A functional androgen receptor is not sufficient to allow estradiol to protect bone after gonadectomy in estradiol receptor–deficient mice
J. Clin. Invest. Natalie A. Sims, et al. 111:1319 doi:10.1172/JCI17246 [Go to this article.]

Figure 6
Testosterone treatment of ERα^–/– females prevents ovariectomy-induced bone loss and high bone turnover. Antiandrogen treatment, but not antiestrogen treatment, partially reproduces the effects of ovariectomy in ERα^–/– females. (a) Representative von Kossa–stained sections of proximal tibiae from sham-operated mice, ovariectomized (Ovx) mice, ovariectomized mice implanted with pellets delivering 2.5 mg/kg/d subcutaneous propiotestosterone (Ovx+T), and sham-operated females treated subcutaneously with the antiestrogen RU58668 (10 mg/kg/d) (Sham+aE) or the antiandrogen RU58642 (30 mg/kg/d) (Sham+aA). (b) Testosterone treatment (light gray bars) prevented the ovariectomy-induced reduction in Tb.BMD and BV/TV in ERα^–/– females. Antiandrogen treatment (dark gray bars), but not antiestrogen treatment (medium gray bars), reduced Tb.BMD and BV/TV to levels not significantly different from post-ovariectomy levels. (c) Testosterone treatment prevented the ovariectomy-induced increase in ObS/BS, BFR/BS, and OcS/BS in ERα^–/– females. Antiandrogen, but not antiestrogen, treatment increased ObS/BS and OcS/BS. Values are mean ± SEM. **P < 0.01, ***P < 0.001 vs. sham-operated of the same genotype; ⁺P < 0.05, ⁺⁺P < 0.01, ⁺⁺⁺P < 0.001 vs. Ovx of the same genotype.