Related Experiment Video
Updated: Aug 11, 2026
Osteoclast Derivation from Mouse Bone Marrow
Published on: November 6, 2014
Androgen-accelerated bone maturation in mice is not attenuated by Faslodex, an estrogen receptor blocker
D F Gunther1, L E Underwood, A S Calikoglu
1Division of Pediatric Endocrinology, University of North Carolina, Chapel Hill, NC, USA.
Abstract:
Androgens accelerate bone maturation, but it is unclear to what extent this process may be mediated by estrogens derived from aromatization of androgens. In this study, we investigated whether an estrogen-blocking agent, Faslodex (ICI 182,780), can attenuate testosterone-accelerated skeletal maturation in immature mice. On days of life 2-8, mouse pups received either testosterone propionate (50 microg/100 g body weight), Faslodex (100 microg/100 g body weight), a combination of Faslodex + testosterone, or vehicle alone. Skeletal maturation was assessed in the forepaw and the lumbar spine. Testosterone caused acceleration of bone maturation (p < 0.05, compared with vehicle), predominantly of axial bones. Faslodex, however, failed to block the effect of testosterone, such that the mice receiving Faslodex + testosterone had skeletal maturation scores similar to those treated with testosterone alone. These results suggest that androgens have the capacity to stimulate bone maturation directly, probably via their own receptors.
Insights
This study found that androgens directly accelerate bone maturation in mice, independent of estrogen conversion. Blocking estrogen receptors did not prevent testosterone
Area of Science:
- Endocrinology
- Skeletal Biology
- Pharmacology
Background:
- Androgens are known to accelerate bone maturation.
- The role of estrogens, derived from androgen aromatization, in this process is not fully understood.
- Investigating the direct effects of androgens on skeletal maturation is crucial.
Purpose of the Study:
- To determine if estrogen blockade can inhibit testosterone-induced acceleration of skeletal maturation in immature mice.
- To elucidate the direct role of androgens in bone maturation, separate from their conversion to estrogens.
Main Methods:
- Immature mice were treated with testosterone propionate, Faslodex (an estrogen-blocking agent), a combination of both, or vehicle.
- Skeletal maturation was assessed in the forepaw and lumbar spine.
- Statistical analysis compared maturation scores between treatment groups.
Main Results:
- Testosterone significantly accelerated bone maturation, particularly in axial bones, compared to the vehicle group.
- Faslodex treatment did not attenuate the bone maturation effects of testosterone.
- Mice receiving both Faslodex and testosterone showed skeletal maturation scores similar to those treated with testosterone alone.
Conclusions:
- Androgens can directly stimulate bone maturation, likely through androgen receptors.
- Estrogen mediation is not the primary mechanism for testosterone-accelerated skeletal maturation in this model.
- These findings highlight the direct anabolic effects of androgens on the developing skeleton.
