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CXCR4 Antagonism to Treat Delayed Fracture Healing

Meeson, R L; Sanghani, A; Coathup, M; Blunn, G

Authors

R L Meeson

A Sanghani

M Coathup

G Blunn



Abstract

A significant number of fractures develop non-union. Stem cell homing is regulated through SDF-1 and its receptor CXCR4. Stem/progenitor cell populations can be endogenously mobilised by administering growth factors with a pharmacological antagonist of CXCR4, AMD3100, which may be a means to improve fracture healing. Methods: A 1.5mm femoral osteotomy in Wistar rats was stabilised with an external fixator. Rats were pre-treated with PBS(P), VEGF(V), IGF-1(I) or GCSF(G) prior to AMD3100. A control group (C) did not receive growth factors or AMD3100. Bone formation after five weeks was analysed. Results: Group P had a significant increase in total bone volume (p=0.01) and group I in % bone in the fracture gap (p=0.035). Group G showed a decrease in bone volume. All treated groups had an increase in trabecular thickness. Histology showed decreased cartilage tissue associated with increased bone in groups with improved healing, and increased fibrous tissue in poorly performing groups. Conclusion: Antagonism of SDF1-CXCR4 axis can boost impaired fracture healing. AMD3100 given alone was the most effective means to boost healing whilst pre-treatment with GCSF reduced healing. AMD3100 is likely mobilizing stem cells into the blood stream that home to the fracture site enhancing healing.

Citation

Meeson, R. L., Sanghani, A., Coathup, M., & Blunn, G. (2019). CXCR4 Antagonism to Treat Delayed Fracture Healing. https://doi.org/10.1089/ten.TEA.2018.0265

Journal Article Type Article
Acceptance Date Jan 1, 2019
Publication Date Jan 5, 2019
Deposit Date Jan 16, 2019
Publicly Available Date Jan 22, 2019
Journal Tissue Engineering Part A
Peer Reviewed Peer Reviewed
Volume 25
Issue 17-18
DOI https://doi.org/10.1089/ten.TEA.2018.0265
Public URL https://rvc-repository.worktribe.com/output/1384092

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