Bernard first established a connection between bone loss and idiopathic scoliosis in the 1980s.[3] Recent epidemiological studies have demonstrated that many patients with scoliosis display lower bone density and quality in both axial and peripheral skeletal regions, suggesting that diminished bone mass may contribute to the pathogenesis of scoliosis.[4–6] Nuclear factor kB receptor activator (RANK), its ligand (RANKL), and osteoprotegerin (OPG) are key regulators of bone loss. This evidence concerns the gene TNFRSF11B and scoliosis.