LAUSR

Synthetic scaffolds, as bone grafts, provide a favorable environment for the repair and growth of new bone tissue at defect sites. However, the lack of angio- and osteo-induction limits the usefulness of artificial scaffolds for bone regeneration. Nitric oxide (NO) performs essential roles in healing processes, such as regulating inflammation and addressing incomplete revascularization. In this study, we developed a polymer capable of controlled NO release to promote the osteogenic capacity in artificial scaffolds. The biological efficiency of the NO compound was assessed by its effect on pre-osteoblasts and macrophages in vitro and the extent of vascularization and bone formation in the calvaria defect model in vivo. The compound did not inhibit cell adhesion or proliferation. NO treatment significantly increased both alkaline phosphatase activity and mineralization in pre-osteoblasts. Macrophages treated with NO secreted high levels of anti-inflammatory factors and adopted the pro-regenerative M2 phenotype. In the critical-sized defect model, the collagen scaffold containing the NO compound enhanced neovascularization and bone formation. The developed NO-releasing system promoted osteogenesis and regeneration of damaged bone tissue. As the multiple functions of NO involve macrophage modulation and angiogenesis, such release systems may be valuable for guiding bone regeneration in critical-sized defects. This article is protected by copyright. All rights reserved.