Comparison of bone loss induced in female rats by hindlimb unloading, ovariectomy, or both

Lecoq, B.; Potrel-Burgot, Céline; Granier, P.; Sabatier, Jean-Pierre; Marcelli, Christian

doi:10.1016/j.jbspin.2005.01.010

Cited by 18 publications

(9 citation statements)

References 24 publications

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“…In line with the fact that trabecular architecture responds more promptly to both homeostases there is the observation that in femoral cortical bone the neo-osteogenesis is abundant later, during the normal diet restoration, as evidenced by bone labeling on the twelfth day. All this agrees with observations of various authors [49,50,51] showing that appendicular skeleton (mostly concerning cortical bone) answers mainly to mechanical demands (i.e., is devoted to the skeletal homeostasis) while axial skeleton (mostly concerning trabecular bone) answers mainly to metabolic demand (i.e., is mainly devoted to the mineral homeostasis).…”

Section: Discussionsupporting

confidence: 92%

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Ferretti

Cavani²,

Rovedatti³

et al. 2019

IJMS

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The present study is the second step (concerning normal diet restoration) of the our previous study (concerning the calcium-free diet) to determine whether normal diet restoration, with/without concomitant PTH (1-34) administration, can influence amounts and deposition sites of the total bone mass. Histomorphometric evaluations and immunohistochemical analysis for Sclerostin expression were conducted on the vertebral bodies and femurs in the rat model. The final goals are (i) to define timing and manners of bone mass changes when calcium is restored to the diet, (ii) to analyze the different involvement of the two bony architectures having different metabolism (i.e., trabecular versus cortical bone), and (iii) to verify the eventual role of PTH (1-34) administration. Results evidenced the greater involvement of the trabecular bone with respect to the cortical bone, in response to different levels of calcium content in the diet, and the effect of PTH, mostly in the recovery of trabecular bony architecture. The main findings emerged from the present study are (i) the importance of the interplay between mineral homeostasis and skeletal homeostasis in modulating and guiding bone’s response to dietary/metabolic alterations and (ii) the evidence that the more involved bony architecture is the trabecular bone, the most susceptible to the dynamical balance of the two homeostases.

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Section: Discussionsupporting

confidence: 92%

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Ferretti

Cavani²,

Rovedatti³

et al. 2019

IJMS

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show abstract

“…In line with the fact that trabecular architecture responds more promptly to both homeostases there is the observation that in femoral cortical bone the neo-osteogenesis is abundant later, during the normal-diet restoration, as evidenced by bone labeling on the twelfth day. All this agrees with observations of various authors [49][50][51] showing that appendicular skeleton (mostly concerning cortical bone) answers mainly to mechanical demands (i.e. is devoted to the skeletal homeostasis) while axial skeleton (mostly concerning trabecular bone) answers mainly to metabolic demand (i.e.…”

Section: Discussionsupporting

confidence: 92%

Interplay among calcium diet content, PTH(1-34) treatment and balance of bone homeostases in rat model: the trabecular bone as keystone

Ferretti¹,

Cavani²,

Rovedatti³

et al. 2019

Preprint

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The present study is the second step (concerning the normal-diet restoration) of the our previous one (concerning the calcium-free diet) to determine whether the normal-diet restoration, with/without concomitant PTH(1-34) administration, can influence amounts and deposition sites of the total bone mass. Histomorphometric evaluations and immunohistochemical analysis for Sclerostin expression were conducted on the vertebral bodies and femurs  in rat model. The final goals are: i) to define timing and manners of bone mass changes when calcium is restored in the diet; ii) to analyze the different involvement of the two bony architectures having different metabolism (i.e. trabecular versus cortical bone); iii) to verify the eventual role of PTH(1-34) administration. Results evidenced the greater involvement of the trabecular bone with respect to the cortical one, in answering to different calcium diet content, and the effect of PTH mostly in the recovery of trabecular bony architecture. The main findings emerged from the present study are: i) the importance of the interplay between mineral homeostasis and skeletal homeostasis in modulating and guiding bone answers to dietary/metabolic alterations and ii) the evidence that the more involved bony architecture is the trabecular one, the most susceptible to the dynamical balance of the two homeostases.

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“…[9][10][11][12][13][14][15][16][17] After estrogen deficiency, bone loss is concentrated in the central part of the metaphysis, whereas disuse leads to overall bone loss. 11,13,17 This finding supports the hypothesis that OVX-induced estrogen deficiency increases the mechanostat threshold, 9 leading to low loaded regions being resorbed first, whereas the main loaded structures would remain.…”

mentioning

confidence: 99%

Comparison of bone loss induced by ovariectomy and neurectomy in rats analyzed by in vivo micro‐CT

Brouwers

Lambers

Rietbergen

et al. 2009

Journal Orthopaedic Research

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ABSTRACT:We hypothesized that osteoporosis due to estrogen deficiency progresses faster than due to disuse and that at the same amount of bone loss, disuse leads to less favorable bone structure and mechanical properties than estrogen deficiency. Adult rats were either ovariectomized (OVX) (n ¼ 9) or neurectomized (NX) (n ¼ 8). At week 0, 1, 2, 3, and 4, in vivo micro-CT scans were made of the proximal tibia. Segmented CT-scans at weeks 0 and 4 were used to build a 3D voxel-based micro finite element model (FEM). Displacement in the longitudinal direction was prescribed at the proximal end leading to a compression step of 1%. The severe reduction in metaphyseal bone volume fraction was not significantly different between OVX and NX. Epiphyseal bone loss was less severe in both groups, and BV/TV was significantly lower after NX. Trabecular separation and degree of anisotropy in the metaphysis and connectivity and trabecular number in the epiphysis were significantly more deteriorated after NX. FEM-derived stiffness decreased in both groups, but more after NX. Osteoporosis due to estrogen-deficiency progressed overall at a rate similar to osteoporosis due to disuse. At the same amount of induced bone loss, disuse led to more deteriorated bone structure and mechanical properties than estrogen deficiency. Keywords: estrogen deficiency; disuse; osteoporosis; rats; in vivo micro-CT Osteoporosis is a degenerative bone disease that can develop with reduced estrogen levels during and after menopause and after long periods of disuse. The rat has been used to study osteoporosis, with estrogen deficiency-associated bone loss induced by ovariectomy (OVX), 1-4 and disuse-associated bone loss induced by sciatic neurectomy (NX), tail suspension, or leg taping. 5,6 Both can severely deteriorate bone structure in these models. Differences exist in cellular activity with these forms of bone loss. 7,8 OVX leads to an increased bone formation and resorption rate, disuse leads to decreased turnover rates and increased bone resorption. [9][10][11] This would suggest that bone loss after OVX might proceed faster than that resulting from disuse.Differences also exist in the resulting deterioration of bone mass and microstructure. 9-17 After estrogen deficiency, bone loss is concentrated in the central part of the metaphysis, whereas disuse leads to overall bone loss. 11,13,17 This finding supports the hypothesis that OVX-induced estrogen deficiency increases the mechanostat threshold, 9 leading to low loaded regions being resorbed first, whereas the main loaded structures would remain. With disuse, however, all bone tissue is unloaded, so a more random pattern of bone loss would be expected. 9 This would suggest that disuse-induced osteoporosis would lead to a more severe loss of the main trabecular structures and thus a more severe loss of stiffness and strength in the main loading direction. Upon reloading, distribution of loads in immobilized bones would be very inhomogeneous, because the adaptation to the loading direction is lost. ...

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Comparison of bone loss induced in female rats by hindlimb unloading, ovariectomy, or both

Cited by 18 publications

References 24 publications

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Interplay among calcium diet content, PTH(1-34) treatment and balance of bone homeostases in rat model: the trabecular bone as keystone

Comparison of bone loss induced by ovariectomy and neurectomy in rats analyzed by in vivo micro‐CT

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