Int J Med Sci 2018; 15(7):723-729. doi:10.7150/ijms.22713 This issue

Research Paper

Propofol attenuates osteoclastogenesis by lowering RANKL/OPG ratio in mouse osteoblasts

Do-Won Lee1, Jae-Young Kwon1✉, Hae-Kyu Kim1, Hyeon-Jeong Lee1, Eun-Soo Kim1, Hyae-Jin Kim1, Hyung-Joon Kim2, Han-Bit Lee1

1. Department of Anesthesia and Pain Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea
2. Department of Oral Physiology, BK21 PLUS Project, and Institute of Translational Dental Sciences, School of Dentistry, Pusan National University, Yangsan, Republic of Korea

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Lee DW, Kwon JY, Kim HK, Lee HJ, Kim ES, Kim HJ, Kim HJ, Lee HB. Propofol attenuates osteoclastogenesis by lowering RANKL/OPG ratio in mouse osteoblasts. Int J Med Sci 2018; 15(7):723-729. doi:10.7150/ijms.22713. Available from

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Bone remodeling plays an important role in the bone healing process; for example, following fracture. The relative ratio of the receptor activator of nuclear factor kappa B ligand (RANKL)/ osteoprotegerin (OPG) controls osteoclast differentiation, thereby playing a pivotal role in the regulation of bone remodeling. Propofol, a widely used anesthetic agent in orthopedic procedures, is considered to possess potential antioxidant properties owing to its structural similarity to α-tocopherol. Antioxidants are known to enhance bone healing. Accordingly, in the present study, we aimed to investigate osteoblastic differentiation and RANKL/OPG expression following propofol administration, in order to assess the potentially beneficial effects of this drug on the bone remodeling process, using calvarial primary osteoblasts from newborn mice. Calvarial pre-osteoblast cells were cultured in media containing clinically relevant concentrations of propofol, and cytotoxicity, effects on cell proliferation, osteogenic activity, and osteoclastogenesis were examined. The present findings indicated that propofol did not exert cytotoxic effects or alter cell proliferation in primary calvarial osteoblasts. Further, propofol did not affect osteoblast differentiation. The RANKL/OPG ratio was found to be decreased following propofol administration, and osteoclastogenesis was significantly reduced, indicating that propofol attenuated the osteoclastogenesis-supporting activity of osteoblasts. The results demonstrate that propofol, at clinically relevant concentrations, exerts beneficial effects on bone remodeling by attenuating osteoclastogenesis via suppression of the RANKL/OPG expression axis.

Keywords: Bone remodeling, Osteoblast, RANKL, OPG, Propofol