INTRODUCTION
Over the last few decades, multiple advancements in skin rejuvenation techniques have provided dermatologists
with a myriad of options for enhancing the cosmetic
appearance of skin. Most important, many of these new technologies produce significant results with minimal downtime and a low incidence of side effects. Microdermabrasion (MDA) remains a popular skin rejuvenation modality that fits this profile.
With approximately 11 million MDA procedures performed worldwide each year, dermatologists should be familiar with the use of MDA and the mechanism behind this popular technology.
Understanding the biochemical, molecular, and histologic effects of MDA treatment can help practitioners focus their clinical
use of the device. While many studies discuss the clinical applications of MDA and their relation to histologic changes found after treatment, few address the basic science behind the technology. This review will shed light on the recent advances made in understanding the molecular pathways activated by this noninvasive treatment. In Part 2, we focus on the innovative
uses of MDA in clinical practice. Individuals interested in the clinical evidence and applications of MDA are recommended to read Karimipour et al.1
Biology of MDA
Achieving the desired clinical and histologic effects of MDA treatment
relies on proper activation of the biomolecular pathways at its core. Unfortunately, this area of investigation remains in its infancy. In recent years, investigators have shown that many of the biologic markers of the wound healing response are modulated
after MDA treatment (Table 1).2This preliminary body of work suggests that the lack of significant posttreatment side effects should not be interpreted as a sign of a lack of clinical efficacy, a stigma often attached to device procedures that show minimal downtime.2
For example, Karimipour et al evaluated molecular changes in the skin of 49 patients after a single MDA treatment. In this study, the authors treated patients with three passes of an aluminum
oxide crystal MDA handpiece and a vacuum pressure of 15 mm Hg. Punch biopsies of treated and untreated skin were obtained at baseline and at different time intervals after treatment,
varying from 15 minutes to 16 days.
Additional molecular analysis by Karimipour and colleagues showed significant elevation of activator protein 1 (AP-1) and nuclear factor kappa B (NF-kB) after a single MDA treatment. These transcription factors are involved in the wound healing response, cell growth and differentiation, apoptosis, and inflammation.
One hour after MDA treatment, the authors noted a ninefold increase in the c-Jun component of AP-1, with a subsequent drop to a 2.8-fold increase after 24 hours (P<.05). Expression was limited to upper epidermal layers. Furthermore, immunohistologic analysis revealed nuclear translocation of NF-kB one hour after MDA treatment. This nuclear translocation activates NF-kB, which is normally constitutively expressed and retained in the cytoplasm in its inactive form. These results are significant because AP-1 and NF-kB induce the expression of interleukin-
1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α), which influence matrix metalloproteinase (MMP) expression and the subsequent degradation of dermal collagen in the remodeling
process. Specifically, TNF-α messenger RNA (mRNA) expression increased fourfold within two hours of MDA treatment,
with persistent twofold elevation up to eight hours after treatment (P<.05). IL-1β gene expression increased 10-fold at one hour (P<.05), followed by a gradual decline.3
Karimipour and colleagues also demonstrated an increase in gene expression of MMP-1, MMP-3, and MMP-9 following MDA treatment in the same study. MMP-1 functions to degrade types I and III collagen, helping initiate the dermal remodeling process. The collagen fragments are then further degraded by MMP-3 and MMP-9. Immunohistologic analysis showed MMP-1 and MMP-3 in the basal epidermis and dermis eight hours after treatment.
