Biomechanical spinal growth modulation and progressive adolescent scoliosis--a test of the 'vicious cycle' pathogenetic hypothesis: summary of an electronic focus group debate of the IBSE

Abstract

There is no generally accepted scientific theory for the causes of adolescent idiopathic scoliosis (AIS). As part of its mission to widen understanding of scoliosis etiology, the International Federated Body on Scoliosis Etiology (IBSE) introduced the electronic focus group (EFG) as a means of increasing debate on knowledge of important topics. This has been designated as an on-line Delphi discussion. The text for this debate was written by Dr Ian A Stokes. It evaluates the hypothesis that in progressive scoliosis vertebral body wedging during adolescent growth results from asymmetric muscular loading in a "vicious cycle" (vicious cycle hypothesis of pathogenesis) by affecting vertebral body growth plates (endplate physes). A frontal plane mathematical simulation tested whether the calculated loading asymmetry created by muscles in a scoliotic spine could explain the observed rate of scoliosis increase by measuring the vertebral growth modulation by altered compression. The model deals only with vertebral (not disc) wedging. It assumes that a pre-existing scoliosis curve initiates the mechanically-modulated alteration of vertebral body growth that in turn causes worsening of the scoliosis, while everything else is anatomically and physiologically 'normal' The results provide quantitative data consistent with the vicious cycle hypothesis. Dr Stokes' biomechanical research engenders controversy. A new speculative concept is proposed of vertebral symphyseal dysplasia with implications for Dr Stokes' research and the etiology of AIS. What is not controversial is the need to test this hypothesis using additional factors in his current model and in three-dimensional quantitative models that incorporate intervertebral discs and simulate thoracic as well as lumbar scoliosis. The growth modulation process in the vertebral body can be viewed as one type of the biologic phenomenon of mechanotransduction. In certain connective tissues this involves the effects of mechanical strain on chondrocytic metabolism a possible target for novel therapeutic intervention.

Figure 1

Spinal growth (T3-L5) during adolescence, as shown by a cross-sectional study of spinal length, and the contributions from total vertebral height, and from total disc height. Lengths were obtained from stereoradiographic reconstructions of patients in a scoliosis clinic [83].

Figure 2

Simulated evolution of the thoracolumbar scoliosis as a result of mechanically modulated asymmetrical growth. The initial geometry (unfilled shapes, and '+' indicating thoracic vertebrae) is the starting geometry at age 11 years (26 degrees Cobb lumbar scoliosis). The final geometry (filled shapes) is averaged from the model-predicted final shapes for all 11 analysed loading directions at age 16 years. Note that only the vertebrae grow asymmetrically and develop progressive wedging in this simulation – the discs do not change shape.

Figure 3

Diagram of vertebral body growth including that from the neurocentral synchondroses (neurosomatic growth cartilages); the latter are shown by the smallest arrows as growing postero-laterally. The increase in dimensions of the vertebral body shown as a concentric (ellipsoid) simulates radial vertebral body growth. It is proposed that the increased girth of the vertebral body leads to increased axial loading indicated by the weights of the larger arrows placed above and below it.