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The ability to safely and effectively treat cutaneous scarring with laser therapy represents an invaluable skill for the practicing laser surgeon. Various types of scarring may result from traumatic injury, surgical procedures, inflammation, or infection. A basic understanding of the pathophysiology of scarring, the different types of scars, and the most appropriate laser therapy for each type is essential to successfully treating cutaneous scars. While a challenging task, successful treatment of scarring generates immense patient satisfaction and renewed patient self-confidence.


Hypertrophic scarring can occur after surgical procedures, inflammatory conditions, or traumatic injury to the skin. This aberrant scarring frequently occurs in predisposed individuals or in wounds under increased tension, pressure, or movement. Histologically, hypertrophic scars consist of compact, thickened collagen bundles and prominent microvasculature. Keloid scars have dense, proliferative nodules of collagen and a paucity of microvasculature compared with hypertrophic scars, and this difference in vessel density may explain, in part, the poor response of keloids to laser therapy. Affected individuals may frequently complain of discomfort or pruritus at the site of these scars, and patients frequently seek medical treatments for symptomatic or cosmetic improvement of hypertrophic scars. Persistent and excessive erythema, to some degree, often accompanies hypertrophic scarring.

The laser treatment of choice for hypertrophic and erythematous scars is the vessel-specific 585/595-nm pulsed dye laser (PDL) (Figure 9-1). Numerous studies have demonstrated efficacy in reducing scar erythema as well as scar volume, texture, and pruritus with PDL treatments. The exact mechanism by which PDL improves hypertrophic scarring is not completely understood. PDL use for these scars is largely based on the concept of selective photothermolysis, in which oxyhemoglobin in scar vasculature selectively absorbs the laser energy resulting in thermal injury and coagulation of microvasculature.1 This selective destruction of scar microvasculature is thought to result in reduced collagen density within the scar and perhaps decreased endothelial cell stimulation of scar fibroblasts. Histologically, the prominence of microvasculature in hypertrophic scars and the relative paucity of microvasculature in keloid scars are notable, and this difference in vessel density may explain, in part, the poor response of keloids to PDL. Other therapeutic effects of PDL correlated to scar improvement include suppression of fibroblast proliferation and activation of fibroblast apoptosis.2 Additionally, suppression of TGF-beta1 expression and upregulation of matrix metalloproteinase have been correlated to scar regression following PDL treatment.3 TGF-beta is known to enhance extracellular matrix, and collagen and fibronectin production by dermal fibroblasts,4 and, based on animal models, overproduction of TGF-beta can produce excessive scar formation.5,6 Inhibition of TGF-beta signaling may explain, in part, the histologic changes seen in scars treated with PDL.

Figure 9–1

A. Erythematous scars resulting from trauma prior to treatment. B. Erythematous scars resulting from trauma 1 month after three treatments with a pulsed dye laser.

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