Bone healing and regeneration following fracture is a complex process, and an influx of inflammatory cells is known to be required for successful healing to occur. Xing and co-authors show that, in mice lacking the CCR2 chemokine receptor, which is required for monocyte trafficking and osteoclast function, fracture repair is significantly delayed. A better understanding of how inflammation regulates bone repair may lead to the development of new methods to optimize healing of traumatic skeletal injuries.

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