Osteoporosis After Oophorectomy in the Mature Female Rat and the Effect of Oestrogen and/or Progestogen Replacement Therapy in Its Prevention

Aitken, J. M.; Armstrong, E.; Anderson, Jamie

doi:10.1677/joe.0.0550079

Cited by 142 publications

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“…The reduction in plasma calcium concentration and the bone calcium content after ovariectomy was consistent with the findings of Saville (1965) Aitken (1972) and Cruess and Hong (1979). How ovariectomy led to hypocalcemia is not yet clear but a suppression of GI calcium absorption and serum 1,25(OH)2D3 was reported in postmenopausal women (Riggs et al, 1981).…”

Section: Discussionsupporting

confidence: 90%

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

1983

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AbstractsThe plasma calcium concentration, urinary calcium excretion, total bone calcium content and the rate of calcium uptake and release by tibias were measured in 6 groups of rats which were kept under various treatment protocols for 8 wk. Ovariectomy led to significant hypocalcemia and a decrease in bone calcium content the former being reversed towards normal by estrogen treatment.Chronic ethanol ingestion reduced the bone calcium content without apparent effect on plasma calcium in intact rat and further reduced (P<0.05) the bone calcium content in ovariectomized rats. The calcium uptake by the bone measured by 45Ca injected ip at zero hour was the same among the 6 groups. When "Ca was injected ip 17 hours earlier, the disappearance of plasma 45Ca was found to be slower in ovariectomized and alcohol treated groups, indicating a higher rate of calcium movement from bone to plasma. Moreover, there was also an increase in the rate of calcium release by tibias after ovariectomy and chronic alcohol ingestion ; the release was slightly greater in the condition of ovariectomy plus alcohol.The present investigation thus, provides evidence that ethanol is likely to have a direct stimulatory effect on bone resorption as well as an indirect effect through disrupting ovarian function during chronic administration.

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Section: Discussionsupporting

confidence: 90%

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

1983

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“…It is well known that rats develop osteopenia after ovariectomy (OVX),' and the OVX rat has been used as a model for postmenopausal osteoporosis (1)(2)(3). Our studies have shown that bone density in rats is reduced 6 mo post-OVX, and that the ratio of femoral cortical thickness to midshaft diameter was significantly lower than normal (x-ray femoral score; Table I).…”

Section: Introductionmentioning

confidence: 57%

Bone deficit in ovariectomized rats. Functional contribution of the marrow stromal cell population and the effect of oral dihydrotachysterol treatment.

Tabuchi¹,

Simmons²,

Fausto³

et al. 1986

J. Clin. Invest.

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This study investigates the proliferative and osteogenic role of marrow stromal/osteoprogenitor cells in the development of the cortical bone deficit in ovariectomized (OVX) female rats. In vitro, clonal growth of marrow stromal cells from OVX rats was significantly impaired (vs. sham-operated controls). Yet in vivo, cells from sham-operated and OVX rats had equal osteogenic potential in several in vivo experimental situations, such as in intraperitoneally implanted millipore diffusion chambers and in intramuscular implants of marrow plus osteoinductive bone matrix (composite grafts). Long-term (6 mo) dihydrotachysterol (DHT) treatment of OVX rats enhanced their in vitro proliferative potential and clonal growth, as well as their osteogenic expression in composite grafts. The observation that the in vivo osteogenic performance of OVX rat marrow stromal cells was normal at extraosseous sites suggests that the mechanisms leading to osteopenia may involve an abnormality in cell-matrix interactions.

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“…Ovariectomy causes osteopenia in rats (22)(23)(24)(25)(26)(27) and has been used as a model for postmenopausal bone loss (25)(26)(27). Wronski et al (27) reported osteopenia and increased bone resorption and formation, estimated by histomorphometry, as early as 14 days after ovariectomy.…”

Section: Discussionmentioning

confidence: 99%

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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Osteoporosis After Oophorectomy in the Mature Female Rat and the Effect of Oestrogen and/or Progestogen Replacement Therapy in Its Prevention

Cited by 142 publications

References 0 publications

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

Bone deficit in ovariectomized rats. Functional contribution of the marrow stromal cell population and the effect of oral dihydrotachysterol treatment.

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

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