Abstract
Fracture healing is a complex physiological process. It involves the coordinated participation of haematopoietic and immune cells within the bone marrow in conjunction with vascular and skeletal cell precursors, including mesenchymal stem cells (MSCs) that are recruited from the surrounding tissues and the circulation. Multiple factors regulate this cascade of molecular events by affecting different sites in the osteoblast and chondroblast lineage through various processes such as migration, proliferation, chemotaxis, differentiation, inhibition, and extracellular protein synthesis. An understanding of the fracture healing cellular and molecular pathways is not only critical for the future advancement of fracture treatment, but it may also be informative to our further understanding of the mechanisms of skeletal growth and repair as well as the mechanisms of aging.
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