CXCR4 Antagonism to Treat Delayed Fracture Healing

Tissue Eng Part A. 2019 Sep;25(17-18):1242-1250. doi: 10.1089/ten.TEA.2018.0265. Epub 2019 Jun 14.

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.

Keywords: AMD3100; CXCR4; delayed union; endogenous mobilization; external fixator; fracture healing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzylamines
  • Cyclams
  • External Fixators
  • Female
  • Fracture Healing / drug effects
  • Fracture Healing / physiology*
  • Heterocyclic Compounds / pharmacology
  • Rats
  • Rats, Wistar
  • Receptors, CXCR4 / antagonists & inhibitors
  • Receptors, CXCR4 / metabolism*
  • Tibial Fractures / diagnostic imaging
  • Tibial Fractures / metabolism
  • X-Ray Microtomography

Substances

  • Benzylamines
  • Cxcr4 protein, rat
  • Cyclams
  • Heterocyclic Compounds
  • Receptors, CXCR4
  • plerixafor