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. 2011 May;212(5):880-8.
doi: 10.1016/j.jamcollsurg.2011.01.006. Epub 2011 Mar 23.

Histologic and biomechanical evaluation of crosslinked and non-crosslinked biologic meshes in a porcine model of ventral incisional hernia repair

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Histologic and biomechanical evaluation of crosslinked and non-crosslinked biologic meshes in a porcine model of ventral incisional hernia repair

Corey R Deeken et al. J Am Coll Surg. 2011 May.

Abstract

Background: The objective of this study was to evaluate the biomechanical characteristics and histologic remodeling of crosslinked (Peri-Guard, Permacol) and non-crosslinked (AlloDerm, Veritas) biologic meshes over a 12 month period using a porcine model of incisional hernia repair.

Study design: Bilateral incisional hernias were created in 48 Yucatan minipigs and repaired after 21 days using an underlay technique. Samples were harvested at 1, 6, and 12 months and analyzed for biomechanical and histologic properties. The same biomechanical tests were conducted with de novo (time 0) meshes as well as samples of native abdominal wall. Statistical significance (p < 0.05) was determined using 1-way analysis of variance with a Fisher's least significant difference post-test.

Results: All repair sites demonstrated similar tensile strengths at 1, 6, and 12 months and no significant differences were observed between mesh materials (p > 0.05 in all cases). The strength of the native porcine abdominal wall was not augmented by the presence of the mesh at any of the time points, regardless of de novo tensile strength of the mesh. Histologically, non-crosslinked materials showed earlier cell infiltration (p < 0.01), extracellular matrix deposition (p < 0.02), scaffold degradation (p < 0.05), and neovascularization (p < 0.02) compared with crosslinked materials. However, by 12 months, crosslinked materials showed similar results compared with the non-crosslinked materials for many of the features evaluated.

Conclusions: The tensile strengths of sites repaired with biologic mesh were not impacted by very high de novo tensile strength/stiffness or mesh-specific variables such as crosslinking. Although crosslinking distinguishes biologic meshes in the short-term for histologic features, such as cellular infiltration and neovascularization, many differences diminish during longer periods of time. Characteristics other than crosslinking, such as tissue type and processing conditions, are likely responsible for these differences.

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Figures

Figure 1
Figure 1
Biomechanical characteristics of mesh-repaired sites over time compared with de novo strength and native porcine abdominal wall. (A) Maximum load (Newton [N]), (B) tensile strength (N/cm), (C) stiffness (N/mm). All 4 meshes were significantly stronger and stiffer at time 0 compared with their corresponding repair sites (mesh-abdominal wall tissue composites) after 1, 6, or 12 months (p < 0.01 for all comparisons). Although significant differences were observed between the strengths and stiffnesses of the 4 meshes at time 0, no significant differences were detected between mesh-repaired sites at 1, 6, or 12 months due to the type of mesh used to repair the defect (p > 0.05 in all cases). In addition, no significant differences in strength or stiffness of the repair site were detected over time for any of the meshes used (p > 0.05 in all cases). Abd, abdominal.
Figure 2
Figure 2
Composite scores for both non-crosslinked meshes (Veritas and AlloDerm) were significantly higher than the composite scores for both crosslinked meshes (Permacol and Peri-Guard), p < 0.05 and Veritas scored higher than AlloDerm; p < 0.05.
Figure 3
Figure 3
Histologic scores, separated by mesh type and length of time in vivo. (A) Cellular infiltration scores demonstrated that the non-crosslinked meshes (Veritas and AlloDerm) initially permitted more cellular infiltration than the crosslinked meshes (Permacoland Peri-Guard); p < 0.008. By 6 and 12 months, this trend disappeared and all meshes achieved equivalent cellular infiltration (p > 0.05). (B) Cell types scores revealed that fewer inflammatory cells and more fibroblasts were detected at 1 and 6 months in Peri-Guard compared with AlloDerm (p < 0.02), and all other comparisons at these time points were not significant (p > 0.05). By 12 months, Veritas exhibited the greatest number of fibroblasts and least inflammatory infiltrate compared with the other 3 materials (p < 0.04). (C) Extracellular matrix (ECM) deposition scores at 1 month demonstrated that the non-crosslinked meshes (Veritas and AlloDerm) initially permitted more cellular infiltration than the crosslinked meshes (Permacoland Peri-Guard); p < 0.02. At 6 months, Veritas, AlloDerm, and Permacol all demonstrated greater ECM deposition than Peri-Guard (p < 0.02), and by 12 months, the only remaining difference was that Veritas exhibited the highest level of ECM deposition compared with Peri-Guard and AlloDerm (p < 0.03). (D) Scaffold degradation scores showed that non-crosslinked meshes (Veritas and AlloDerm) were markedly more degraded at 1 and 6 months compared with the crosslinked meshes (Permacoland Peri-Guard); p < 0.03. Veritas also exhibited significantly more scaffold degradation than the other non-crosslinked mesh, AlloDerm, at both 1 and 6 months (p = 0.010 and p = 0.002, respectively). (E) Fibrous encapsulation scores revealed that Veritas was significantly less encapsulated (higher score means less encapsulation) than all other meshes at 1 month (p < 0.01). By 6 months, both non-crosslinked materials (AlloDerm and Veritas) scored similarly, and both were significantly less encapsulated than the crosslinked meshes (p < 0.001). However, at 12 months, the crosslinked meshes showed decreasing levels of encapsulation, suggesting that this process might be reversible. (F) Neovascularization scores were significantly higher for both non-crosslinked meshes (Veritas and AlloDerm) at 1 and 6 months compared with both crosslinked meshes (Permacoland Peri-Guard); p < 0.05. By 12 months, however, Veritas and AlloDerm reached significance only in comparison with Peri-Guard, but not Permacol (p < 0.01).
Figure 4
Figure 4
Photographs of hematoxylin and eosin–stained specimens of each mesh-repaired site after 1, 6, and 12 months in vivo (100× magnification).

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