FU, cryotherapy, pressure therapy, silicone gels or sheets, laser therapy, and radiotherapy have all been previously described in the literature¹² (see Chapters 10 and 13). However, treatment results are not consistent and frequently disappointing. Furthermore, treatment-related complications such as atrophy and dyspigmentation are especially problematic in skin of color. Ultimately, the selected treatment course depends on a variety of factors such as patient expectations and needs, scar classification, constitutive skin pigmentation, procedural pain, treatment cost, number of visits, and potential downtime and adverse effects, particularly PIH risk in skin of color (Table 18-4). Scar location, functional disturbance resulting from scar contractures, and their overall psychosocial impact are important points to consider so that the treatment objective can match the patients’ expectations (see Chapter 18).

The application of silicone-based gel sheeting up to 12 hours per day for 2 to 6 months’ duration is a well-established and well-tolerated choice for hypertrophic scars and is used widely in clinical practice for prophylaxis of pathologic scars.²⁰ Although surgical intervention for keloids is tempting, particularly for the seemingly ubiquitous earlobe keloid, surgery should be approached with extreme caution and not without a management plan beginning immediately after surgery. This is due to an extremely high relapse rate of at least 50% after surgical excision and difficulty in predicting the treatment course. Additional management options for keloids, either alone or as adjuncts to surgical excision, include pressure therapy, intralesional corticosteroids and 5-FU, and radiotherapy. In general, multiple treatment sessions and many months, even years, may be required for significant improvements in pathologic scar appearance and symptoms. The treatment aims are cosmetic improvement, relief of symptoms such as pain and itch, and mitigation of scar contractures that limit limb movement. In the experience of the authors, it takes an average of 3 years to achieve treatment goals for pathologic scars on the face. Intralesional corticosteroid plus 5-FU injection every 4 to 6 weeks remains the mainstay of treatment in the early stage. The injection interval can be gradually spaced out to every 2 to 3 months depending on the response. It is more cost-effective to initiate PDL to improve telangiectasias and scar erythema at later stages of management, when the scars are almost flattened. The appearance and texture of scars can then be further improved by fractional laser resurfacing.

Lesional factors affecting the treatment response include the age of the scar, color (hyperpigmentation or hypopigmentation), location, and lesional stability (active growth). In general, younger scars respond better to treatment. Less invasive, safer, and simpler interventions with minimal side effects are generally preferred in ethnic skin. A palliative approach can be adopted with the aim of improving pliability, reducing scar volume, erythema, and dyspigmentation, and to relieve symptoms such as pain and itch. It is also imperative to communicate with the patient adequately to educate them on the course of treatment and the expected response and risk.

Scar origin does not seem to be as important as morphology when developing a treatment plan. The standard treatment
for keloids and hypertrophic scars resulting from acne is similar to that of other excessive scarring that results from trauma and surgery. Intralesional corticosteroids decrease collagen synthesis and inhibit fibroblast proliferation.²¹ PDL therapy has been shown to downregulate the expression of TGF-β and upregulate MMP-13, which results in reduced fibroblast proliferation and collagen type III deposition.²² Laser therapy improves erythema and vascularity as well as scar texture and elevation. Radiotherapy is reserved for recalcitrant keloids; it penetrates into the dermis and inhibits fibroblast proliferation effectively. However, its usefulness is limited by its considerable adverse effects, which include mottled dyspigmentation, radiation dermatitis, and a low risk of carcinogenesis.¹⁴ A combination of the various treatment modalities is often adopted to achieve the optimal cosmetic results (see Chapter 16).

Corticosteroids (such as triamcinolone acetonide suspension at doses of 10 to 40 mg per mL) and antitumor agents such as 5-FU and bleomycin can be injected directly into the pathologic scars, either alone or in combination. Hyperpigmentation is a major side effect of intralesional bleomycin in darker skin types, affecting 71.4% of patients in one study.²³ Corticosteroids can inhibit TGF-β, can decrease fibroblast proliferation, and have vasoconstrictive effects. Common side effects associated with intralesional corticosteroids include injection site pain, local skin atrophy, telangiectasia, and hypopigmentation. Iatrogenic Cushing’s syndrome following repeated corticosteroid injections for keloids has been reported.²⁴ 5-FU, as a potent inhibitor of TGF-β/SMAD signaling, is capable of blocking TGF-β-induced, SMAD-driven upregulation of α2 type I collagen (COL1A2) gene expression in a c-Jun N-terminal kinase (JNK)-dependent manner.²⁵ 5-FU is contraindicated in pregnant and pediatric patients. Injections are performed with a 30-gauge needle every 4 to 8 weeks; injection site pain can be ameliorated with a cooling agent or the use of topical anesthesia. Clinical improvement of keloidal and hypertrophic sternotomy scars after treatment with intralesional corticosteroid alone or combined with 5-FU, 5-FU alone, and PDL appeared comparable, though intralesional corticosteroid with or without 5-FU achieved faster resolution and greater improvement of induration of scars than PDL in a randomized controlled study.²⁶ In the experience of the authors, multimodal treatments combining intralesional corticosteroid with 5-FU and laser treatment sessions can reduce the number of treatments to reach treatment goals compared to either modality alone (Table 18-5).