Purpose: Complex ventral hernia repair is frequently performed with human acellular dermal matrix (HADM), as it remodels readily. Studies have yet to evaluate the tissue source, timing, and quantity of cellular and vascular infiltration into HADMs for ventral hernia repair. The impact of the biomaterial basement membrane (BM) on cellular and vascular infiltration also remains to be determined. We evaluated the in vivo metrics of fibrovascular remodeling with focus on the relative contribution from adjacent tissue (musculofascia versus fat) and BM effects on cellular and vascular infiltration in HADM.
Methods: An established acute ventral hernia model was used. Fifty-six guinea pigs underwent inlay, bridged ventral hernia repair with HADM (AlloDerm; LifeCell, Branchburg, NJ). HADMs were oriented with the BM toward or away from the peritoneal cavity. At postoperative week 1, 2, or 4, abdominal wall repairs were excised. Repair site adhesions (tenacity and surface area) were quantified. Histologic and immunohistochemical (factor VIII) analyses were performed to quantify cellular and vascular density within repair-site cross-sections, as well as within the interface (dorsal to musculofascial edge) and center (dorsal to subcutaneous fat) mesh zones. Subgroup analyses were performed; the quantity of cellular and vascular infiltration was compared as functions of BM orientation, location within the HADM, and post-implantation time.
Results: HADM infiltration with host cells and vessels increased over time in all groups. There were no differences in adhesion strength or surface area between groups. BM oriented away from the peritoneal cavity reduced vascular infiltration at all timepoints. The greatest magnitude of difference in vascular infiltration occurred in week 4 (68+/-36 versus 129+/-35 vessels/mm2; p = 0.002). In addition, vascular infiltration from the interface zone was greater than that from the center at all timepoints. Cellular infiltration was not significantly affected by BM orientation or adjacent tissue type (cross-section zone) at any timepoint.
Conclusion: HADM undergoes robust cellular and vascular infiltration within 4 weeks. HADM cellularization was not significantly affected by BM orientation or location within the repair site. However, HADM vascularization was delayed by the BM and slower underneath subcutaneous fat. These results suggest that both subcutaneous fat and musculofascia contribute to cellularization and vascularization of bridged HADM repairs, and that orienting the BM toward the peritoneal cavity may be advantageous for fibrovascular remodeling.