A prospective study of change in bone mass with age in postmenopausal women

Hui, Siu L.; Wiske, Prescott S.; Norton, James A.; Johnston, C. Conrad

doi:10.1016/0021-9681(82)90095-9

Cited by 96 publications

(31 citation statements)

References 12 publications

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“…Similar although less detailed observations have been made on other bones [ 13,36]. In the radius, continued periosteal apposition combined with slowing down of net endosteal loss may actually increase the amount of cortical bone during the 9th and 10th decades [41]. The rate of periosteal bone expansion in the adult is only about 1-3% of the rate during growth, suggesting a different mechanism [13].…”

Section: Periosteal Expansionmentioning

confidence: 66%

Age-related structural changes in trabecular and cortical bone: Cellular mechanisms and biomechanical consequences

1984

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It is proposed that there are two structurally different forms of bone loss with different rates, cellular mechanisms, and biomechanical effects. Rapid bone loss is the result of excessive depth of osteoclastic resorption cavities. This leads in trabecular bone to perforation of structural elements, increased size of marrow cavities, and discontinuity of the bone structure, and in cortical bone to subendosteal cavitation and conversion of the inner third of the cortex to a trabecularlike structure, which then undergoes the same changes as the trabecular bone originally present. These structural characteristics reduce the strength of the bones to a greater extent than the reduction in the amount of bone by itself would suggest. Slow bone loss results from incomplete refilling by osteoblasts of resorption cavities of normal or reduced size. This leads to simple thinning of residual structural elements in both trabecular and cortical bone, and reduces the strength of the bones in proportion to the reduction in the amount of bone. This concept, although derived mainly from an examination of postmenopausal bone loss, may be applicable to other osteopenic states. At the same time as bone loss is occurring on the endosteal surface, rapidly or slowly, bone is being added to the periosteal surface, but much more slowly than during growth. The cellular mechanism is the converse of that causing slow bone loss, consisting of slight overfilling of shallow resorption cavities. Slow periosteal gain serves to partly offset the structural weakness resulting from endosteal loss, but is not directly compensatory.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Periosteal Expansionmentioning

confidence: 66%

Age-related structural changes in trabecular and cortical bone: Cellular mechanisms and biomechanical consequences

1984

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“…In the most widely accepted model for age-related bone loss, there is no change in BMD in women from ages 25 to 40 yr; BMD then decreases minimally until the menopause, when large losses occur for at least a decade followed by a slowing of the rate of loss (2,11,12). This model has been based almost entirely on BMD measurements in the predominantly cortical bone of the appendicular skeleton.…”

Section: Resultsmentioning

confidence: 99%

Rates of bone loss in the appendicular and axial skeletons of women. Evidence of substantial vertebral bone loss before menopause.

Riggs

Wahner

Melton³

et al. 1986

J. Clin. Invest.

466

109

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We made longitudinal measurements of bone mineral density (BMD) in 139 normal women (ages 20-88 yr) at midradius (99% cortical bone) and lumbar spine (-70% trabecular bone) by single-and dual-photon absorptiometry. BMD was measured 2-6 (median, 3) times over an interval of 0.8-3.4 yr (median, 2.1 yr). For midradius, BMD did not change (+0.48%/yr, NS) before menopause but decreased (-1.01%/yr, P < 0.001) after menopause. For lumbar spine, there was significant bone loss both before (-132%/yr, P < 0.001) and after (-0.97%/yr, P = 0.006) menopause; these rates did not differ significantly from each other. Our data show that before menopause little, if any, bone is lost from the appendicular skeleton but substantial amounts are lost from the axial skeleton. Thus, factors in addition to estrogen deficiency must contribute to pathogenesis of involutional osteoporosis in women because about half of overall vertebral bone loss occurs premenopausally.

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“…Analyses of the spine and the wrist did not detect significant h 2 for OF, thus no estimate of r G is available. As with many previous studies, weight significantly affects BMD and OF risk [e.g., Hui et al, 1982;Pouilles et al, 1995; Tables II and III, the alternative model given is either the general model against which the current model is tested as a restricted model or is the restricted model for which the current model serves as a general model for testing. For example, for Model III in this table, in the alternative Models I and II, model I is the general model against which Model III is tested and Model II is the restricted model for which Model III serves as a general model for testing.…”

Section: Discussionmentioning

confidence: 97%

Relevance of the genes for bone mass variation to susceptibility to osteoporotic fractures and its implications to gene search for complex human diseases

Deng

Mahaney

Williams

et al. 2001

Genetic Epidemiology

121

109

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We investigate the relevance of the genetic determination of bone mineral density (BMD) variation to that of differential risk to osteoporotic fractures (OF). The high heritability (h(2)) of BMD and the significant phenotypic correlations between high BMD and low risk to OF are well known. Little is reported on h(2) for OF. Extensive molecular genetic studies aimed at uncovering genes for differential risks to OF have focussed on BMD as a surrogate phenotype. However, the relevance of the genetic determination of BMD to that of OF is unknown. This relevance can be characterized by genetic correlation between BMD and OF. For 50 Caucasian pedigrees, we estimated that h(2) at the hip is 0.65 (P < 0.0001) for BMD and 0.53 (P < 0.05) for OF; however, the genetic correlation between BMD and OF is nonsignificant (P > 0.45) and less than 1% of additive genetic variance is shared between them. Hence, most genes found important for BMD may not be relevant to OF at the hip. The phenotypic correlation between high BMD and low risk to OF at the hip (approximately -0.30) is largely due to an environmental correlation (rho(E) = -0.73, P < 0.0001). The search for genes for OF should start with a significant h(2) for OF and should include risk factors (besides BMD) that are genetically correlated with OF. All genes found important for various risk factors must be tested for their relevance to OF. Ideally, employing OF per se as a direct phenotype for gene hunting and testing can ensure the importance and direct relevance of the genes found for the risk of OF. This study may have significant implications for the common practice of gene search for complex diseases through underlying risk factors (usually quantitative traits).

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A prospective study of change in bone mass with age in postmenopausal women

Cited by 96 publications

References 12 publications

Age-related structural changes in trabecular and cortical bone: Cellular mechanisms and biomechanical consequences

Age-related structural changes in trabecular and cortical bone: Cellular mechanisms and biomechanical consequences

Rates of bone loss in the appendicular and axial skeletons of women. Evidence of substantial vertebral bone loss before menopause.

Relevance of the genes for bone mass variation to susceptibility to osteoporotic fractures and its implications to gene search for complex human diseases

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