Mechanical loading modifies ovariectomy-induced cancellous bone loss

Lin, Bai Yun; Jee, Webster S. S.; Chen, Meng Meng; Yan, Fei; Ke, Hua Zhu; Li, Xiao Jian

doi:10.1016/s0169-6009(08)80239-5

Cited by 38 publications

(21 citation statements)

References 13 publications

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“…However, mechanically induced bone formation appears not to be dependent upon prior bone resorption (31,32), possibly because coupling itself might occur through resorption-enhanced mechanical stimuli (11,25). Indeed, mechanical stimulation suppresses bone resorption (15,33). In the present experiment, we noted no inhibition of the mechanical response by bisphosphonate.…”

Section: Discussioncontrasting

confidence: 48%

Estrogen suppresses activation but enhances formation phase of osteogenic response to mechanical stimulation in rat bone.

Jagger¹,

Chow²,

Chambers³

1996

J. Clin. Invest.

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We used a model whereby mechanical stimulation induces bone formation in rat caudal vertebrae, to test the effect of estrogen on this osteogenic response. Unexpectedly, estrogen administered daily throughout the experiments (8-11 d) suppressed, and ovariectomy enhanced, mechanically induced osteogenesis. Osteogenesis was unaffected by the resorption-inhibitor pamidronate, suggesting that the suppression of bone formation caused by estrogen was not due to suppression of resorption. We found that estrogen did not significantly reduce the proportion of osteocytes that were induced by mechanical stimulation to express c-fos and IGF-I mRNA; and estrogen suppressed mechanically induced osteogenesis whether administration was started 24 h before or 24 h after loading. This suggests that estrogen acts primarily not on the strain-sensing mechanism itself, but on the osteogenic response to signals generated by strain-sensitive cells. We also found that when estrogen administration was started 3 d after mechanical stimulation, by which time osteogenesis is established, estrogen augmented the osteogenic response. This data is consistent with in vitro evidence for estrogen responsiveness in two phenotypically distinct bone cell types: stromal cells, whose functional activities are suppressed, and osteoblasts, which are stimulated, by estrogen. ( J. Clin. Invest. 1996. 98:2351-2357.)

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Section: Discussioncontrasting

confidence: 48%

Estrogen suppresses activation but enhances formation phase of osteogenic response to mechanical stimulation in rat bone.

Jagger¹,

Chow²,

Chambers³

1996

J. Clin. Invest.

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“…Bone turnover rates decrease after disuse, while after estrogen deficiency they increase. [9][10][11] Despite these differences in underlying mechanisms, our findings indicate that deterioration of bone mass after estrogen deficiency and disuse proceeds at the same rate in the metaphysis. In the epiphysis, however, bone loss after disuse developed faster than after estrogen deficiency.…”

Section: Discussionmentioning

confidence: 65%

“…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.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

“…[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.…”

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confidence: 99%

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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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Evaluation of an injectable bone substitute (βTCP/hydroxyapatite/hydroxy‐propyl‐methyl‐cellulose) in severely osteopenic and aged rats

Blouin

Moreau

Weiss

et al. 2006

J Biomedical Materials Res

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The use of injectable biomaterials is of interest in osteoporotic patients to locally restore bone mass in sites at risk of fracture. An injectable bone substitute (IBS1 made of betaTCP/hydroxyapatite as a calcium phosphate substitute and hydroxy-propyl-methyl-cellulose as a polymer carrier) was used in a severely osteopenic rat model obtained by combining orchidectomy (ORX) and disuse (paralysis induced by botulinum toxin - BTX). Fifty-six aged male rats were randomized into three groups: 18 were SHAM operated; 38 were ORX and BTX injected in the right hindlimb; they constituted the OP (osteoporotic) group. One month after ORX-BTX surgery, 20 of these OP rats received a IBS1 injection in the right femur (OP-IBS1 rats). Animals were studied at the time of IBS1 injection 1 month post ORX-BTX (M1), 1 month (M2) and 2 months (M3) after IBS1 injection. Bone mass (BV/TV) and microarchitectural parameters were measured by microCT. BV/TV was decreased after ORX-BTX; ORX and BTX had cumulative effects on bone loss (differences maximized on the right femur). BV/TV (combining the volume of both bone and material in OP-IBS1 rats) was elevated at M1 but decreased at M2. Marked bone formation was found onto the biomaterial granules but bone had a woven texture. A marked increase in the number of nonosteoclastic TRAcP+ cells was found in the implanted area. IBS1 induced new bone formation shortly after implantation but both IBS1 and woven bone were resorbed without inducing lamellar bone. Biomaterial trials must be conducted with long-term implantation periods, in aged osteoporotic animals.

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Mechanical loading modifies ovariectomy-induced cancellous bone loss

Cited by 38 publications

References 13 publications

Estrogen suppresses activation but enhances formation phase of osteogenic response to mechanical stimulation in rat bone.

Estrogen suppresses activation but enhances formation phase of osteogenic response to mechanical stimulation in rat bone.

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

Evaluation of an injectable bone substitute (βTCP/hydroxyapatite/hydroxy‐propyl‐methyl‐cellulose) in severely osteopenic and aged rats

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