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The composites showed appropriate physical and biological properties creating more biologically active scaffolds that may support bone growth.
In this study, we investigated whether coimplantation of MSCs which have been predifferentiated in vitro into SMCs (SMC MSCs) may enable pbEPCs to form blood vessels upon implantation and, if this would be the case, whether the resulting enhanced vascularization may support bone regeneration.
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Thus, siPHD2 had the opportunity to act on other cells besides the bone precursors, although the siPHD2-driven vascular phenotype may support the regeneration of bone by supporting the nutrient supply to the growing bone.
Based on these findings, we speculate that the induction of these three pro-angiogenic genes may support new vasculature for bone induction during ME.
These results may support our findings that the bone marrow present in the NCB increases the strength and stiffness and therefor PE treatment itself is not the only parameter responsible for the alteration of the biomechanical properties of CBG.
The resulting loss of supporting bone may lead to loosening of the implants requiring difficult revision surgery.
Individuals with a history of periodontitis and loss of supporting bone may experience more implant loss and complications around implants than non-periodontitis patients [ 4].
These results may support a role of cell-mediated inflammation in bone metabolism.
The behaviour in this biomimetic in vitro system suggests that ESLs may support the recruitment of CTCs from circulation to the bone endothelium in vivo.
Differences in protein adsorption may support the initial colonization of tumor cells extravasated from blood vessels into the bone microenvironment.
It may be manifested by materials supporting bone cell attachment, proliferation and differentiation (biocompability/osteconductivity), and/or by materials inducing/promoting the expression of multiple bone-related genes that drive osteogenesis (osteoinductivity).
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