Dimitri P, Jacques R M, Paggiosi M, King D, Walsh J, Taylor Z A, Frangi A F, Bishop N, Eastell R
Department of Paediatric Endocrinology (P.D., D.K.), Sheffield Children's NHS Foundation Trust, Sheffield, S10 2TH, United Kingdom; School of Health and Related Research (R.M.J.), The Mellanby Centre for Bone Research (M.P., J.W., N.B., R.E.), Academic Unit of Bone Metabolism, and Centre for Computational Imaging and Simulation Technologies in Biomedicine, Department of Mechanical Engineering (Z.A.T., A.F.F.), University of Sheffield, Sheffield, S10 2TN, United Kingdom.
J Clin Endocrinol Metab. 2015 Feb;100(2):594-602. doi: 10.1210/jc.2014-3199. Epub 2014 Nov 20.
Bone mass is low and fracture risk is higher in obese children. Hormonal changes in relation to skeletal microstructure and biomechanics have not been studied in obese children.
The objective of the study was to ascertain the relationships of obesity-related changes in hormones with skeletal microstructure and biomechanics.
High resolution peripheral quantitative computed tomography (HR-pQCT) was used to compare three-dimensional cortical and trabecular microstructure and biomechanics at load-bearing and nonload bearing sites in obese and lean children. The relationship between leptin, adiponectin, testosterone, estrogen, osteocalcin and sclerostin and skeletal microstructure was also determined.
The study was conducted at a tertiary pediatric endocrine unit in the United Kingdom.
Obese and lean children were matched by gender and pubertal stage.
Radial cortical porosity (mean difference -0.01 [95% CI: -0.02, -0.004], P = .003) and cortical pore diameter (mean difference -0.005 mm [95% CI: -0.009, -0.001], P = .011) were lower in obese children. Tibial trabecular thickness was lower (mean difference -0.009 mm [95% CI: -0.014, -0.004], P = .003), and trabecular number was higher (mean difference 0.23 mm(-1) [95% CI: 0.08, 0.38], P = .004) in obese children. At the radius, fat mass percentage negatively correlated with cortical porosity (r = -0.57, P < .001) and pore diameter (r = -0.38, P = .02) and negatively correlated with trabecular thickness (r = -0.62, P < .001) and trabecular von Mises stress (r = -0.39, P = .019) at the tibia. No difference was observed in the other biomechanical parameters of the radius and tibia. Leptin was higher in obese children (805.3 ± 440.6 pg/ml vs 98.1 ± 75.4 pg/ml, P < .001) and was inversely related to radial cortical porosity (r = 0.60, 95% CI: [-0.80, -0.30], P < .001), radial cortical pore diameter (r = 0.51, 95% CI [-0.75, -0.16], P = .002), tibial trabecular thickness (r = 0.55, 95% CI: [-0.78, -0.21], P = .001) and tibial trabecular von Mises stress (r = -0.39, 95% CI: -0.65, 0.04, P = .02).
Childhood obesity alters radial and tibial microstructure. Leptin may direct these changes. Despite this, the biomechanical properties of the radius and tibia do not adapt sufficiently in obese children to withstand the increased loading potential from a fall. This may explain the higher incidence of fracture in obese children.
肥胖儿童的骨量较低且骨折风险较高。肥胖儿童中与骨骼微观结构和生物力学相关的激素变化尚未得到研究。
本研究的目的是确定与肥胖相关的激素变化与骨骼微观结构和生物力学之间的关系。
使用高分辨率外周定量计算机断层扫描(HR-pQCT)比较肥胖和瘦儿童承重和非承重部位的三维皮质和小梁微观结构及生物力学。还确定了瘦素、脂联素、睾酮、雌激素、骨钙素和硬化蛋白与骨骼微观结构之间的关系。
该研究在英国一家三级儿科内分泌科进行。
肥胖和瘦儿童按性别和青春期阶段进行匹配。
肥胖儿童的桡骨皮质孔隙率(平均差异-0.01 [95%CI:-0.02,-0.004],P = 0.003)和皮质孔径(平均差异-0.005mm [95%CI:-0.009,-0.001],P = 0.011)较低。肥胖儿童的胫骨小梁厚度较低(平均差异-0.009mm [95%CI:-0.014,-0.004],P = 0.003),小梁数量较高(平均差异0.23mm-1 [95%CI:0.08,0.38],P = 0.004)。在桡骨处,脂肪量百分比与皮质孔隙率(r = -0.57,P < 0.001)和孔径(r = -0.38,P = 0.02)呈负相关,与胫骨处的小梁厚度(r = -0.62,P < 0.001)和小梁冯·米塞斯应力(r = -0.39,P = 0.019)呈负相关。桡骨和胫骨的其他生物力学参数未观察到差异。肥胖儿童的瘦素水平较高(分别为805.3±440.6pg/ml和98.1±75.4pg/ml,P < 0.001),且与桡骨皮质孔隙率(r = 0.60,95%CI:[-0.80,-0.30],P < 0.001)、桡骨皮质孔径(r = 0.51,95%CI [-0.75,-0.16],P = 0.002)、胫骨小梁厚度(r = 0.55,95%CI:[-0.78,-0.21],P = 0.001)和胫骨小梁冯·米塞斯应力(r = -0.39,95%CI:-0.65,0.04,P = 0.02)呈负相关。
儿童肥胖会改变桡骨和胫骨的微观结构。瘦素可能引导这些变化。尽管如此,肥胖儿童桡骨和胫骨的生物力学特性并未充分适应,无法承受跌倒时增加的负荷潜力。这可能解释了肥胖儿童骨折发生率较高这一现象。