Equivalent deficits in bone mass of the vertebral body and posterior processes in women with vertebral fractures: implications regarding the pathogenesis of spinal osteoporosis.
Reduced bone mass of the spine in women with vertebral fractures is attributed to excessive trabecular bone loss from the vertebral body. However, the measurement obtained by posteroanterior (PA) scanning includes the posterior processes and the vertebral body, each comprising about 50% of the total vertebral mass. Thus, the deficit in bone mass by PA scanning may be due to deficits in one or both of these structures. We asked two questions: (1) In healthy women, is the age-related diminution in bone mass of the vertebral body greater than the diminution at the posterior processes? (2) In women with vertebral fractures, is the deficit in bone mass at the vertebral body, the fracture site in spinal osteoporosis, greater than at the posterior processes? Bone mass of the posterior processes and vertebral body of the third lumbar vertebra was measured by lateral scanning using dual-energy X-ray absorptiometry (DXA). Compared with 27 premenopausal women, deficits in 27 postmenopausal women at the posterior processes and vertebral body, respectively, were 35.9 +/- 3.7 and 25.2 +/- 4.1% (p < 0.05); t score, -1.5 +/- 0.2 and -1.1 +/- SD (p = 0.09). Compared with the postmenopausal (age-matched) women, deficits in 21 women with vertebral fractures at the posterior processes and vertebral body, respectively, were 22.6 +/- 4.9 and 24.5 +/- 8.3% (p = NS); Z score, -0.8 +/- 0.2 and -0.8 +/- 0.3 (p = NS). In vivo the bone mass of the vertebral body as a percentage of the whole vertebra was 45.7 +/- 0.1 in premenopausal women, 48.9 +/ 1.9 in postmenopausal women, 51.5 +/- 1.1 in women with low bone mass but no fractures, 52.7 +/- 2.4 in women with vertebral fractures, and 51.9 +/- 2.5% in vitro, based on autopsy specimens from 19 postmenopausal women aged 65 - 95 years. The lower spinal bone density measured using PA scanning in women with spine fractures may not be due to excessive or disproportionate trabecular bone loss from the vertebral body because comparable deficits are found at the posterior processes. Whether these deficits are due to reduced peak bone mass, trabecular bone loss, cortical bone loss, or varying combinations of these mechanisms remains to be established.
Seeman
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Department of Endocrinology, University of Melbourne, Austin Hospital, Australia.
Formica
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Mosekilde
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D015502:Absorptiometry, Photon; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000473:pathology / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D015519:Bone Density / Q000502:physiology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008159:Lumbar Vertebrae / Q000473:pathology* / Q000502:physiology; D008875:Middle Aged; D015663:Osteoporosis, Postmenopausal / Q000209:etiology / Q000503:physiopathology*; D016103:Spinal Fractures / Q000209:etiology / Q000503:physiopathology*; D011795:Surveys and Questionnaires