Microarchitecture osseuse chez des adolescents garçons avec un trouble du spectre de l'autisme

Traduction partielle: G.M.

Bone. 2017 Jan 11. pii: S8756-3282(17)30009-1. doi: 10.1016/j.bone.2017.01.009.

Bone microarchitecture in adolescent boys with autism spectrum disorder

Neumeyer AM¹, Sokoloff NC², McDonnell E³, Macklin EA⁴, McDougle CJ⁵, Misra M⁶.

Author information

• ¹Lurie Center for Autism, Massachusetts General Hospital, Lexington, MA 02421, United States; Harvard Medical School, Boston, MA 02115, United States. Electronic address: aneumeyer@mgh.harvard.edu
• ²Lurie Center for Autism, Massachusetts General Hospital, Lexington, MA 02421, United States.
• ³Biostatistics Center, Massachusetts General Hospital, Boston, MA 02114, United States.
• ⁴Harvard Medical School, Boston, MA 02115, United States; Biostatistics Center, Massachusetts General Hospital, Boston, MA 02114, United States.
• ⁵Lurie Center for Autism, Massachusetts General Hospital, Lexington, MA 02421, United States; Harvard Medical School, Boston, MA 02115, United States.
• ⁶Harvard Medical School, Boston, MA 02115, United States; Pediatric Endocrine and Neuroendocrine Units, Massachusetts General Hospital, Boston, MA 02114, United States.

Abstract

BACKGROUND:

Les garçons avec trouble du spectre de l'autisme (TSA) ont une densité minérale osseuse de surface (DMOs) inférieure à celle des témoins qui développent typiquement (DT). Des études sur la DMO volumétrique (MDOv) et sur la microarchitecture osseuse fournissent des informations sur le risque de fracture au-delà de celles fournies par la DMOs mais manquent actuellement dans le TSA.
Boys with autism spectrum disorder (ASD) have lower areal bone mineral density (aBMD) than typically developing controls (TDC). Studies of volumetric BMD (vBMD) and bone microarchitecture provide information about fracture risk beyond that provided by aBMD but are currently lacking in ASD.

OBJECTIVES:

To assess ultradistal radius and distal tibia vBMD, bone microarchitecture and strength estimates in adolescent boys with ASD compared to TDC.

DESIGN/METHODS:

Cross-sectional study of 34 boys (16 ASD, 18 TDC) that assessed (i) aBMD at the whole body (WB), WB less head (WBLH), hip and spine using dual X-ray absorptiometry (DXA), (ii) vBMD and bone microarchitecture at the ultradistal radius and distal tibia using high-resolution peripheral quantitative CT (HRpQCT), and (iii) bone strength estimates (stiffness and failure load) using micro-finite element analysis (FEA). We controlled for age in all groupwise comparisons of HRpQCT and FEA measures. Activity questionnaires, food records, physical exam, and fasting levels of 25(OH) vitamin D and bone markers (C-terminal collagen crosslinks and N-terminal telopeptide (CTX and NTX) for bone resorption, N-terminal propeptide of Type 1 procollagen (P1NP) for bone formation) were obtained.

RESULTS:

ASD participants were slightly younger than TDC participants (13.6 vs. 14.2years, p=0.44). Tanner stage, height Z-scores and fasting serum bone marker levels did not differ between groups. ASD participants had higher BMI Z-scores, percent body fat, IGF-1 Z-scores, lower lean mass and aBMD Z-scores than TDC at the WB, WBLH, and femoral neck (P<0.1). At the radius, ASD participants had lower trabecular thickness (0.063 vs. 0.070mm, p=0.004), compressive stiffness (56.7 vs. 69.7kN/mm, p=0.030) and failure load (3.0 vs. 3.7kN, p=0.031) than TDC. ASD participants also had 61% smaller cortical area (6.6 vs. 16.4mm², p=0.051) and thickness (0.08 vs. 0.22mm, p=0.054) compared to TDC. At the tibia, ASD participants had lower compressive stiffness (183 vs. 210kN/mm, p=0.048) and failure load (9.4 vs. 10.8kN, p=0.043) and 23% smaller cortical area (60.3 vs. 81.5mm², p=0.078) compared to TDC. A lower proportion of ASD participants were categorized as "very physically active" (20% vs. 72%, p=0.005). Differences in physical activity, calcium intake and IGF-1 responsiveness may contribute to group differences in stiffness and failure load.

CONCLUSION:

Les paramètres micro-architecturaux osseux sont altérés dans le TSA, avec des réductions des estimations de la résistance osseuse (rigidité et rupture de charge) au niveau du radius ultradistal et du tibia distal. Cela peut résulter d'une diminution de l'activité physique et de l'apport en calcium, et d'une diminution de la sensibilité à l'IGF-1.
Bone microarchitectural parameters are impaired in ASD, with reductions in bone strength estimates (stiffness and failure load) at the ultradistal radius and distal tibia. This may result from lower physical activity and calcium intake, and decreased IGF-1 responsiveness.

Copyright © 2016. Published by Elsevier Inc.

PMID: 28088646

DOI: 10.1016/j.bone.2017.01.009