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G59 Bone microarchitecture and strength in obese children – a new insight into fracture risk
  1. P Dimitri1,
  2. D King1,
  3. M Paggiosi2,
  4. J Walsh3,
  5. N Bishop4,
  6. R Eastell3
  1. 1Department of Paediatric Endocrinology, Sheffield Children’s NHS Foundation Trust, Sheffield, UK
  2. 2Department of Metabolic Bone Disease, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK
  3. 3The Academic Unit of Bone Metabolism, University of Sheffield, Sheffield, UK
  4. 4The Academic Unit of Child Health, the University of Sheffield, Sheffield, UK


Introduction Obese children have a greater fracture risk. Studies utilising DXA and pQCT have demonstrated that bone mass and size relative to body size is reduced in obese children. However, these imaging modalities cannot quantify alterations in bone microstructure and strength in obese children. The advent of High Resolution peripheral Quantitative Computed Tomography (HRpQCT – isotropic voxel size 82 mm) provides the resolution required to accurately determine 3-dimensional in-vivo bone microstructure; microfinite element (microFE) analysis of HRpQCT images provides insight into skeletal biomechanical properties.

Methods Children aged 8–15 years were recruited into lean and obese groups according to BMI percentile. Prepubertal children were matched by age and gender; pubertal children were matched by gender and Tanner stage (18 pairs). Cortical and trabecular skeletal parameters were quantified using HRpQCT. MicroFE software was used to determine bone stiffness, estimated failure load, load carried by the trabecular and cortical bone, and the average Von Mises stresses in trabecular and the cortical bone. The tibial and radial Bone Strength Index was calculated using the formula [BSI(mg2/mm4) = Densitytotal 2 x Areatotal].

Results The mean age of lean and obese children was 12.9 ± 1.9 years and 12.6 ± 1.9 years (p = 0.63) respectively. There was no difference in height SDS between the two groups (1.12 ± 1.34 vs 0.96 ± 1.41). Radial cortical pore diameter was lower in obese children (0.140 ± 0.007 mm vs 0.145 ± 0.005, p = 0.01). In contrast, tibial trabecular thickness was lower (0.065 ± 0.008 mm vs 0.074 ± 0.009 mm, p = 0.003) and trabecular number (2.5 ± 0.31 mm–1 vs 2.26 ± 0.31 mm–1) was higher in obese children. There were no other observed differences in cortical/trabecular bone microstructure. There was no significant difference in bone strength indices at the distal radius and tibia between groups.

Conclusion An increase in total body fat mass does not result in a change in cortical and trabecular bone microstructure and strength at the radius. In contrast, there appears to be an alteration in trabecular microarchitecture at the tibia. Obese children are at a greater risk of falling. Failure of bone to adapt to excess fat at the radius and a change in trabecular architecture at the tibia may increase the risk of fracture relative to the greater load imparted during a fall.

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