Improving Cutaneous Scar Formation by Controlling the Mechanical Environment Large Animal and Phase I Studies ANNALS OF SURGERY Gurtner, G. C., Dauskardt, R. H., Wong, V. W., Bhatt, K. A., Wu, K., Vial, I. N., Padois, K., Korman, J. M., Longaker, M. T. 2011; 254 (2): 217-225


To test the hypothesis that the mechanical environment of cutaneous wounds can control scar formation.Mechanical forces have been recognized to modulate myriad biologic processes, but the role of physical force in scar formation remains unclear. Furthermore, the therapeutic benefits of offloading cutaneous wounds with a device have not been rigorously tested.A mechanomodulating polymer device was utilized to manipulate the mechanical environment of closed cutaneous wounds in red Duroc swine. After 8 weeks, wounds subjected to different mechanical stress states underwent immunohistochemical analysis for fibrotic markers. In a phase I clinical study, 9 human patients undergoing elective abdominal surgery were treated postoperatively with a stress-shielding polymer on one side whereas the other side was treated as standard of care. Professional photographs were taken between 8 and 12 months postsurgery and evaluated using a visual analog scale by lay and professional panels. This study is registered with, number NCT00766727.Stress shielding of swine incisions reduced histologic scar area by 6- and 9-fold compared to control and elevated stress states, respectively (P < 0.01 for both) and dramatically decreased the histologic expression of profibrotic markers. Closure of high-tension wounds induced human-like scar formation in the red Duroc, a phenotype effectively mitigated with stress shielding of wounds. In the study on humans, stress shielding of abdominal incisions significantly improved scar appearance (P = 0.004) compared with within-patient controls.These results indicate that mechanical manipulation of the wound environment with a dynamic stress-shielding polymer device can significantly reduce scar formation.

View details for DOI 10.1097/SLA.0b013e318220b159

View details for Web of Science ID 000292908700007

View details for PubMedID 21606834