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Objective . Redox imbalance contributes to bone fragility. We have evaluated the in vivo role of nuclear factor erythroid derived 2-related factor-2 (Nrf2), an important regulator of cellular responses to oxidative stress, in bone metabolism using a model of postmenopausal osteoporosis.  Methods . Ovariectomy was performed in both wild-type and mice deficient in Nrf2 (Nrf2 −/− ). Bone microarchitecture was analyzed by  μ CT. Serum markers of bone metabolism were also measured. Reactive oxygen species production was determined using dihydrorhodamine 123.  Results . Sham-operated or ovariectomized Nrf2 −/−  mice exhibit a loss in trabecular bone mineral density in femur, accompanied by a reduction in cortical area in vertebrae. Nrf2 deficiency tended to increase osteoblastic markers and significantly enhanced osteoclastic markers in sham-operated animals indicating an increased bone turnover with a main effect on bone resorption. We have also shown an increased production of oxidative stress in bone marrow-derived cells from sham-operated or ovariectomized Nrf2 −/−  mice and a higher responsiveness of bone marrow-derived cells to osteoclastogenic stimuli in vitro.  Conclusion . We have demonstrated in vivo a key role of Nrf2 in the maintenance of bone microarchitecture.

Effects of Nrf2 Deficiency on Bone Microarchitecture in an Experimental Model of Osteoporosis