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It is customary to analyse scoliosis as a mechanical failure: first there is a straight spine (=normal), then an habitual and collapsing posture (=disease) and finally, structural remodelling (Hueter-Volkmann effect = scoliosis). This hypothesis makes two practical predictions:

  1. There is a disease process causing the pathological posture. The purpose of gatherings such as this is to identify this pathology, thus far without success.

  2. Early diagnosis will permit early non-operative treatment which will halt or reverse the remodelling and reduce the occurrence of severe deformity and the need for corrective spinal surgery.

The failure of school scoliosis screening to achieve this end is well documented, but the consequence for the underlying hypothesis has not been analysed. Screening failed, not because it was unable to detect scoliosis, but because scoliosis did not behave as the hypothesis predicted.

Disease process: All theories presume some form of neurological or muscular deficit as the final pathway but while the variety is wide, e.g. (historically) anterior poliomyelitis; more recently proprioceptive defect, melatonin or calmodulin disorder, there is no clear evidence for such a deficit in adolescent idiopathic scoliosis (AIS). Of 1342 screening referrals to this centre, 10 had a neurological diagnosis (most of which were already known to the patients) and 598 had radiologically confirmed AIS. In contrast, 1707 referrals to the general clinics included 410 syndromic cases and 420 AIS. Patients with a neurological problem, by and large, find their own way to medical attention. The hypothesis does not explain the natural history or the aetiology, and awkward observations, such as the association with growth (Goldberg et al Spine.18(5):529–535.1993, Eur Spine J.2:29–36.1993 and, most recently, Ylikoski M. Journal of Pediatric Orthopaedics B.14:320–324, 2005) or the higher incidence in ballet dancers (Warren et al. New England Journal of Medicine.314(21):1348–1353.1986) and rhythmic gymnasts (Tanchev et al. Spine.25(11):1367–1372.2000) are ignored.

Screening: Screening programmes (e.g. Goldberg et al., Spine.20(12):1368–1374, 1995) showed that there was no precise demarcation between “scoliosis” and “normal,” and that there was no benefit in terms of the need for surgical correction from screening or bracing, (Goldberg et al. Spine.26(1):42–47, 2001).

Discussion: his information has been in the public domain for some years and, in the meanwhile, there have been huge advances in biology and medicine which must have relevance. When the predictions of a hypothesis are not confirmed, that hypothesis must at least be re-examined, and it is not necessary to wait until a replacement can be suggested. The undisputed aspects of scoliosis, such as association with growth rate and maturation, lateralisation, gender predominance, normal distribution of Cobb angle and asymmetry over the wider population, essential health and normality of those with even severe deformity, increased incidence in other conditions, all suggest a different model. This is an opportune time to pause and reconsider the underlying model of scoliosis in the light of what we have learned about scoliosis and what is now known in other disciplines about how morphology is determined and evolved.

Correspondence should be addressed to Jeremy C T Fairbank at The Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX7 7LD, UK