The Effects of Hormones on Bone in Growing Rats

Tapp, E.

doi:10.1302/0301-620x.48b3.526

Cited by 42 publications

(21 citation statements)

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“…We also noted that E2 inhibited longitudinal bone growth due to a reduction in the growth of epiphyseal cartilage, as found by others (8,20). The question arises of whether decreased longitudinal growth could contribute to the increased Although estrogen clearly has a potent antiresorptive effect, which has made a separate anabolic effect difficult to identify, it seems reasonable that a hormone implicated in the maintenance ofbone mass should be both anabolic and anticatabolic.…”

Section: Discussion One Tormationsupporting

confidence: 81%

Estrogen maintains trabecular bone volume in rats not only by suppression of bone resorption but also by stimulation of bone formation.

Chow¹,

Tobias²,

Colston³

et al. 1992

J. Clin. Invest.

244

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Estrogen is generally considered to maintain bone mass through suppression of bone resorption. We have previously demonstrated that administration of pharmacologic doses of estrogen increases bone formation in ovary-intact rats. To assess the effects of physiological concentrations of estrogen on bone formation, estrogen was administered to ovariectomized rats in which bone resorption was suppressed by the bisphosphonate 3-amino-1-hydroxypropylidene-1-bisphosphonate (AHPrBP). Animals receiving exogenous 170t-estradiol (E2) (1, 10, and 100 ,g/kg daily for 17 d) showed a dose-dependent increase in trabecular bone volume of 1.9, 25.8, and 43.6%, respectively, compared with those rats treated with AHPrBP alone. The increase in bone volume was associated with an increase in bone formation in E2-treated animals, in which bone resorption had been almost completely suppressed by AHPrBP. Neither ovariectomy, AHPrBP, nor E2 treatment had a significant effect on the volume or rate of formation of cortical bone. Thus, the increased bone resorption, which is a consequence of estrogen-deficiency, entrains increased bone formation, which masks a simultaneous reduction in estrogendependent bone formation. Therefore, in addition to the nonspecific effect of estrogen to depress formation via coupling, we have identified a specific effect of estrogen to increase formation independent of coupling. Thus it appears that estrogen maintains bone volume not only through inhibition of bone resorption, but also through stimulation of bone formation. (J.

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Section: Discussion One Tormationsupporting

confidence: 81%

Estrogen maintains trabecular bone volume in rats not only by suppression of bone resorption but also by stimulation of bone formation.

Chow¹,

Tobias²,

Colston³

et al. 1992

J. Clin. Invest.

244

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“…This possibility could not be ruled out from the present study. Our present findings, nevertheless, are in contrast to earlier suggestions that osteoclasts are scanty, rarely formed, or even absent in estrogentreated animals Wrist et al, 1948;Tapp, 1966;Silberberg and Silberberg, 1971), but are in accord with the observations of osteoclast cell-surface changes showing retraction of ruffled borders and vacuoles from the bone surface a t the completion of egg shell calcification in egg-lying quail (Miller, 1977), a time when mobilization of mineral is no longer needed.…”

Section: Discussionsupporting

confidence: 78%

Bone‐cell changes in estrogen‐induced bone‐mass increase in mice: Dissociation of osteoclasts from bone surfaces

Liu

Howard

1991

Anat. Rec.

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Early studies in certain avian and mammalian species have described estrogen-associated bone-cell changes, which were based on bone cells that were neither quantified nor identified histochemically (osteoclasts). In the experiments described here, weanling female mice were given a pharmacological dose of 17 beta-estradiol benzoate (1 mg/week) for 1 and 4 weeks, and changes in osteoclasts and osteoblasts were assessed in tibial metaphyses and diaphyses. In the proximal metaphysis, the number of osteoclasts/mm surface length was significantly reduced by estrogen at 1 week (43%) and 4 weeks (64%), which was accompanied by significant increases in the number of osteoclasts in the marrow space not in contact with bone surfaces (no./mm2: 382% and 999%, respectively). These increases, along with observations of decreased osteoclast size (19%), of changes in osteoclast morphology, and of numerous acid-phosphatase-positive fragments in the marrow space, suggest that estrogen treatment causes the dissociation and disintegration, and thus decreased activity, of osteoclasts. The above changes were accompanied by more than 48% increases in the number of trabecular osteoblasts. In the diaphysis, the number of endosteal osteoclasts was significantly decreased by estrogen at 1 week (32%), but was not significantly changed at 4 weeks. These changes were attended by significant increases in the number of osteoclasts in the marrow space not in contact with bone surfaces (no./mm2: 393% at 1 week and 342% at 4 weeks). The number of endosteal osteoblasts was also increased by estrogen at 1 week (132%), and so was the size of endosteal osteoblasts (39% at 1 week and 81% at 4 weeks). Comparable results were obtained when a lower dose of 17 beta-estradiol benzoate (20 micrograms/week) was given to ovariectomized mice. The increase in bone mass and its associated cell changes following estrogen treatment were also found in athymic nude mice, suggesting that these bone/bone cell changes are independent of the thymus.

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“…38 In addition to parathyroid hormone, bone resorptive activity is also regulated by L-thyroxine. 39,40 Thyroid hormone plays a crucial role in normal growth and development of vertebrate bones. 41 The administration of high doses of TX has been shown to increase bone resorption.…”

Section: Doxycycline and L-thyroxinementioning

confidence: 99%

An Extensive Review of Literature: Considering Bone Reaction To Different Agents In Orthodontically Induced Root And Alveolar Resorption

2017

IJDA

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ABSTRACT:Orthodontically induced root resorption is a common problem in day to day practice. If such root resorption could be prevented, it would be an important contribution toward reducing risk factors in orthodontic treatment. The aim of the review is to focus on different agents which can be therapeutically useful in orthodontic tooth movement. The article reviews various agents inhibiting as well as promoting root and alveolar bone resorption to orthodontic tooth movement based on advanced PUBMED, Cochrane database, Wiley online search of the English language literature from the year 1951 to present in order to help us select the most suitable among them fulfilling the desired criteria of being safe, having less adverse effects, minimal contraindications, rare cross reactions, economically viable, having a scope to be used for successful prognosis and possibly not requiring any special considerations to interpret the results.Forty-nine articles were included in the review, but their interpretation was hindered by the variability in experimental design, magnitude of force applied during tooth movement, and medication regimens. Corticosteroid hormones, parathyroid hormone, and thyroxin have all been shown to increase tooth movement. Bisphosphonates had a strong inhibitory effect.By this review, we conclude that low laser therapy and RGD peptide emerges as the clear winner and can result in better prognosis in orthodontic treatment. These techniques are new and cannot replace the conventional agents as a whole.

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The Effects of Hormones on Bone in Growing Rats

Cited by 42 publications

References 0 publications

Estrogen maintains trabecular bone volume in rats not only by suppression of bone resorption but also by stimulation of bone formation.

Estrogen maintains trabecular bone volume in rats not only by suppression of bone resorption but also by stimulation of bone formation.

Bone‐cell changes in estrogen‐induced bone‐mass increase in mice: Dissociation of osteoclasts from bone surfaces

An Extensive Review of Literature: Considering Bone Reaction To Different Agents In Orthodontically Induced Root And Alveolar Resorption

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