William Kuzon, Jr, MD, PhD
Professor, Plastic Surgery
Section Head, Plastic Surgery
University of Michigan Health Systems
2130 Taubman Center
1500 East Medical Center Drive
Ann Arbor, MI 48109-0340
Pathogenesis of Ventral Hernia
Ventral hernia is a common clinical condition causing significant clinical morbidity. Over 200,000 incisional hernia repairs performed each year in the United States with direct costs estimated to exceed $2.5 billion. Current surgical techniques for hernia repair are inadequate; the recurrence rate after primary ventral hernia repair ranges from 20-55%. We hypothesize that compensatory change in the abdominal wall musculature after ventral hernia formation result in an inhospitable mechanical environment that contributes to the failure of ventral hernia repairs. Previously, we have developed an extensive understanding of the mechanisms governing the pathomechanics of skeletal muscle after denervation and reinnervation, tenotomy, and aging. This understanding led us to the realization that the changes we observed in rat hindlimb muscles would certainly be observed in the abdominal muscles of animals after the creation of midline, ventral hernias. Based on that realization, we have generated new data using our unique rat ventral hernia model demonstrating that muscle fiber denervation, changes in muscle collagen content, and changes in muscle fiber type composition are observed after ventral herniation. We have preliminary data that suggest these morphologic changes reflect significant changes in the active and passive mechanical properties of the abdominal muscles in rats with ventral hernias and that these changes are more pronounced in the abdominal muscles of old animals compared with young animals with ventral hernias.
Acellular Myofascial Constructs for Ventral Hernia Repair
Conventional tissue prostheses for ventral hernia repair are inadequate as evidenced by a 20-50% recurrence rate after ventral hernia repair. We propose using acellularized myofascial (AM) constructs tissue engineered in our own lab for abdominal wall reconstruction and incisional hernia repair. AM constructs mimic the high compliance, low stiffness, and sub-maximal breaking strength of the "native" abdominal wall, and are highly biocompatible. Preliminary data using our rat hernia model show that AM constructs are associated with a significantly lower recurrence rate than prolene mesh or Alloderm. In addition, AM constructs incorporate into the native abdominal wall via tissue ingrowth. Further studies will utilize AM constructs seeded with cultured autologous dermal fibroblasts. Because fibroblasts are expected to improve extracellular matrix deposition and local cellular recruitment, we hypothesize that this tissue engineered construct will be superior to acellular constructs for ventral hernia repair.