Page 296 - Prevention and Treatment of Incisional Hernia- New Techniques and Materials

Chapter 14
found in performance between the crosslinked meshes. In previous studies, the possible e ect of crosslinking on the occurrence of infectious complications was not addressed. This experiment is the rst step in acquiring more knowledge on the e ect of crosslinking on the occurrence of infectious complications after implantation of biological meshes in a contaminated environment.
In abdominal wall repair with a biological mesh, resistance to degradation is critical to prevent recurrence of hernia. During the remodelling process, after implantation a delicate balance exists between ECM degradation and deposition of host collagen. The donor material of the ECM seems to in uence the rapidity of degradation of the mesh. High levels of hydroxyproline in collagenase assay suggest low resistance of the submucosa-based mesh to enzymatic degradation(37). This was illustrated in the present and previous experiments by the complete disappearance of the small intestine submucosa– based Surgisis, which makes long-term hernia repair questionable(34, 38). Meshes derived from dermis were observed to have little surface reduction in the present experiment, with a 20% reduction in non-crosslinked Strattice and 1% in crosslinked Permacol after 6 months.
Chemical crosslinking is performed to make biological meshes more resistant to matrix metalloproteases and native and bacterial collagenase. Our experiment also showed decreased surface reduction in the crosslinked group; however, when only dermal meshes were investigated, there was no di erence in surface reduction between non-crosslinked and crosslinked meshes. In the present experiment, under contaminated conditions, crosslinked meshes showed poor incorporation in the abdominal wall. The best incorporation was 21% by Permacol after 90 days, which was decreased to only 6% at 180 days. This disappointing incorporation of crosslinked meshes can be explained by delayed collagen degradation, leading to decreased angiogenesis and in ammation due to foreign body reaction resulting in poor tissue integration and adhesion formation(14, 24, 26, 27). This foreign body reaction can be provoked by exposure of antigenic epitopes known to hinder successful xenotransplantation. For example, galactose-alpha-1,3- galactose (alpha-gal) is proven to be present in the ECM of non-crosslinked Surgisis(39). Crosslinking can initially mask these antigenic epitopes, but with mesh degradation, epitopes become exposed(40, 41). Exposure of epitopes leads to production of antibodies in humans and primates activating humoral immune and complement response(39, 42). Adhesion formation seems to be
294