CXCR4 Antagonism to Treat Delayed Fracture Healing.

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.

VEGF with AMD3100 endogenously mobilizes mesenchymal stem cells and improves fracture healing.

A significant number of fractures develop non-union. Mesenchymal stem cell (MSC) therapy may be beneficial, however, this requires cell acquisition, culture and delivery. Endogenous mobilization of stem cells offers a non-invasive alternative.