The early 1980s brought about a revolution in dermatologic laser treatment with Anderson and Parrish’s1 publication detailing the theory of selective photothermolysis. Selective photothermolysis describes the use of specific absorptions of laser energy to achieve temperature-mediated localized injury in a target. This theory led to the invention of pulsed lasers that are target-specific and highly selective. Increased selectivity decreased the amount of thermal damage to healthy tissue, thereby decreasing scarring and other adverse effects.

The first laser used in the treatment of hypertrophic scars and keloids was a continuous-wave argon laser. While initial reports were encouraging, subsequent studies did not confirm its efficacy. Similarly, use of the continuous wave neodymium:yttrium-aluminum-garnet (Nd:YAG) laser (1064 nm), which selectively inhibits collagen production by a direct photobiologic effect and creates tissue infarction with subsequent charring and sloughing of the treated area, also showed initial clinical improvement. Results, however, were transient and scar recurrences were common. Similar recurrences were observed when hypertrophic scars and keloids were excised or vaporized with a continuous-wave carbon dioxide laser (CO2). When treated with the carbon dioxide laser, scars universally recurred within 1 year.

By the early 1990s, the effectiveness of the vascular-specific 585-nm pulsed dye laser (PDL) in treating a variety of vascular lesions (eg, port-wine stain, telangiectasia) was widely known. The first series of studies on the successful use of the 585-nm flashlamp-pumped PDL in the treatment of hypertrophic scars and keloids had been published. In 1993, Dr. Alster and colleagues reported prolonged improvement in argon laser–induced port-wine stain scars treated with PDL irradiation. Skin surface texture analysis performed by optical profilometry with accompanying clinical assessment revealed that laser-irradiated scars approximated normal skin characteristics. No scar recurrences were noted 4 years following treatment.

In 1994, Alster reported clinical and textural improvement in long-standing erythematous and hypertrophic scars. An improvement rate ranging from 57-83% was observed following 1-2 PDL treatments, respectively. Dierickx and colleagues corroborated these findings the following year; they reported an average scar improvement of 77% after 1.8 laser treatments. Not surprisingly, in 1995, Alster and Williams compared the clinical, textural, histologic, and symptomatic responses of irradiated scar halves with untreated control halves. Significant improvement was observed for all clinical parameters. Histologic evaluation revealed increased numbers of regional mast cells. Because mast cells also elaborate a variety of cytokines, the presence of mast cells following laser irradiation and accompanying tissue revascularization may provide an explanation for the therapeutic outcome following microvasculature destruction in terms of stimulating collagen remodeling.

Subsequent studies also showed improvement in keloid scars following PDL treatment. In 1996, Alster and McMeekin also reported improvement in erythematous and hypertrophic facial acne scars following 585-nm pulsed dye irradiation.

Improvement in nonerythematous, minimally hypertrophic scars was also achieved following combination treatment involving pulsed dye technology and carbon dioxide laser vaporization. In 1998, Alster and Lewis treated selected scars by performing carbon dioxide laser de-epithelialization followed by PDL irradiation. Significant and prolonged clinical and textural improvement was observed in all treatment areas. In a 1995 report, Goldman and Fitzpatrick also described a combination approach to scar management. They used intralesional corticosteroids concomitantly with 585-nm PDL irradiation in 11 of 37 patients with hypertrophic scars.

No consensus exists regarding the mechanism by which PDLs achieve these additional clinical effects. Plausible explanations include laser-induced tissue hypoxia (leading to collagenesis from decreased microvascular perfusion), collagen fiber heating with dissociation of disulfide bonds and subsequent collagen realignment, selective photothermolysis of vasculature, suppression of TGF-β1 expression, and mast cell factors (eg, histamine, interleukins, various immunofactors) that may affect collagen metabolism.

In 1996, McDaniel and colleagues reported using the same 585-nm PDL to effect an improvement in the appearance of striae. They observed an improvement not only in skin surface appearance, but also in increased dermal elastin after low-fluence laser irradiation. In a 1998 report, Alster and colleagues7 also found that low-fluence PDL irradiation was superior compared with pulsed dye treatment at regular (scar) fluences and pulsed carbon dioxide vaporization. Both groups postulate that the improvement may be due to laser-induced effects on elastin, collagen, or other undiscovered factors.

In 2003, Nouri and colleagues showed that the 585-nm PDL can improve the quality and appearances of surgical scars when used as early as the day of suture removal. Scars were treated 3 times at monthly intervals and were significantly more improved compared with controls in overall Vancouver Burn Scar Scale (ie, vascularity, pliability, height, and cosmetic appearance) comparisons.

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