Vitamin B3 Rescues Mandibular Osteoporosis in Bmi-1–Deficient Mice by Regulating Autophagy

Abstract

Abstract Background Mandible osteoporosis is gaining attention as it causes dental dysfunction and fragility; however, existing anti-osteoporosis therapies do not specifically target mandibular bone and may have negative side effects. Methods Osteoporosis mice were further treated with Vitamin B3(1mg ml-1), compared with a control set of osteoporosis without treatment and a set of wild-type group. Results Here, we demonstrated that Vitamin B3, the precursor of NAD+, significantly rescue osteoporosis in Bmi-1 deficient mice, a well-known premature induced osteoporosis animal modle. Our research found Vitamin B3 significantly enhanced the bone mineral density and bone volume in Bmi-1 deficient mice, promoted the osteogenic differentiation of both in human dental follicle precursor cells (DFPCs) and Bmi-1 deficient mice. Further analysis reveals the level of autophagy and mitophagy is also notably improved in mandible and cells, however the osteogenic effect of Vitamin B3 in hDFPCs was abolished when autophagy inhibition was added. Conclusion Herein, we suggest that Vitamin B3 alleviated the mandible osteoporosis of Bmi-1-deficient mice via enhancing autophagy level, paving the way for using as a potential therapy for aging osteoporosis.