Abstract
Adolescent idiopathic scoliosis is a three-dimensional deformity of the spine and trunk that primarily affects previously healthy children. It is a classic orthopedic disorder. Despite many years of dedicated research into the etio-pathogenesis of idiopathic scoliosis, there is not one distinct cause for this condition and its etiology is called
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multifactorial. At present, no adequate causal treatment or preventive measures are available and apart from the impact of the spinal deformity on quality of life, scoliosis patients are also a considerable economic burden to society.
Adolescent idiopathic scoliosis is related exclusively to humans. The fully upright human posture and bipedal ambulation differs considerably from other bipedal species. Therefore, the way the upright human spine is biomechanically loaded, with its consequences for stability of the spine, is a unique feature of man. For better understanding the factors that play a role in the etio-pathogenesis of idiopathic scoliosis, the evolutionary features of upright spino-pelvic alignment and the role of posterior shear loads, rotational stability and pre-existent rotation, were explored in this thesis, using innovative image processing techniques.
Evidence from multiple imaging studies is provided that supports the hypothesis that the unique, fully upright spinal biomechanics of man play an important role in the initiation and progression of idiopathic scoliosis. We observed that the sagittal spinal profile determines why scoliosis occurs more in girls than in boys around the adolescent growth spurt. Our studies also demonstrated that once the spine decompensates into an idiopathic scoliosis it will follow the pre-existent rotational pattern of the nonscoliotic spine. This spinal deformation ultimately leads to a rather uniform pattern of rotated curvatures and has significant impact on quality of life.
We can conclude that adolescent idiopathic scoliosis has an intrinsic biomechanical basis: An imbalance between the biomechanical loading of the upright human spine (i.e. posteriorly directed shear loading) on the one hand and the body’s compensating mechanisms on the other. Our results support the posterior shear theory for the causation of this complex spinal disorder.
As research continues on the pathogenesis of idiopathic scoliosis, it can be expected that the role of biomechanics in the pathogenesis of AIS can be revealed, and possible risk factors for the development and progression of AIS can be identified at an early stage, when less invasive treatment is still an opportunity.
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