Mechanical Determinants of Peak Bone Mass

Meulen, Marjolein C.H. van der; Carter, Dennis R.

doi:10.1016/b978-012098655-2/50012-0

Cited by 6 publications

(5 citation statements)

References 48 publications

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“…Intriguingly, by the end of the experiment at 56 days, this newly formed trabecular bone was no longer observed by pQCT analysis. We interpret this data to indicate that cells expressing human BMP4 induced formation of excess trabecular bone that was subsequently resorbed by normal remodeling processes, as predicted by Wolff's law 50, 51.…”

Section: Discussionmentioning

confidence: 62%

Local ex vivo gene therapy with bone marrow stromal cells expressing human BMP4 promotes endosteal bone formation in mice

Zhang

Linkhart

Chen

et al. 2004

The Journal of Gene Medicine

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Section: Discussionmentioning

confidence: 62%

Local ex vivo gene therapy with bone marrow stromal cells expressing human BMP4 promotes endosteal bone formation in mice

Zhang

Linkhart

Chen

et al. 2004

The Journal of Gene Medicine

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“…(34) Our findings also show that sexual dimorphic skeletal changes occurred in mice during puberty as in the case of humans. (4) This sexual dimorphism may be attributed to greater bone size and cortical thickness in men than in women, (35) which in turn may be caused by a later start and a longer pubertal growth period in boys than girls. (5) However, volumetric bone mineral density (BMD) does not appear to be different between the two sexes in humans.…”

Section: Discussionmentioning

confidence: 99%

“…( 1,2 ) About 60–70% of variance in peak bone density is determined genetically,( 3 ) and 40–50% of peak bone density is accumulated during puberty. ( 4 ) Elucidation of the mechanisms regulating this dramatic increase in skeletal mass during puberty is important in the effort to identify potential preventive or interventive measures that would lower the risk of developing osteoporosis.…”

Section: Introductionmentioning

confidence: 99%

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Postnatal and Pubertal Skeletal Changes Contribute Predominantly to the Differences in Peak Bone Density Between C3H/HeJ and C57BL/6J Mice

Richman

Kutı́lek

Miyakoshi

et al. 2001

Journal of Bone and Mineral Research

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Previous studies have shown that 60 -70% of variance in peak bone density is determined genetically. The higher the peak bone density, the less likely an individual is to eventually develop osteoporosis. Therefore, the amount of bone accrued during postnatal and pubertal growth is an important determining factor in the development of osteoporosis. We evaluated the contribution of skeletal changes before, during, and after puberty to the development of peak bone density in C3H/HeJ (C3H) and C57BL/6J (B6) mice. Volumetric bone density and geometric parameters at the middiaphysis of femora were measured by peripheral quantitative computed tomography (pQCT) from days 7 to 56. Additionally, biochemical markers of bone remodeling in serum and bone extracts were quantified. Both B6 and C3H mice showed similar body and femoral weights. B6 mice had greater middiaphyseal total bone area and thinner cortices than did C3H mice. Within strains, males had thicker cortices than did females. C3H mice accumulated more minerals throughout the study, with the most rapid accumulation occurring postnatally (days 7-23) and during pubertal maturation (days 23-31). C3H mice had higher volumetric bone density as early as day 7, compared with B6 mice. Higher serum insulin-like growth factor I (IGF-I) was present in C3H mice postnatally at day 7 and day 14. Until day 31, B6 male and female mice had significantly higher serum osteocalcin than C3H male and female mice, respectively. Alkaline phosphatase (ALP) was found to be significantly higher in the bone extract of C3H mice compared with B6 mice at day 14. These data are consistent with and support the hypothesis that the greater amount of bone accrued during postnatal and pubertal growth in C3H mice compared with B6 mice may be caused by increased cortical thickness, increased endosteal bone formation, and decreased endosteal bone resorption. (1,2) About 60 -70% of variance in peak bone density is determined genetically, (3) and 40 -50% of peak bone density is accumulated during puberty.(4) Elucidation of the mechanisms regulating this dramatic increase in skeletal mass during puberty is important in the effort to identify potential preventive or interventive measures that would lower the risk of developing osteoporosis.*The view, opinions, and/or findings contained in this report are those of the author(s) and should not be construed as a position, policy, decision, or endorsement of the Federal Government or the National Medical Technology Testbed, Inc. 1 J.L. Pettis

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“…It has been well established that the pubertal growth period is a critical period in time when rapid increase in bone accretion takes place. We and others (19,32,48) have demonstrated in both humans and mice that 40 -50% of bone accretion occurs during puberty. Understanding the mechanisms involved in regulating bone accretion during this period of rapid growth is of considerable importance in the prevention and treatment of osteoporosis.…”

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confidence: 99%

Prepubertal OVX increases IGF-I expression and bone accretion in C57BL/6J mice

Govoni

Wergedal²,

Chadwick³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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It is generally well accepted that the pubertal surge in estrogen is responsible for the rapid bone accretion that occurs during puberty and that this effect is mediated by an estrogen-induced increase in growth hormone (GH)/insulin-like growth factor (IGF) action. To test the cause and effect relationship between estrogen and GH/IGF, we evaluated the consequence of ovariectomy (OVX) in prepubertal mice (C57BL/6J mice at 3 wk of age) on skeletal changes and the GH/IGF axis during puberty. Contrary to our expectations, OVX increased body weight (12-18%), bone mineral content (11%), bone length (4%), bone size (3%), and serum, liver, and bone IGF-I (30 -50%) and decreased total body fat (18%) at 3 wk postsurgery. To determine whether estrogen is the key ovarian factor responsible for these changes, we performed a second experiment in which OVX mice were treated with placebo or estrogen implants. In addition to observing similar results compared with our first experiment, estrogen treatment partially rescued the increased body weight and bone size and completely rescued body fat and IGF-I levels. The increased bone accretion in OVX mice was due to increased bone formation rate (as determined by bone histomorphometry) and increased serum procollagen peptide. In conclusion, contrary to the known estrogen effect as an initiator of GH/IGF surge and thereby pubertal growth spurt, our findings demonstrate that loss of estrogen and/or other hormones during the prepubertal growth period effect leads to an increase in IGF-I production and bone accretion in mice. osteoporosis; estrogen; puberty; bone size; bone mineral density OSTEOPOROSIS IS A MAJOR HEALTH concern in humans, and this disease is characterized by a low bone mineral density (BMD), which leads to increased bone fragility and risk of fractures. BMD is an important determinant of bone strength, and low BMD is the result of increased bone resorption and decreased bone formation. It has been well established that the pubertal growth period is a critical period in time when rapid increase in bone accretion takes place. We and others (19,32,48) have demonstrated in both humans and mice that 40 -50% of bone accretion occurs during puberty. Understanding the mechanisms involved in regulating bone accretion during this period of rapid growth is of considerable importance in the prevention and treatment of osteoporosis.In terms of the potential messenger molecules that contribute to rapid skeletal growth during puberty, it has been suggested that the growth hormone (GH)/insulin-like growth factor (IGF) axis is a key regulator of early bone development (34, 55). Recent studies using transgenic mouse models lacking IGF-I or GH have provided convincing evidence for a key role for GH/IGF axis in the regulation of skeletal growth that occurs during puberty (28). It is well accepted that increased IGF-I during sexual maturation is regulated by increased GH production and/or action as demonstrated by reduced IGF-I and bone density in mice lacking GH (28). In addition, we and ot...

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Mechanical Determinants of Peak Bone Mass

Cited by 6 publications

References 48 publications

Local ex vivo gene therapy with bone marrow stromal cells expressing human BMP4 promotes endosteal bone formation in mice

Local ex vivo gene therapy with bone marrow stromal cells expressing human BMP4 promotes endosteal bone formation in mice

Postnatal and Pubertal Skeletal Changes Contribute Predominantly to the Differences in Peak Bone Density Between C3H/HeJ and C57BL/6J Mice

Prepubertal OVX increases IGF-I expression and bone accretion in C57BL/6J mice

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