Microstructure of trabecular bone in a mouse model for down syndrome

Authors

  • Trish Parsons,

    1. Department of Anthropology, Pennsylvania State University, University Park, Pennsylvania
    Current affiliation:
    1. Faculty of Medicine, University of Calgary, Calgary, Canada
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  • Timothy M. Ryan,

    1. Department of Anthropology, Pennsylvania State University, University Park, Pennsylvania
    2. Center for Quantitative Imaging, Pennsylvania State University, University Park, Pennsylvania
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  • Roger H. Reeves,

    1. Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland
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  • Joan T. Richtsmeier

    Corresponding author
    1. Department of Anthropology, Pennsylvania State University, University Park, Pennsylvania
    2. Centers for Craniofacial Development and Disorders and Functional Anatomy and Evolution, Johns Hopkins University School of Medicine, Baltimore, Maryland
    • Department of Anthropology, Pennsylvania State University, 409 Carpenter Building, University Park, PA 16802
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    • Fax: 814-863-1474.


Abstract

Down syndrome (DS) is caused by trisomy of human chromosome 21 (Hsa21) and results in a suite of dysmorphic phenotypes, including effects on the postcranial skeleton and the skull. We have previously demonstrated parallels in the patterns of craniofacial dysmorphology in DS and in the Ts65Dn mouse model for DS. The specific mechanisms underlying the production of these changes in craniofacial shape remain unknown. High-resolution computed tomography scan data were collected for the presphenoid bone of euploid and aneuploid mice. Three-dimensional morphometric parameters of trabecular bone were quantified and compared between euploid and aneuploid mice using nonparametric statistical tests. Aneuploid presphenoid bones were smaller than those of their euploid littermates and had lower bone volume fraction and fewer, more rod-like trabeculae. The differences in cancellous bone structure suggest that bone development, perhaps including bone modeling and remodeling, is affected by aneuploidy. These differences may contribute to the observed dysmorphology of skull and postcranial skeletal phenotypes in DS. Anat Rec, 2007. © 2007 Wiley-Liss, Inc.

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