Jeffrey L Van Eps, MD1, Joseph S Fernandez-Moure, MD, MS1, Fernando J Cabrera, MD2, Bradley K Weiner, MD1, Ennio Tasciotti, PhD2, Brian J Dunkin, MD, FACS3, Warren A Ellsworth IV, MD, FACS4. 1Houston Methodist Hospital & Surgical Advanced Technology Lab, Houston Methodist Research Institute, 2Surgical Advanced Technology Lab, Houston Methodist Research Institute, 3Houston Methodist Hospital, Methodist Institute for Technology, Innovation and Education (MITIE), 4Houston Methodist Hospital
Introduction: High hernia recurrence rates witnessed with use of acellular dermal matrices (ADMs) for ventral hernia repair (VHR) have largely relegated them to bridging therapy before definitive synthetic mesh repair or breast surgery. PRP is a universally available, personalized product that when activated, releases a host of growth factors capable of augmenting soft tissue repair. Its effectiveness has been validated in many plastic surgery and orthopedic applications, but its benefit has not been explored as it applies to VHR. We hypothesized that the addition of PRP would enhance Strattice™ longevity via increased tissue deposition and protection from immunologic degradation, thus resulting in decreased hernia recurrence due to mesh failure at 6 months in a rodent model of chronic VHR.
Methods/Procedures: Chronic ventral hernias were created in 42 Lewis rats via a 3cm incision of the linea alba, followed by skin closure and hernia maturation for >28 days. Rats were randomly assigned to either a Strattice™ control (A) or PRP-treated Strattice™ (B) group and either 3 or 6-month time point. All repairs were done in underlay fashion. Autologous PRP (1×106 platelets/uL) was isolated preoperatively for experimental rats via double-centrifugation of whole blood (8mL), activated with thrombin, and applied to the mesh surface at the time of implantation. Animals were sacrificed at 3 and 6 months postoperatively, specimens harvested en bloc with surrounding abdominal wall, and either histologically processed to compare tissue deposition, neovascularization, mesh thickness and integrity (N=24), or preserved by vitrification for biaxial biomechanical stress testing (N=18). Adhesion severity was scored at necropsy according to a modified Hopkins Adhesion Scoring system.
Results: At 3 months, no hernia recurrence was noted in either group. However, at 6-month necropsy, all control rats displayed mesh failure and hernia recurrence compared to none of group B PRP-treated rats. Group B rats also had lower adhesion severity scores at both 3 months (2.17 +/- 0.58 vs. 3.25 +/- 0.62) and 6 months (2.00 +/- 0.74 vs. 3.17 +/- 0.41) (Figure 1). PRP-treated mesh underwent significantly less degradation, with residual mesh thickness over 3-fold greater than control at both areas of muscular overlap and mesh center (p<0.05, Figure 2). Histologically, PRP-treated mesh displayed enhanced tissue deposition/incorporation and more robust neovascularization than controls. Final biomechanical stress testing results are pending, but preliminary data supports greater tensile strength in PRP-treated samples of Group B.
Conclusions: Our data supports PRP’s ability to safely augment VHR with ADM at the macroscopic level, with less frequent or severe adhesion formation, less hernia recurrence, and greater long-term mechanical longevity – all due to its microscopic local tissue effects that favor a regenerative response of neovascularization, tissue incorporation, and avoidance of immunologic degradation. PRP is a safe, personalized, and universally available resource with apparent usefulness in surgery and regenerative medicine, and such evidence supports ongoing investigation into its role in VHR and soft tissue repair. Future randomized human studies would help answer this query and are warranted.
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