Collectively, our results suggest that GTE precludes excessive bone loss due to postmenopausal osteoporosis by inducing bone formation through Bmp2-Smads 1/5/8-Runx2 signaling and interrupts osteoclastogenesis via RANKL/OPG binding and lowered Nox-4 activity (Figure 6E). Here, TNFRSF11B is linked to postmenopausal osteoporosis.