Effect of Estrogen Deficiency on Cancellous and Cortical Bone Structure and Strength of the Femoral Neck in Rats

Bagi, Cedo M.; Ammann, Patrick; Rizzoli, René; Miller, Scott C.

doi:10.1007/s002239900344

Cited by 86 publications

(63 citation statements)

References 41 publications

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“…It is likely that the increases in both osteoclast number and osteoclast activity caused by estrogen deficiency (Henriksen et al 2007) play an important role in postmenopausal osteoporosis. Similar to our simulations of increases in F res and V cl , estrogen deficiency decreased trabecular thickness and trabecular number, and increased trabecular separation in rats (Bagi et al 1997). In the model, a decrease in osteocyte density negatively affected the bone architecture, because osteocytes promote osteoblastic bone formation in response to mechanical load.…”

Section: Discussionsupporting

confidence: 87%

Analysis of bone architecture sensitivity for changes in mechanical loading, cellular activity, mechanotransduction, and tissue properties

Cox

Rietbergen

Donkelaar

et al. 2010

Biomech Model Mechanobiol

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Bone has an architecture which is optimized for its mechanical environment. In various conditions, this architecture is altered, and the underlying cause for this change is not always known. In the present paper, we investigated the sensitivity of the bone microarchitecture for four factors: changes in bone cellular activity, changes in mechanical loading, changes in mechanotransduction, and changes in mechanical tissue properties. The goal was to evaluate whether these factors can be the cause of typical bone structural changes seen in various pathologies. For this purpose, we used an established computational model for the simulation of bone adaptation. We performed two sensitivity analyses to evaluate the effect of the four factors on the trabecular structure, in both developing and adult bone. According to our simulations, alterations in mechanical load, bone cellular activities, mechanotransduction, and mechanical tissue properties may all result in bone structural changes similar to those observed in various pathologies. For example, our simulations confirmed that decreases in loading and increases in osteoclast number and activity may lead to osteoporotic changes. In addition, they showed that both increased loading and decreased bone matrix stiffness may lead to bone structural changes similar to those seen in osteoarthritis. Finally, we found that the model may help in gaining a better understanding of the contribution of individual

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Section: Discussionsupporting

confidence: 87%

Analysis of bone architecture sensitivity for changes in mechanical loading, cellular activity, mechanotransduction, and tissue properties

Cox

Rietbergen

Donkelaar

et al. 2010

Biomech Model Mechanobiol

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“…Our results are in agreement with a previous study of 29 inbred mouse lines showing that genes affecting strength by varying BMD are different than those that affect strength by altering cross-sectional geometry (Wergedal et al 2005) and likely from those altering intracortical remodeling. Cortical porosity has been reported in several earlier studies and seems to differ greatly among animal models, with low values for rodents (Bagi et al 1997;Lauritzen et al 1993) and higher values for sheep (Chavassieux et al 2001) and dogs (Sietsema 1995;Wilson et al 1998). In agreement with the μCT data, showing increased intracortical porosity, we demonstrated an increase in intracortical calcein labeling and TRAP staining and a lack of new lamellar bone, indicating increased intracortical bone remodeling/turnover in WT mice that favors resorption over formation.…”

Section: Discussionsupporting

confidence: 91%

Low levels of plasma IGF-1 inhibit intracortical bone remodeling during aging

Courtland

Kennedy²,

et al. 2012

AGE

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Studies linking insulin-like growth factor-1 (IGF-1) to age-related bone loss in humans have been reported but remain only correlative. In this investigation, we characterized the bone phenotype of aged WT C57BL/6J male mice in comparison to that of C57BL/ 6J mice with reduced serum IGF-1 levels arising from an igfals gene deletion (ALS knockout (ALSKO)). During the aging process, WT mice showed an increase in fat mass and decrease lean mass while ALSKO mice had stable lean and fat mass values. Skeletal analyses of femora from WT mice revealed an expansion of the marrow area and a significant accumulation of intracortical porosity associated with increased intracortical remodeling. In contrast, ALSKO mice showed only small age-related declines in the amount of cortical bone tissue and minimal intracortical porosity, at 2 years of age. Accordingly, mechanical tests of femora from 2-year-old WT mice revealed reduced stiffness and maximal load when compared to bones from ALSKO mice. We show here that lifelong reductions in serum IGF-1 compromise skeletal size in development leading to slender bones; they are also associated with decreased intracortical bone remodeling and preservation of bone strength during aging.

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“…The OVX rat is a commonly used model for testing ways to prevent and treat postmenopausal osteoporosis. Estrogen deficiency increases bone turnover with excess bone resorption, and leads to a net loss of trabecular bone (Bagi et al 1997). In cortical bone, an increase in the rate of bone turnover results in endocortical resorption.…”

mentioning

confidence: 99%

Pharmacological treatment of osteopenia induced by gastrectomy or ovariectomy in young female rats

Andersson

Surve

Lehto-Axtelius

et al. 2004

Acta Orthopaedica Scandinavica

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Background Both gastrectomy (GX) and ovariectomy (OVX) induce osteopenia in man and experimental animals. The present study addresses the question -can alendronate, estrogen or parathyroid hormone (PTH) be used to treat established GX-or OVX -evoked osteopenia?Methods Rats were GX-, OVX-or SHAM-operated 8 weeks before starting the treatment with drugs. Each group was then treated for 8 weeks with 50 µg/kg/day alendronate, 10 µg/kg/day estrogen or 75 µg/kg/day PTH(1-84); n = 8 rats/group. Peripheral Quantitative Computed Tomography (pQCT) was used to measure trabecular bone mineral density (BMD) and various cortical bone parameters.Results At killing, 16 weeks after surgery, GX and OVX rats had a greatly reduced trabecular BMD in the metaphysis of the distal femur (GX -44% and OVX -55%). Alendronate increased the trabecular BMD by 44% in GX rats and by 64% in OVX rats, while PTH increased it by 51% and 115%, respectively. However, estrogen increased the trabecular BMD in GX rats (35%), but not in OVX rats (15%, not significant). Cortical bone parameters were adversely (but moderately) affected by GX, but not by OVX or by treatment with the three drugs.Interpretation Alendronate, estrogen and PTH restored the trabecular bone loss in rats with an established GX-evoked osteopenia. In contrast, alendronate and PTH, but not estrogen, restored the trabecular bone loss after OVX. Hence, the mechanism underlying GX-evoked bone loss differs from that underlying OVXevoked bone loss. The ability of alendronate, estrogen

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Effect of Estrogen Deficiency on Cancellous and Cortical Bone Structure and Strength of the Femoral Neck in Rats

Cited by 86 publications

References 41 publications

Analysis of bone architecture sensitivity for changes in mechanical loading, cellular activity, mechanotransduction, and tissue properties

Analysis of bone architecture sensitivity for changes in mechanical loading, cellular activity, mechanotransduction, and tissue properties

Low levels of plasma IGF-1 inhibit intracortical bone remodeling during aging

Pharmacological treatment of osteopenia induced by gastrectomy or ovariectomy in young female rats

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