Molecular Mechanisms Controlling Bone Formation during Fracture Healing and Distraction Osteogenesis

By Z. S. AI-Aql, A. Alagl, D. Graves, L. Gerstenfeld, T. Einhorn. Journal of dentistry research, 2008

691 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Bone regeneration strategies: engineered scaffolds, bioactive molecules and stem cells Current stage and future perspectives (2018, positive): “The local hypoxia at the fracture site induces production of angiogenic factors such as VEGF to stimulate neo-angiogenesis [21].”
Fracture healing under healthy and inflammatory conditions (2012, background): “A large number of proinflammatory cytokines (IL-1, IL-6, TNF, receptor activator of nuclear factor κB ligand [RANKL], macrophage colony-stimulating factor 1) and members of the transforming growth factor (TGF)-β superfamily (bone morphogenetic protein [BMP]-2, BMP-4, BMP-5, BMP-6) are released early”
The roles of vascular endothelial growth factor in bone repair and regeneration (2016, background): “Unlike bone repair, bone regeneration is a process in which a relatively large amount of new bone is formed in response to external stimulators, such as mechanical force, exogenous bony tissues or bone forming cells [1].”