3D-printed bone regeneration scaffolds modulate bone metabolic homeostasis through vascularization for osteoporotic bone defects.

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  • Additional Information
    • Source:
      Publisher: Elsevier Science Country of Publication: Netherlands NLM ID: 8100316 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-5905 (Electronic) Linking ISSN: 01429612 NLM ISO Abbreviation: Biomaterials Subsets: MEDLINE
    • Publication Information:
      Publication: <1995-> : Amsterdam : Elsevier Science
      Original Publication: [Guilford, England] : IPC Science and Technology Press, 1980-
    • Subject Terms:
      Bone Regeneration*/drug effects ; Printing, Three-Dimensional* ; Osteoporosis*/metabolism ; Osteoporosis*/therapy ; Rats, Sprague-Dawley* ; Mesenchymal Stem Cells*/metabolism ; Mesenchymal Stem Cells*/cytology ; Tissue Scaffolds*/chemistry ; Osteogenesis*/drug effects ; Homeostasis* ; Neovascularization, Physiologic*/drug effects; Animals ; Polyesters/chemistry ; Cell Differentiation/drug effects ; Female ; Rats ; Endothelial Progenitor Cells/metabolism ; Bone and Bones/metabolism
    • Abstract:
      The treatment of osteoporotic bone defects poses a challenge due to the degradation of the skeletal vascular system and the disruption of local bone metabolism within the osteoporotic microenvironment. However, it is feasible to modulate the disrupted local bone metabolism imbalance through enhanced vascularization, a theory termed "vascularization-bone metabolic balance". This study developed a 3D-printed polycaprolactone (PCL) scaffold modified with EPLQLKM and SVVYGLR peptides (PCL-SE). The EPLQLKM peptide attracts bone marrow-derived mesenchymal stem cells (BMSCs), while the SVVYGLR peptide enhances endothelial progenitor cells (EPCs) vascular differentiation, thus regulating bone metabolism and fostering bone regeneration through the paracrine effects of EPCs. Further mechanistic research demonstrated that PCL-SE promoted the vascularization of EPCs, activating the Notch signaling pathway in BMSCs, leading to the upregulation of osteogenesis-related genes and the downregulation of osteoclast-related genes, thereby restoring bone metabolic balance. Furthermore, PCL-SE facilitated the differentiation of EPCs into "H"-type vessels and the recruitment of BMSCs to synergistically enhance osteogenesis, resulting in the regeneration of normal microvessels and bone tissues in cases of femoral condylar bone defects in osteoporotic SD rats. This study suggests that PCL-SE supports in-situ vascularization, remodels bone metabolic translational balance, and offers a promising therapeutic regimen for osteoporotic bone defects.
      Competing Interests: Declaration of competing interest The author has no conflict of interest.
      (Copyright © 2024 Elsevier Ltd. All rights reserved.)
    • Contributed Indexing:
      Keywords: 3D printing; Bone metabolism regulation; Bone regeneration; Osteoporotic bone defects; Porous PCL scaffold
    • Accession Number:
      0 (Polyesters)
      24980-41-4 (polycaprolactone)
    • Publication Date:
      Date Created: 20240709 Date Completed: 20240804 Latest Revision: 20240804
    • Publication Date:
      20240805
    • Accession Number:
      10.1016/j.biomaterials.2024.122699
    • Accession Number:
      38981153