S54
Surgical Forum Abstracts
CONCLUSIONS: The bioengineered silk mesh bioresorbed at an ideal rate to transfer load bearing responsibility to developing host repair tissue. Results indicate development of functional native tissue.
CD1d-restricted NKT cells regulate the inflammatory phase of cutaneous wound healing David F Schneider, MD, Julia M Tulley, MS, Jessica L Palmer, MS, Richard L Gamelli, MD, FACS, Douglas E Faunce, PhD Loyola University Medical Center, Maywood, IL INTRODUCTION: NKT cells are innate lymphocytes known for their regulation of immune responses in cancer, autoimmunity, and microbial infection. Here, we present the novel finding that NKT cells are key regulators of cutaneous wound repair. Using an in vivo mouse model of cutaneous injury in conjunction with antibodies that block NKT cell activation, we show that NKT cells critically regulate the wound inflammatory milieu and the overall kinetics of wound closure. METHODS: BALB/c mice were given full thickness 3mm excisional wounds followed by systemic administration (i.v.) of either antiCD1d mAb or control IgG. Wound closure was determined at one, three, five, and seven days post injury by digital photography and wound cytokine content was quantified by ELISA. RESULTS: Most strikingly, wounds from anti-CD1d treated mice closed approximately 30% faster than those from IgG treated animals. Accelerated wound closure in anti-CD1d treated mice correlated with increased local concentrations (two-fold) of IL-6 and TNF alpha in samples obtained at one and three days post injury. Additionally, we observed that wounds collected from anti-CD1d treated mice at one, three, and seven days after injury contained nearly two-fold greater levels of the fibrogenic cytokine, TGF beta 1. CONCLUSIONS: Together, our results demonstrate the novel observation that NKT cells contribute to cutaneous wound repair via regulation of the local inflammatory response. Moreover, our findings implicate NKT cells as potential targets for innovative therapeutic interventions in aberrant wound healing such as what occurs in diabetes, keloids, and burns.
Comparative healing of surgical incisions created by a standard bovie, PEAK electrosurgical cutting tool, and standard scalpel blade Shang A Loh, MD, Grace A Carlson, MD, MBA, Eric Huang, MD, PhD, Keith L Duncan, MD, PhD, Geoffrey C Gurtner, MD, FACS Stanford University, Stanford, CA INTRODUCTION: The pulsed electron avalanche knife (PEAK) is a new electrosurgical cutting tool that uses pulsed radiofrequency energy to generate a plasma field at the tip of a titanium cutting blade. This creates an effective cutting edge while maintaining the blade near body temperature. A comparative study of skin incision healing was conducted to evaluate the characteristics of this technology.
J Am Coll Surg
METHODS: Full thickness incisions were made with a bovie, PEAK, and scalpel blade on pigs at days 0, 21, 28, 35, and 42 and reapproximated. Gauze pads used to absorb bleeding were weighed to estimate blood loss. Wounds were harvested on day 42, tested for wound strength, and examined histologically. RESULTS: Bleeding was significantly reduced in the PEAK wounds versus the scalpel wounds (p ⫽.003). Wound sections showed greatly reduced acute thermal damage from the PEAK compared with the bovie (p ⫽ .02). Bovie incisions showed 63% less strength than both PEAK and scalpel wounds at week 6. Histological scoring for injury showed no difference between the PEAK and scalpel incisions; both were significantly less than the bovie group at weeks 1 and 2 (p⫽ .015 and .02). Scar formation was similar between scalpel and PEAK groups, but significantly less than the bovie incisions (p ⫽ .02 and .03). Bovie wounds healed with heavy scarring unlike the PEAK and scalpel incisions that healed with good cosmetic results. CONCLUSIONS: The PEAK instrument is a promising new technology which provides atraumatic, scalpel-like cutting, and bovielike hemostasis, resulting in minimal bleeding, tissue injury, and scar formation.
Effect of human beta-defensin-3 expression in a novel infected diabetic porcine wound model Tobias Hirsch, MD, Malte Spielmann, Baraa Zuhaili, MD, Magdalena Fossum, MD, PhD, Hans-Ulrich Steinau, MD, PhD, Feng Yao, PhD, Andrew B Onderdonk, PhD, Lars Steinstraesser, MD, PhD, Elof Eriksson, MD, PhD, FACS Brigham and Women’s Hospital, Harvard Medical School, Boston, MA INTRODUCTION: Wound infections in diabetic patients are challenging. Increasing morbidity underlines the need for new therapeutic options. Host Defense Peptides are part of the innate immune system. Particularly human beta Defensin-3 (hBD-3) has broad antimicrobial and immunomodulatory activity in vitro. We developed a large-animal wound model to investigate the effect of hBD-3 expression in infected diabetic wounds. METHODS: Wounds were created on Streptozotocin induced diabetic Yorkshire pigs and microseeded using adenoviral vectors coding for hBD-3 transgene. The wounds were enclosed in a sealed polyurethane chamber and inoculated with 2x10E8 CFU Staphylococcus aureus. Tissue biopsies were taken for histological and microbiologic analysis. RESULTS: The animal model showed a sustained S. aureus infection over the time course with up to 8x10E7 cfu/g per gram of tissue (⬎10E5 CFU/g tissue for 12 days). No cross contamination between wounds could be detected. Diabetes promoted invasive wound infection and wound healing delay (59% versus 84%; p⬍ 0.05). hBD-3 gene transfer showed significant (p⬍ 0.01) improved wound healing (75% versus 50% reepithelialization). Antibacterial activity was significant (p⬍ 0.001) on day 4 (2.1x10E8 CFU/g in hBD-3 versus 1.3x10E9 CFU/g in controls) and there was no detectable difference on the final day of experiment.