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BACKGROUND: There are several commercially available acellular dermal matrices (ADM), whose properties vary according to their proprietary manufacturing processes. Survival and durability of any of these ADM depends on effective host cellular invasion and neovascularization. As cellular invasion and vascularization are crucial for ADM incorporation and survival, interventions that could expedite this process should be explored. We sought to quantitatively determine whether perforating ADM scaffolds would result in more rapid host cell invasion in a murine model of graft incorporation.
METHODS: 6mm diameter StratticeTM and XenmatrixTM scaffolds were created using a biopsy punch and perforated with a 26G needle, resulting in an evenly distributed “spoke and wheel” pattern of 1 perforation/1mm2 of scaffold surface area. Biomechanical testing was performed on perforated and non-perforated samples using a MTS Criterion™ Universal Test Systems machine. Scaffolds were implanted subcutaneously in the dorsa of C57BL6 mice and harvested after 14 and 28 days. Representative sections from post-harvest samples were stained and imaged. Immunohistochemical analysis was performed for CD31 (platelet endothelial cell adhesion molecule-1). Scaffolds were divided into 4 layers of 50 microns with increasing depth, and cell density was calculated using ImageJ. Densities were plotted according to layer depth, yielding an exponential decay graph. Exponential regression equations were then created and used to determine an “invasion coefficient.” Higher invasion coefficients correspond with increased degrees of cellular invasion in each layer of the ADM.
RESULTS: Biomechanical testing of perforated StratticeTM and XenmatrixTM demonstrated similar tensile strengths and failure forces when compared with their respective non-perforated samples. CD31 expression, a widely used marker for endothelial cells, was present at the 14 day time point only for perforated StratticeTM samples. At 28 days, CD31 positivity was noted in perforated and non-perforated StratticeTM samples. After 14 and 28 days, perforated StratticeTM exhibited a lower invasion coefficient when compared with non-perforated StratticeTM (0.464 vs. 0.498 and 0.627 vs. 0.657, respectively). Only with XenmatrixTM at 14 days was there a moderately higher invasion coefficient seen in perforated compared with non-perforated XenmatrixTM (0.472 vs. 0.450). After 28 days, the invasion coefficient for perforated XenmatrixTM was identical to non-perforated XenmatrixTM (0.475 vs. 0.474).
CONCLUSIONS: We have demonstrated that perforation of ADM likely does not alter the rate of cellular invasion after both 14 and 28 days. Biomechanical testing revealed that perforating ADM did not significantly diminish its tensile strength. CD31 expression in certain ADM suggests that there is, indeed, neovascularization in these scaffolds. These findings indicate that incorporating perforations of this size (464 µm in diameter) into ADM does not significantly improve scaffold cellular invasion or decrease the time to neovascularization and incorporation, leaving open the possibility that perforations of a different size may lead to improved clinical outcomes.