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Samir Aït Saïd, a French gymnast, took to the mat in Rio to prepare for a qualifying round of vaulting during the recent summer Olympics. As he landed from an aerial display of backflips,
the impact broke both the tibia and fibula in his left leg; a brutal set of injuries that will most likely cut short a young career. Beyond the Olympics and professional athletics, these
kinds of injuries can also have long-term health consequences, especially as people age and their bones become more fragile. Science and technology in orthopedic medicine have improved
dramatically in recent decades, but researchers continue to look for improved methods to help accelerate healing in damaged bones. Credit: Sciepro, Getty Ling Qin, professor at the
Musculoskeletal Research Laboratory at the Chinese University of Hong Kong, specializes in studying musculoskeletal injuries and developing methods to facilitate bone formation, or
osteogenesis. Previous work from Qin's lab has demonstrated the importance of magnesium for bone growth, but a recent paper in _Nature Medicine_ provides a number of novel mechanistic
insights and a new tool that could translate into the clinic (http://dx.doi.org/10.1038/nm.4162; published online 20 August 2016). Using pure magnesium rods surgically implanted into intact
and fractured femurs of rodent models, Qin and colleagues studied how signaling from sensory nerves located in the periosteum—connective tissue that covers the surface of bone—can affect
osteogenesis. Compared to animals with implanted stainless steel rods, animals with magnesium rods showed increased osteogenesis, but removing the sensory nerves to the periosteum, through
capsaicin ablation of dorsal root ganglia (DRG), eliminated these gains. Qin's team looked more deeply into the molecular mechanism and found that magnesium-induced bone growth was
accompanied by increased levels of neuronal calcitonin gene-related polypeptide-α (CGRP), a peptide released by DRG neurons. The team established a causative role for CGRP-signaling using
functional knockdown and overexpression of _Calcrl_ and _Ramp1_, genes that encode CGRP receptors. While these mechanistic details provide a better understanding of how magnesium induces
bone growth, the authors noted that the magnesium rods failed to fix femoral fractures in experimental animals, most likely owing to magnesium's rapid degradation after implantation and
deterioration of mechanical support for the bone. To enable real-world application of magnesium's osteogenic properties, they developed a magnesium intramedullary nail (Mg-IMN) that
supplies magnesium, but resists structural breakdown. Their results showed accelerated healing of fractures with the Mg-IMN compared to traditional IMNs, giving the rats—and perhaps one day
humans—a leg up on bone healing. Authors * Dustin M. Graham View author publications You can also search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and
permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Graham, D. A leg up on bone-fracture healing. _Lab Anim_ 45, 347 (2016). https://doi.org/10.1038/laban.1124 Download citation * Published: 21
September 2016 * Issue Date: October 2016 * DOI: https://doi.org/10.1038/laban.1124 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get
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