CXCR4 Antagonism to Treat Delayed Fracture Healing.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 30612520.
- Also identified by DOI 10.1089/ten.TEA.2018.0265 and PMC identifier 6864747.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Currently ∼10% of fractures progress to delayed or nonunion with significant morbidity and economic impact. Endogenous mobilization of stem cells by pharmacological antagonism of their homing and migration receptor CXCR4 with AMD3100 experimentally reduced delayed union development. Endogenous mobilization may, therefore, translate as a low risk means to boost healing and could potentially be given as a prophylaxis to patients with fractures at risk of delayed healing or nonunion. These patients may include fragility fractures, comminuted tibial fractures, or when treating established nonunions. This approach could have promise for other conditions that may benefit from stem cell treatments.
Medical subject headings
- Fracture Healing
- Receptors, CXCR4