Bone Abstracts

Adolescent idiopathic scoliosis (AIS) is associated with low bone mineral density (BMD) which has been reported to be an important prognostic factor for curve progression. In addition to BMD, high-resolution peripheral quantitative computed tomography (HR-pQCT) allows measurement of volumetric BMD, bone morphology, trabecular micro-architecture, and evaluation with structure model index (SMI) and finite element analysis (FEA) for mechanical property assessment. The aim of this study was to compare the trabecular micro-architecture configuration and bone mechanical properties between AIS and matched adolescent controls.

101 AIS girls aged 12–14 years and equal number of age and gender-matched normal controls were recruited. Detail anthropometric data, dietary food and standardised physical activities questionnaires were collected. Bilateral femoral necks and non-dominant distal radius were scanned by DXA for areal BMD and HR-pQCT for bone morphology, volumetric BMD, micro-architecture, SMI and FEA respectively. Based on their areal BMD, subjects were classified as osteopenic if the Z-score < −1. Bone mechanical properties including stiffness, failure load and apparent modulus were calculated from FEA. Multivariate linear regression model was used to control confounding from age, physical activity level (PA) and dietary calcium intake (Ca).

The mean age of AIS and controls were 12.94±0.66 and 13.06±0.50 years respectively. The mean Cobb angle of the major curve for AIS subjects was 21.5°±6.0°. AIS was associated with lower failure load and apparent modulus (β=−130.16 and −141.72, P=0.048 and 0.032) after adjusting for age, and lower apparent modulus (β=−125.70, P=0.046) after adjusting for age, PA and Ca. Osteopenic AIS was associated with higher SMI when compared with non-osteopenic AIS (%diff=14.5%, P<0.001) whereas no difference was found between osteopenic and non-osteopenic controls.

AIS girls were associated with deranged trabecular micro-architecture and lower bone biomechanical properties with characteristic SMI profile seen with osteopenia. This might be the result of abnormal regulation and modulation of bone metabolism as well as bone modelling during growth in AIS. Further longitudinal studies to determine the implication of these abnormalities that characterize AIS are warranted.

Disclosure: The authors declared no competing interests.