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.

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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 (; 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.