Tamoxifen Impairs Both Longitudinal and Cortical Bone Growth in Young Male Rats

  title={Tamoxifen Impairs Both Longitudinal and Cortical Bone Growth in Young Male Rats},
  author={Elham Karimian and Andrei S. Chagin and Jennifer Gjerde and Terhi J. Heino and Ernst Asbj{\o}rn Lien and Claes Ohlsson and Lars S{\"a}vendahl},
  journal={Journal of Bone and Mineral Research},
Tamoxifen (Tam) has been used experimentally to treat boys with gynecomastia and girls with McCune‐Albright syndrome. This drug was recently shown to inhibit the growth of cultured fetal rat metatarsal bones and thus might also affect bone growth in vivo. Four‐week‐old Sprague‐Dawley rats were gavaged daily with vehicle alone (peanut oil), Tam (40 mg/kg/d; 1 or 4 wk), or estradiol (40 μg/kg/d; 4 wk). Five of the 10 rats in each group were killed after 4 wk and the other five after 14 wk of… 

Resveratrol Treatment Delays Growth Plate Fusion and Improves Bone Growth in Female Rabbits

It is concluded thatTrans-resveratrol has the potential to improve longitudinal bone growth and was associated with a delay of growth plate fusion resulting in increased final length and accompanied by a profound suppression of VEGF and laminin expression.

Regulation of bone growth via ligand-specific activation of estrogen receptor alpha.

The data show that estrogenic effects on bone growth and growth plate maturation are mainly mediated via ERα, and may have direct implications for the development of new and more selective treatment modalities of extreme tall stature using selective estrogen receptor modulators that may have low side effects than high-dose E2 treatment.


The studies described here demonstrate that SERMs have the potential to influence growth plate cartilage in such a manner as to affect the longitudinal bone growth, and in ovariectomized rabbits, resveratrol improves both axial and appendicular bone growth.

Skeletal and Uterotrophic Effects of Endoxifen in Female Rats

The results demonstrate that endoxifen elicits beneficial effects on bone in ovary‐intact rats and protects against bone loss following ovariectomy and that it elicits partial agonistic effects on the uterus and skeleton in ovariectomized animals.

Assessment of a nonsteroidal aromatase inhibitor, letrozole, in juvenile rats.

The observed effects in juvenile rats were considered predictable and primarily related to the mechanism of action of letrozole upon estrogen synthesis.

Antifibrotic effect of tamoxifen in a model of progressive renal disease.

Tamoxifen exhibits antifibrotic effects in the L-NAME model of hypertensive nephrosclerosis, likely through the inhibition of TGF-β1, suggesting that it may have therapeutic use in CKD treatment.

of an in vitro model for growth plate physiology: do mesenchymal stem cells differentiating into chondrocytes show a phenotype

  • Biology, Medicine
  • 2010
The animal studies on AIs show that for the analysis of drugs that intervene with sex steroid signaling, rodents are not an optimal model, and the in vitro model of MSCs differentiating into epiphyseal chondrocytes can be used in future studies aimed at a better understanding of the physiology of the epiphysis.

Estrogen signaling in growth plate cartilage.

It is well known that sex steroids, in particular estrogens, play an important role in longitudinal bone growth during puberty. High doses of estrogen therapy can reduce the final height of an

Melatonin abrogates liver, ovarian, and uterine toxicities induced by tamoxifen in a breast cancer mouse model

The results have demonstrated that tamoxifen when used as combination therapy with melatonin serve as an effective anti-breast cancer molecule with minimum liver, ovarian and uterus toxicities.



The Effect of Tamoxifen on Bone Metabolism and Skeletal Growth is Different in Ovariectomized and Intact Rats

The findings indicate that TAM exerts an effect of estrogen agonist on bone metabolism and skeletal growth in OVX rats, however, it does not affect them in intact rats.

Tamoxifen stimulates cancellous bone formation in long bones of female mice.

Selective estrogen receptor modulators (SERMs) have been developed as a means of targeting estrogen's protective effect on the skeleton in the treatment of postmenopausal osteoporosis. Although it is

17 beta-estradiol stimulates cancellous bone formation in female rats.

Results suggest that stimulation of cancellous bone formation is a physiological action of E2 in the rat, and Stimulation of bone formation by estrogen showed a similar pattern of dose-responsiveness to recognized physiological targets of E1: suppression of longitudinal growth and uterine growth.

Effects of estrogen on growth plate senescence and epiphyseal fusion

The data suggest that epiphyseal fusion is triggered when the proliferative potential of growth plate chondrocytes is exhausted; and estrogen accelerates the programmed senescence of the growth plate, thus causing earlier proliferative exhaustion and consequently earlier fusion.

Raloxifene acts as an estrogen agonist on the rabbit growth plate.

It is concluded that raloxifene acts as an estrogen agonist on the growth plate, accelerating growth plate senescence and thus hastening epiphyseal fusion.

Growth retardation induced by dexamethasone is associated with increased apoptosis of the growth plate chondrocytes.

It is concluded that apoptosis is one mechanism involved in growth retardation induced by glucocorticoids, and premature loss of resting/proliferative chondrocytes by apoptosis could contribute to incomplete catch-up seen after prolonged glucoc Corticoid treatment.

Comparison of tamoxifen and testosterone propionate in male rats: differential prevention of orchidectomy effects on sex organs, bone mass, growth, and the growth hormone-IGF-I axis.

Tamoxifen prevented ORX effects on bone and cholesterol in male rats without affecting sex organs or PRL and might be useful for men who must avoid androgens.

Preliminary in situ identification of estrogen target cells in bone

It is suggested that osteocytes are major skeletal estrogen target cells and may be involved in coordinating the response of surface bone cells to the hormone, and further that chondrocytes may beinvolved in estrogen‐induced epiphyseal growth plate fusion.

The role of estrogen in bone growth and maturation during childhood and adolescence

  • G. Cutler
  • Medicine, Biology
    The Journal of Steroid Biochemistry and Molecular Biology
  • 1997