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Why Does Carbon Dioxide Resurfacing Work?  A Review

E. Victor Ross, MD; Joseph R. McKinlay, MD; R. Rox Anderson, MD
Arch Dermatol. 1999;135(4):444-454. doi:10.1001/archderm.135.4.444.
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Despite the unquestionable efficacy of carbon dioxide laser skin resurfacing, mechanisms for cosmetic enhancement remain poorly characterized. Histological studies have provided some insight into the cascade of events from initial laser impact to final skin rejuvenation. However, there are few comprehensive studies of gross and microscopic wound healing. Additionally, the literature is fragmented; excellent individual articles appear in journals from widely disparate disciplines. For example, some reports relevant to laser skin resurfacing are "sequestered" in the engineering literature. This article is intended to update the physician on laser skin resurfacing based on the broadest review of the current literature. It proceeds from a discussion of initial laser-tissue interactions, such as collagen denaturation, to examination of long-term biological sequlae. At some cost to scientific rigor, mathematical models describing laser-tissue interactions are not presented.

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Figure 1.

A, This graph shows the effects of pulse duration and fluence for a low power density, 60 W/cm2. This scenario occurs, for example, when treating a wart with a setting of 5 W and a 3-mm spot (defocused). Note that by the end of 1 second, residual thermal damage (RTD) has increased to nearly 500 µm. Ablation is negligible at this power density. B, Note the depths of ablation and RTD for a high power density, 10,000 W/cm2 (like that used in laser skin resurfacing (LSR) over the same time scale. By the end of 1 second, ablation has increased to deeper than 6 mm, but RTD has remained relatively constant at 150 to 200 µm. In LSR, we restrict the exposure time to 0.5 to 5 milliseconds (part of graph denoted by arrow). With longer exposures, ablation depth increases rapidly. This might be desirable when cutting tissue, for example, and can be accomplished by focusing 5 W into a 0.2-mm beam. C, This graph depicts the influence of pulse duration and fluence (for power density × 10,000 W/cm2) over the narrow range of parameters used in LSR for photodamage. The graph is an enlarged version of the small region denoted by the arrow in B. Note the narrow ranges of both RTD and ablation.

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Figure 2.

The relative fluence of a representative Gaussian beam.

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Figure 3.

A, Pigskin dermis after 1 pass with millisecond-domain carbon dioxide laser, average fluence 10 J/cm2, 1-mm spot, Gaussian beam profile (arrow indicates where local surface fluence is approximately 3 J/cm2; original magnification ×100). B, After 10 passes, average fluence 10 J/cm2 (original magnification ×40) (bar=400 µm, hematoxylin-eosin stain, both A and B).

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Figure 4.

Graph of residual thermal damage vs fluence for a millisecond-domain carbon dioxide laser. Arrow designates ablation threshold. Dotted line indicates predicted residual thermal damage with ablation. Note resemblance of the graph to the inverted profile of denatured collagen at the edge of Figure 3, A (arrow). This graph is based on a simple model for tissue heating using the Beer law.

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Figure 6.

Pigskin 2 days after carbon dioxide laser skin resurfacing, 3 passes, with wiping, 7 J/cm2, millisecond laser, with only petrolatum applied to the wound. Most of the basophilic zone has already sloughed. Note necrotic fibroblasts in the transition zone (which extends to the level of the short arrows, where there is a subtle change in collagen staining). At the base of the photograph are a few plump, viable fibroblast nuclei (long arrow) (hematoxylin-eosin, original magnification ×200).

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Figure 5.

Pigskin 7 days after carbon dioxide laser skin resurfacing, 3 passes, with wiping, 7 J/cm2, millisecond laser, with occlusive dressings (OpSite; Smith and Nephew, Largo, Fla). Note areas of retained basophilic-staining collagen intermixed and subjacent to neoepidermis (arrow). This may serve as a shrunken template for new collagen deposition (hematoxylin-eosin, original magnification ×200).

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The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
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