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Published in: Calcified Tissue International 6/2016

Open Access 01-12-2016 | Original Research

Osthole Promotes Endochondral Ossification and Accelerates Fracture Healing in Mice

Authors: Zhongrong Zhang, Wing Nang Leung, Gang Li, Yau Ming Lai, Chun Wai Chan

Published in: Calcified Tissue International | Issue 6/2016

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Abstract

Osthole has been found to restore bone mass in preclinical osteoporotic models. In the present study, we investigated the effects of osthole on bone fracture repair in mice. Adult C57BL/6 mice were subjected to transverse femoral fractures and administrated orally with 20 mg/kg osthole and vehicle solvent daily from week 1 post-operation. Fracture callus were analyzed by plain radiography, micro-computed tomography, histology, molecular imaging and immunohistochemistry and tartrate-resistant acid phosphatase staining. Results demonstrated that osthole treatment enhanced removal of cartilage and bony union during reparative stage without significant interfering on remodeling process. In vivo molecular imaging showed bone formation rate of the treatment group was almost twofold of control group at week 2 post-operation. Osthole augmented the expression of alkaline phosphatase and collagen type X in hypertrophic chondrocytes as well as expression of bone morphogenetic protein-2, osteocalcin and alkaline phosphatase in osteoblastic cells, indicating it promoted mineralization of hypertrophic cartilage and woven bone growth simultaneously during endochondral healing. In summary, osthole promotes endochondral ossification via upregulation of maturation osteogenic marker genes in chondrocytes and subsequently accelerates fracture repair and bony fusion.
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Metadata
Title
Osthole Promotes Endochondral Ossification and Accelerates Fracture Healing in Mice
Authors
Zhongrong Zhang
Wing Nang Leung
Gang Li
Yau Ming Lai
Chun Wai Chan
Publication date
01-12-2016
Publisher
Springer US
Published in
Calcified Tissue International / Issue 6/2016
Print ISSN: 0171-967X
Electronic ISSN: 1432-0827
DOI
https://doi.org/10.1007/s00223-016-0189-4

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