Vertebral Bone Mass, Size, and Volumetric Density in Women with Spinal Fractures

Authors

  • Yunbo Duan,

    1. Department of Endocrinology, Austin and Repatriation Medical Center, University of Melbourne, Melbourne, Australia
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  • A. Michael Parfitt,

    1. Division of Endocrinology and Metabolism and Center for Osteoporosis and Metabolic Bone Disease, University of Arkansas for Medical Sciences, Little Rock, Arkansas, U.S.A.
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  • Ego Seeman

    Corresponding author
    1. Department of Endocrinology, Austin and Repatriation Medical Center, University of Melbourne, Melbourne, Australia
    • Address reprint requests to: Ego Seeman, M.D. Austin and Repatriation Medical Centre Heidelberg, Melbourne 3084, Australia
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Abstract

Bone densitometry provides a measure of bone mass expressed as bone mineral content (BMC) or areal bone mineral density (aBMD). BMC is unadjusted for bone size while aBMD is adjusted for the projected area of the region scanned but not its depth. Because patients with fractures often have reduced bone size, the deficit in BMC or aBMD relative to controls may be partly the result of the comparison of a smaller bone in patients with fractures with a bigger bone in controls without fractures. We asked, what proportion of the deficit in BMC and aBMD found in women with spine fractures relative to controls is attributable to smaller vertebral size? We measured BMC (g), volume (cm3, derived from projected area3/2), aBMD (g/cm2), and volumetric BMD (vBMD, g/cm3) of the third lumbar vertebra by dual-energy X-ray absorptiometry in 270 premenopausal women aged 18–43 years, 163 postmenopausal women with spine fractures aged 54–83 years, and 209 women without fractures aged 54–87 years. The regression of BMC and aBMD on volume in the premenopausal women was used to calculate volume adjusted BMC and aBMD in postmenopausal women with and without fractures (adjusted BMC = observed BMC + [50 – observed volume] × 0.29; adjusted aBMD = observed aBMD + [50 – observed volume] × 0.0044). The data were expressed in the original units and as standard deviation scores (SD) above or below the young normal mean (T scores) or the age predicted mean (Z scores). All results were expressed as mean ± SEM. Women with spine fractures had reduced BMC (T = –2.35 ± 0.07 SD, Z = –1.18 ± 0.06 SD), volume (T = –1.08 ± 0.08 SD, Z = –0.82 ± 0.08 SD), aBMD (T = –3.06 ± 0.09 SD, Z = –1.14 ± 0.06 SD) and vBMD (T = –2.67 ± 0.10 SD, Z = – 0.94 ± 0.07 SD) (all p < 0.001). About 48% of the difference in BMC between postmenopausal women with and without spine fractures, and about 16% of the difference in aBMD was explained by the difference in vertebral volume between them. When women with and without spine fractures were intentionally matched by aBMD (and age, height, and weight), vertebral volume was reduced (Z = –0.66 ± 0.13 SD, p < 0.001). When women with and without fractures were intentionally matched by vertebral volume (and age, height, and weight), vBMD was reduced (Z = –1.07 ± 0.10 SD, p < 0.001). Women with spine fractures have smaller vertebrae with less bone in the smaller bone. About half the deficit in BMC relative to controls is due to their smaller bone size. The remainder may be due to reduced bone accrual, increased bone loss, or both. Thus, the pathogenesis of bone fragility is heterogeneous. Factors responsible for a deficit in bone mass (due to reduced accrual or excess bone loss) are unlikely to be identified when reduced bone size exaggerates the deficit, and increased bone size obscures it. Understanding the pathogenesis of bone fragility requires acknowledgment of this heterogeneity and the description of its varied morphological basis. This can be achieved by the study of the periosteal and endosteal surfaces of bone because the absolute and relative changes in these surfaces during growth and aging determine skeletal size, its mass, and architecture.

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