Molecular mechanisms of nonablative fractionated laser resurfacing

Nonablative fractionated laser resurfacing improves the texture of treated skin, but little is known about the molecular mechanisms that underlie clinical improvements.

We sought to examine and quantify the time course and magnitude of dermal matrix changes that occur in response to nonablative fractionated laser resurfacing, with the dual goals of better understanding the molecular mechanisms that underlie clinical improvements and of gaining knowledge that will enable evidence-based treatment parameter optimization.

Twenty patients (mean age 58 years) with photodamaged skin were focally treated on dorsal forearms with a nonablative fractionated laser. Serial skin samples were obtained at baseline and at various times after treatment. Biopsies were examined with real-time polymerase chain reaction technology and immunohistochemical techniques.

Laser treatment resulted in an initial inflammatory response as indicated by statistically significant induction of proinflammatory cytokines (interleukin-1β and tumour necrosis factor-α). This was followed by substantial increases in levels of several matrix metalloproteinases and later by significant induction of type I collagen. Dermal remodelling was noted with both low and high microbeam energy treatment parameters.

Nonablative fractionated laser resurfacing induces a well-organized wound-healing response that leads to substantial dermal remodelling and collagen induction. Surprisingly, only minimal differences were observed between lower and higher microbeam energy settings. These data suggest that lower microbeam energy/higher microbeam density treatment parameters, which are generally better tolerated by patients, may yield dermal changes similar to those that result from higher microbeam energy/lower microbeam density treatment parameters.