Idiopathic scoliosis: biomechanics and biology.

For whatever reason, right-left asymmetry has attracted an illogical proportion of research effort. Non-structural scoliosis, for example secondary to a leg length inequality, is indeed a problem of right-left asymmetry, but structural scoliosis is a complex three-dimensional deformity involving all planes. Biomechanical, biological and clinical evidence indicates clearly that the problem is one of front-back asymmetry and not right-left. The importance of biological factors lies in their ability to bring the spinal column to and beyond its buckling threshold. Thus a taller and more slender spine is more liable to bend and, being stiffer in the sagittal plane, favours movement into other planes. This epitomises the spine of the scoliosis patient who is growing faster with a spinal template similar to other family members allowing idiopathic scoliosis to express itself genetically. It is the opposite condition to idiopathic hyperkyphosis (Scheuermann's disease), but this deformity is rotationally stable, thus remaining in the sagittal plane. The presence of an adjacent area of lordo-scoliosis below the region of hyperkyphosis testifies to the common nature of the pathogenesis of idiopathic scoliosis and Scheuermann's disease. It is the area of compensatory hyperlordosis below the Scheuermann's area that has obligatorily buckled and represents a human model supporting the lordosis theory, as does surgically tethering the back of the young growing human spine, which crankshafts accelerated progression. Similarly the only successful animal model of the formation of idopathic follows creation of a lordotic spinal segment in an otherwise kyphotic spine. For centuries, engineers have recognised that the mechanical behaviour of a column under load is influenced by geometry, as well as by material properties; it is clear that the spinal column also obeys these well-described laws.