A Short Commentary about Efficacy of an Flowable Matrix (Integra) in the Treatment ofDFU

What is it about?

Collagen scaffolds must prevent the scarring response and therefore the contracture; the scar by nature is populated by myofibroblasts and contracted, the matrix serves to prevent this and regenerate a tissue as similar as possible to the original tissue. The peculiar skill to regeneration of collagen-based scaffolds particularly open structure and very large, was related with a decrease in wound contraction. However, collagen-based scaffolds do not all have the same regenerative depending on detailed structural features. The level of activity depends on often subtle but distinct structural differences: pore structure, degradation rate and surface chemistry.

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Why is it important?

The average pore diameter required should remain within a range 20-125μm. A pore size of less than 20μm does not allow the cells to come in; at the high end of the pore size range the cells do not come into direct contact with the scaffold surface, but are organized in cell-cell clusters. Wound contraction is further inhibited and dermis regeneration induced when the scaffold degradation rate is about 2-3 weeks in skin. MFB are known to migrate inside the scaffold and adhere on the scaffold surface during this period [23]; in so doing, these cells lose cell-cell contacts that appear to be required for development of large contractile forces. They differed, however, in their cross-link density which is known to control the degradation half-life of the two scaffolds to different level . In skin lesions treated with a scaffold that degradation rate is about 2-3 weeks a MFB reductions was viewed. Disorganization with loss of alignment in the same plane of MFB, drastic reduction in MFB density was relieved in skin lesion treated with Derma Regeneration Template scaffolds [21]. A change in the phenotype of MFB was directly observed as, dispersion of MFB assemblies and when Derma Regeneration Template (DRT-integra). This change is explained most simply by inhibition of MFB-MFB binding and facilitation instead of MFB-DRT binding, by MFB integrins (α1 β1 and α2 β1) and ligands on the DRT scaffold.

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