Endosteal-Bone Formation in Estrogen-Treated Mice

Budy, Ann M.; McLean, Franklin C.

doi:10.2106/00004623-195032010-00014

Cited by 100 publications

(33 citation statements)

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“…This is consistent with the results of others who have found no decrease in cortical bone area in the diaphysis of ovariectomized rats, while the metaphysis becomes osteopenic following ovariectomy (24,25), and also is consistent with the generally different responsiveness of dynamic histomorphometric parameters in metaphyseal and cortical bone to ovariectomy and hormone replacement (7,(25)(26)(27)(28). Bone also accumulates in the metaphysis after PTH therapy (29, 30), during high dose estrogen therapy (31)(32)(33)(34), and before egg production in birds (35). It is intriguing to speculate that estrogen may induce and maintain bone at this site as an estrogen-dependent quantum of bone (24) that is available as a metabolic reserve.…”

Section: Discussion One Tormationsupporting

confidence: 91%

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: 91%

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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“…A major unanswered question is whether estrogen action on bone in vivo is direct or indirect (4,(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41). It has been suggested that in vivo estrogen promotes the systemic production of growth factors, so-called estromedins, or the removal of growth inhibitors, estrocolyons, elsewhere in the body (42).…”

Section: Discussionmentioning

confidence: 99%

“…In vivo studies have yielded controversial findings regarding estradiol stimulation of bone formation (4,22,24,29,41). Although some studies in women and mice suggest that estrogen increased bone formation and bone mineral content (4,29,41) The localized action of 17,fE2 was evident from the lack of changes in the untreated contralateral femora and especially in the proximal region of 17,fE2-infused femora.…”

Section: Discussionmentioning

confidence: 99%

“…Although some studies in women and mice suggest that estrogen increased bone formation and bone mineral content (4,29,41) The localized action of 17,fE2 was evident from the lack of changes in the untreated contralateral femora and especially in the proximal region of 17,fE2-infused femora. As expected, no estrogenic effects on body and uterine weights could be detected in these experiments, whereas systemic administration of estradiol to OVX rats clearly increases uterine weight (49) and decreases body weight (22).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Direct effects of 17 beta-estradiol on trabecular bone in ovariectomized rats.

Takano‐Yamamoto

Rodan

1990

Proc. Natl. Acad. Sci. U.S.A.

163

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High-affinity nuclear binding sites for 17 (3-estradiol (17(3E2) were recently found in bone cells; however, the mechanism by which estrogen exerts its effect on bone in vivo is still unknown. To study if estrogen acts on bone directly, we used an experimental model in which test substances are infused locally into rat femur trabecular bone. SpragueDawley rats weighing 150-160 g were ovariectomized (OVX) and 14 days later a polyethylene tube (1 mm in diameter) connected to an Alzet osmotic minipump was implanted into the distal femur 9 mm from the joint. 17fiE2 (24 pl/day at 0.01-1 nM), 17a-estradiol (17aE2) (24 pl/day at 1 nM), or phosphatebuffered saline (NaCl, 8 g/liter; KCI, 0.2 g/liter; KH2PO4, 0.2 g/liter; Na2HPO4-7H2O, 2.16 g/liter) was infused for 8 days.The contralateral limb remained intact. Animals were sacrificed and bones were examined by histomorphometry. Ovariectomy caused a 50% loss in trabecular bone volume (TBV) in the secondary spongiosa (from 20.3% ± 1.7% to 9.6% + 1.1%; mean ± SEM), a 2-fold increase in osteoclast number (to 4.0 ± 0.4 per mm), a 3-fold increase in relative resorption surfaces (to 24.8% ± 2.9%), a 9-fold increase in osteoblast number (to 11.3 ± 2.1 per mm), and an 8-fold increase in relative osteoid surface (to 9.6% ± 1.7%). The local infusion of 17fiE2 for 8 days into OVX rats (t) restored the TBV dose dependently to 75% and 85% of control (non-OVX) levels, at 0.1 nM and 1 nM 17(3E2, respectively; (it) decreased osteoclast number and the relative resorption surface to control (non-OVX) levels; and (iii) further increased osteoblast number and the relative osteoid surface dose dependently (by 5-fold at 1 nM 173E2). Phosphate-buffered saline infusion was without effect.Infusion of 17ciE2 had no effect on TBV, osteoclast number, or resorption surface but increased slightly the osteoblast number and the osteoid surface. Its potency was 1/100 that of 1713E2. The local infusion of 17fiE2 or 17aE2 had no effect on body or uterine weight. We conclude from these rmdings that estrogen delivered directly to the bone of OVX rats in vivo at 2.4 and 24 fmol/day acted locally to inhibit bone resorption and stimulate bone formation.About 50 years ago, Albright et al.(1) suggested a link between postmenopausal osteoporosis and estrogen deficiency. The lack of estrogen is associated with increased bone remodeling rates, accelerated bone loss, and a negative calcium balance (2). Estrogen replacement therapy decreases bone turnover and the rate ofbone resorption and reduces the occurrence of fractures in postmenopausal osteoporosis. However, the mechanism by which estrogen exerts its effects on bone is still unknown (3,4 2172The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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“…The femurs and pelvis of mice are the bones most responsive to estrogens.ls It may be that the relatively low ash content and lack of consistent excessive bone in the estrogen-treated mice is the result of late reversal of the bone changes after long term treatment. 20 There was no consistent relationship between the quantity of bone in the femur, as measured either by the cross-sectional area of cortex or the ash content, adjusted for differences in length, and the occurrence of arthritis in the various experimental groups of DBA/2JN mice. The presence of joint disease did not affect the cross-sectional area of the femur shaft in 3 additional male DBA/BJN mice with osteoarthritis in which this was studied.…”

mentioning

confidence: 88%

Sex hormones, bone changes and osteoarthritis in DBA/2JN mice

Sokoloff¹,

Varney²,

Scott³

1965

Arthritis & Rheumatism

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Several possible mechanisms by which sex hormones may influence development of osteoarthritis in mice have been investigated. No relationship existed between the joint disease and mineral content of the bone. A sexual dimorphism in femur length is described for the first time. Strain differences in the effect of sex hormones on the joints of STR/lN and other strains of mice cannot be accounted for by a proposed "dyschondrogenesis."Esseva investigate plure possible mechanismos per que hormones sexual pote influentiar le disveloppamento de osteoarthritis in muses. Nulle relation esseva trovate le inter le morbo articular e le contento mineral del osso. Un dimorphismo sexual in le Iongor del femore es describite pro le prime vice. Differentias inter muses STR/lN e altere lineas con respecto a1 effect0 del hormones de sex0 super le articulationes non pote esser explicate per un proponite "dyschondrogenese."

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Endosteal-Bone Formation in Estrogen-Treated Mice

Cited by 100 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.

Direct effects of 17 beta-estradiol on trabecular bone in ovariectomized rats.

Sex hormones, bone changes and osteoarthritis in DBA/2JN mice

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