If you are a member of the network, please log in to access Network content and tools. If you do not have a username, contact your site principal investigator or site coordinator and request that they complete a membership request for you. If you have forgotten your password, you may CLICK HERE.


You are here

Bone Microarchitecture in Autism Spectrum Disorder.

TitleBone Microarchitecture in Autism Spectrum Disorder.
Publication TypeConference Abstract
Year of Publication2016
AuthorsNeumeyer, AM, Cano-Sokoloff, N, McDonnell, E, Macklin, EA, McDougle, CJ, Misra, M
Conference NamePAS.

Background: Children with Autism Spectrum Disorder (ASD) have lower areal bone mineral density (aBMD) than typically developing controls (TDC). Bone microarchitecture provides information about fracture risk beyond that provided by dual energy x-ray absorptiometry (DXA) measures of aBMD. Studies have not examined bone microarchitecture in ASD.

Objective: To assess distal radius and tibial microarchitecture in adolescent boys with ASD compared to TDC.

Design/Methods: In a cross-sectional study of 34 boys (16 ASD, 18 TDC), aBMD was measured at the whole body less head (WBLH), hip and spine using DXA, and volumetric BMD (vBMD) and microarchitecture using high-resolution peripheral quantitative CT. Activity questionnaires, food records, and fasting levels of 25(OH) vitamin D and bone markers (CTX and NTX for bone resorption, P1NP for bone formation) were obtained. Data are represented as mean (SE).

Results: ASD boys were slightly younger than TDC [13.5 (0.5) vs. 14.4 (0.5), P=0.05]. Tanner stage, BMI z-scores, height z-scores, serum vitamin D and P1NP did not differ between groups. ASD boys had lower aBMD Z-scores than TDC at the WBLH, femoral neck and total hip (P<0.01). At the radius, ASD boys had lower cortical vBMD [632.7 (26.5) vs. 687.3 (10.5) mgHA/cm, P<0.01], log-transformed cortical area [1.81 (0.56) vs. 3.02 (0.15) log(mm2), P=0.01], trabecular thickness [0.064 (0.002) vs. 0.071 (0.003) mm, P<0.01], stiffness [56.7 (6.8) vs. 74.8 (6.1) kN/mm, P=0.02], and failure load [3.0 (0.3) vs. 3.9 (0.3) kN, P=0.02]. At the tibia, ASD boys had lower cortical vBMD [719.1 (21.1) vs. 753.1 (10.0) mgHA/cm, P=0.05], log-transformed cortical area [4.04 (0.14) vs. 4.38 (0.08) log(mm2), p<0.01], cortical thickness [0.60 (0.08) vs. 0.74 (0.07) mm, P<0.01], stiffness [170.0 (12.2) vs. 216.8 (14.9) kN/mm, P<0.01] and failure load [8.8 (0.6) vs. 11.1 (0.7) kN, P<0.01]. Most group differences persisted after controlling for age. A lower proportion of ASD boys was categorized as “very physically active” (19% vs. 72%, P<0.01). Bone resorption markers were higher in ASD (P<0.03).

Conclusion: For the first time, we show impaired cortical parameters in ASD, with reductions in bone strength estimates (stiffness and failure load) at the distal radius and tibia. This may be consequent to lower physical activity causing increased bone resorption.