There are many conflicting actiological theories for adolescent idiopathic scoliosis. We present a simple new model of scoliosis and a mechanism by which it is initiated and progresses. This mechanism provides a final common pathway for the multiple aetiological factors. A simple model of the spine, incorporating its fundamental mechanical features, was constructed. The model consisted of interconnected anterior compression and posterior tension columns. It allowed normal spinal movements, with flexion limited by the posterior column and rotation centered around the anterior column. It also allowed deformities to develop. The ends of the model were fixed in the position of the vertebrae they represented. Overgrowth of the anterior column relative to the posterior column caused the model to take up the shape of an idiopathic scoliosis. The greater the overgrowth, the more marked the deformity. Normally anterior and posterior column growth are coupled. During the growth spurt the thoracic kyphosis flattens indicating that anterior growth temporarily exceeds posterior growth. If this over-growth is marked a scoliosis will develop, as demonstrated by the model. Once this occurs the coupling is lost, anterior growth further outstrips posterior growth and the deformity progresses. Not all scolioses worsen, as the tendency to progress is balanced by neuromuscular factors and remodelling. Factors that increase the growth rate, induce asymmetry or decrease the inherent stability of the spine all encourage the development and progression of a scoliosis. This explains the complex biomechanics of scoliosis and provides a final common pathway by which the multiple aetiological factors can induce idiopathic scoliosis. It has important implications for the understanding and treatment of this condition.