Relative anterior spinal overgrowth in adolescent idiopathic scoliosis--result of disproportionate endochondral-membranous bone growth? Summary of an electronic focus group debate of the IBSE

Abstract

There is no generally accepted scientific theory for the etiology 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 EFG was written by Professor Jack Cheng and his colleagues who used whole spine magnetic resonance imaging (MRI) to re-investigate the relative anterior spinal overgrowth of progressive AIS in a cross-sectional study. The text is drawn from research carried out with his co-workers including measurement of the height of vertebral components anteriorly (vertebral body) and posteriorly (pedicles) in girls with AIS and in normal subjects. The findings confirm previous anatomical studies and support the consensus view that in patients with thoracic AIS there is relatively faster growth of anterior and slower growth of posterior elements of thoracic vertebrae. The disproportionate anteroposterior vertebral size is associated with severity of the scoliotic curves. In interpreting the findings they consider the Roth/Porter hypothesis of uncoupled neuro-osseous growth in the spine but point out that knowledge of normal vertebral growth supports the view that the scoliosis deformity in AIS is related to longitudinal vertebral body growth rather than growth of the canal. In the mechanical mechanism (pathomechanism) they implicitly adopt the concept of primary skeletal change as it affects the sagittal plane of the spine with anterior increments and posterior decrements of vertebral growth and, in the biological mechanism (pathogenesis) propose a novel histogenetic hypothesis of uncoupled endochondral-membranous bone formation. The latter is viewed as part of an 'intrinsic abnormality of skeletal growth in patients with AIS which may be genetic'. The hypothesis that AIS girls have intrinsic anomalies (not abnormalities) of skeletal growth related to curve progression and involving genetic and/or environmental factors acting in early life is not original. While the findings of Professor Cheng and his colleagues have added MRI data to the field of relative anterior spinal overgrowth in AIS their interpretation engenders controversy. Three new hypotheses are proposed to interpret their findings: (1) hypoplasia of articular processes as a risk factor for AIS; (2) selection from the normal population to AIS involves anomalous vertebral morphology and soft tissue factors--this hypothesis may also apply to certain types of secondary scoliosis; and (3) a new method to predict the natural history of AIS curves by evaluating cerebro-spinal fluid (CSF) motion at the cranio-cervical junction. What is not controversial is the need for whole spine MRI research on subjects with non-idiopathic scoliosis.