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Body mass index in relation to truncal asymmetry of healthy adolescents, a physiopathogenetic concept in common with idiopathic scoliosis: summary of an electronic focus group debate of the IBSE

Theodoros B Grivas1, R Geoffrey Burwell2 and Peter H Dangerfield345*

Author Affiliations

1 Department of Trauma and Orthopedics, “Tzanio” General Hospital, Tzani and Afendouli 1st, Piraeus 18536, Greece

2 Centre for Spinal Studies and Surgery, Nottingham University Hospitals Trust, Queen’s Medical Centre Campus, Derby Road, Nottingham NG7 2UH, UK

3 University of Liverpool, Ashton Street, L69 3GE, Liverpool, UK

4 Staffordshire University, Leek Road, Stoke-on-Trent ST4 2DF, UK

5 Royal Liverpool Children’s Hospital, Eaton Road, Liverpool L12 2AP, UK

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Scoliosis 2013, 8:10  doi:10.1186/1748-7161-8-10

Published: 25 June 2013


There is no generally accepted scientific theory for the cause 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 TB Grivas. It is based on published research from Athens, Greece evaluating schoolchildren age 11–17 years for the relation of body mass index (BMI) to each of truncal asymmetry (TA) and menarcheal status. Girls with relatively lower BMI were found to have a significant excess of severe TAs and significantly later menarche confirming the well-known relation of BMI to menarche. Together with other evidence linking nutritional status to skeletal growth, the observations suggest energy balance via the hypothalamus is related to trunk asymmetry. As with a recent speculative hypothesis for the pathogenesis of AIS in girls, Grivas et al. suggest that the severe TAs involve a genetically-determined selectively increased sensitivity (up-regulation) of the hypothalamus to circulating leptin with asymmetry as an adverse response to stress (hormesis). The TA is expressed bilaterally via the sympathetic nervous system to produce left-right asymmetry in ribs and/or vertebrae leading to severe TAs when beyond the capacity of postural mechanisms of the somatic nervous system to control the shape distortion in the trunk. This EFG discusses the findings and interpretations of the paper by Grivas and colleagues as research at the borderland between the genesis of TA (physiogenesis) and AIS (pathogenesis). It is suggested that TAs, here regarded in common with AIS, result from the combination of secondary sexual development affecting body composition, adolescent skeletal growth velocity, and an asymmetry process. The possible involvement of epigenetic factors is not considered.