On Exposure to Anorexia Nervosa, the Temporal Variation in Axial and Appendicular Skeletal Development Predisposes to Site-Specific Deficits in Bone Size and Density: A Cross-Sectional Study

Authors

  • Ego Seeman M.D.,

    Corresponding author
    1. Endocrine Unit and Department of Medicine, Austin and Repatriation Medical Center, University of Melbourne, Melbourne, Australia
    • Department of Endocrinology, Austin and Repatriation Medical Center, Heidelberg, Melbourne, 3084, Australia
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  • Magnus K. Karlsson,

    1. Endocrine Unit and Department of Medicine, Austin and Repatriation Medical Center, University of Melbourne, Melbourne, Australia
    Current affiliation:
    1. Department of Orthopedic Surgery, Malmö General Hospital, Malmö, Sweden
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  • Yunbo Duan

    1. Endocrine Unit and Department of Medicine, Austin and Repatriation Medical Center, University of Melbourne, Melbourne, Australia
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Abstract

Skeletal development is heterogeneous. Throughout growth, bone size is more maturationally advanced than the mineral being accrued within its periosteal envelope; before puberty, appendicular growth is more rapid than axial growth; during puberty, appendicular growth slows and axial growth accelerates. We studied women with differing age of onset of anorexia nervosa to determine whether this temporal heterogeneity in growth predisposed to the development of deficits in bone size and volumetric bone mineral density (vBMD), which varied by site and severity depending on the age at which anorexia nervosa occurred. Bone size and vBMD of the third lumbar vertebra and femoral neck were measured using dual-energy X-ray absorptiometry in 210 women aged 21 years (range, 12–40 years) with anorexia nervosa. Results were expressed as age-specific SDs (mean ± SEM). Bone width depended on the age of onset of anorexia nervosa; when the onset of anorexia nervosa occurred (1) before 15 years of age, deficits in vertebral body and femoral neck width did not differ (−0.77 ± 0.27 SD and −0.55 ± 0.17 SD, respectively); (2) between 15 and 19 years of age, deficits in vertebral body width (−0.95 ± 0.16 SD) were three times the deficits in femoral neck width (−0.28 ± 0.14 SD; p < 0.05 comparing the deficits), (3) after 19 years of age, deficits in the vertebral body width (−0.49 ± 0.26 SD; p = 0.05) were half that in women with earlier onset of anorexia nervosa. No deficit in bone width was observed at the femoral neck. Deficits in vBMD at the vertebra and femoral neck were independent of the age of onset of anorexia nervosa but increased as the duration of anorexia nervosa increased, being about 0.5 SD lower at the vertebra than femoral neck. We infer that the maturational development of a region at the time of exposure to disease, and disease duration, determine the site, magnitude, and type of trait deficit in anorexia nervosa. Bone fragility due to reduced bone size and reduced vBMD in adulthood is partly established during growth.

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