Scoliosis BioMed Central Review Open Access 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 Ian AF Stokes1, R Geoffrey Burwell*2 and Peter H Dangerfield3 Address: 1Department of Orthopaedics and Rehabilitation, University of Vermont, Burlington, Vermont 05405, USA, 2The Centre for Spinal Studies & Surgery, Queen's Medical Centre, Nottingham, NG7 2UH, UK and 3Sherrington Buildings, Ashton Street, Liverpool, L69 3GE, UK Email: Ian AF Stokes - [email protected]; R Geoffrey Burwell* - [email protected]; Peter H Dangerfield - [email protected] * Corresponding author Published: 18 October 2006 Received: 08 August 2006 Accepted: 18 October 2006 Scoliosis 2006, 1:16 doi:10.1186/1748-7161-1-16 This article is available from: http://www.scoliosisjournal.com/content/1/1/16 © 2006 Stokes et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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. Background pragmatic with a very incomplete scientific basis. The In the absence of any generally accepted scientific theory International Federated Body on Scoliosis Etiology (IBSE) for the etiology of idiopathic scoliosis, treatment remains [1] introduced the Electronic Focus Group (EFG) as a Page 1 of 21 (page number not for citation purposes) Scoliosis 2006, 1:16 http://www.scoliosisjournal.com/content/1/1/16 means of increasing debate of knowledge on important calculated loading asymmetry of a growing spine with topics. The text for this debate was written by Dr Ian scoliosis created by a neuromuscular activation strategy, Stokes who addresses the concept of mechanical modula- together with (2) the measured bone growth sensitivity to tion of vertebral body growth in the pathogenesis of pro- altered compression could explain (3) the observed rate of gressive adolescent scoliosis generally attributed to the scoliosis progression during adolescent growth. The Hueter-Volkmann or Delpech effect [1-25] in which con- model assumes that (1) a pre-existing scoliosis curve of stant pathologic strong pressure inhibits endochondral unknown etiology initiates the mechanically modulated longitudinal growth while reduced compression acceler- alteration of growth that in turn causes worsening of the ates growth [2-4]; pressure exerted eccentrically causes an scoliosis, (2) everything else is anatomically and physio- active change in the direction of growth [2,5-7]. Brace logically 'normal', and (3) loading sustained over a sub- treatment is based on this effect although the efficacy of stantial proportion of the day modulates endochondral bracing continues to be debated and questioned [26-39] bone growth, whereas transient loading does not. The while exercises are not even considered by many clini- forces due to muscle activation are generally of greater cians. Guidelines for the conservative management of sco- magnitude than forces due to superimposed body weight liosis by physical therapy, intensive rehabilitation and [52]. The simulations employ newly-available data on the brace treatment have been published recently [37,38]; on magnitude of asymmetric loading imposed on the spine evidence-based medicine [40,41] bracing and exercises gave as a function of the scoliosis curve, and of the resulting a grade of evidence C (level of evidence IV)[37] (i.e. expert mechanically altered vertebral growth. The effects of committee reports or opinions and/or clinical experience intervertebral disc wedging were included only indirectly of respected authorities indicating that directly applicable by prior knowledge of their relationship to vertebral clinical studies of good quality are absent). Since it is gen- wedging. The findings are consistent with the vicious cycle erally recognized that multi-level arthrodesis of the spine hypothesis of pathogenesis namely that in progressive ado- is not a desirable outcome, currently there is renewed lescent idiopathic scoliosis (AIS) frontal plane vertebral interest in modifying vertebral growth by early surgical body wedging during growth results from asymmetric interventions [42-44] including stapling and, in young neuromuscular loading. children, fusionless scoliosis surgery [45] which is being evaluated experimentally in animals [46-48]. The research engenders controversy, including: The mechanical modulation of vertebral growth in the 1. Are the results applicable to humans who lack ossified presumed asymmetrically loaded spine with scoliosis was vertebral body epiphyses and have "ring" apophyses? described by Stokes as a 'vicious cycle' and interpreted by his vicious cycle hypothesis of pathogenesis [3,4]. Roaf [10] 2. Are there separate initiating (? discal, vertebral, costal or had previously used the term 'vicious circle' to describe the neuromuscular) and progressive (mechanical and non- effects of gravity on thoracic vertebral endplate physes in mechanical) factors for AIS pathogenesis? Scheuermann's disease whatever the primary cause of that deformity. The implication is that independent of 3. Are vertebral endplate physes normal when the growth whether a scoliosis is congenital, neuromuscular, or idio- modulation starts? pathic, mechanical factors become predominant relative to initiating factors during rapid adolescent growth, when 4. Whether healthy adolescents can spontaneously gener- the risk of curve progression is greatest [49-51]. While ate asymmetrical vertebral growth and deformity by inap- qualitatively attractive, the validity of this mechanical propriate neuromuscular activation strategies. stress-growth relationship hypothesis remains to be proven. Proof requires quantitative information about the loading 5. Do the findings have relevance to treatment? Or, is the state of the spine with scoliosis, consequential growth resurrection of exercise programs for AIS a step too far? alterations and geometrical changes all of which are addressed here. 6. Why does asymmetric loading on the spine from pelvic tilt scoliosis not lead to curve progression? The Statement of this EFG is drawn from biomechanical studies that Dr Stokes has pursued in recent years relating 7. Does movement asymmetry of both hips during gait to a mathematical simulation of the vicious cycle hypothesis cause idiopathic scoliosis? for the pathogenesis of adolescent scoliosis. A frontal plane model was designed because very little is known 8. Why do normal sagittal spinal curves not progress from about the details of how the loads are transmitted through front-back asymmetric vertebral loading? the spine in three-dimensions. The model, involving geo- metric recursive/growth analysis, tested whether (1) the Page 2 of 21 (page number not for citation purposes) Scoliosis 2006, 1:16 http://www.scoliosisjournal.com/content/1/1/16 9. Might not patients with severe curves have, in addition dimensional quantitative models that incorporate to the hypokyphosis, a slightly postero-lateral asymmetric intervertebral discs and simulate thoracic as well as lum- load on endplate physes? bar scoliosis. An urgent challenge is to be able to distin- guish the factors that predict whether a curve is 10. Do neurogenic thoracic scolioses result from different progressive