Affiliations: Department of Orthopaedic Surgery, Toho University School of Medicine 6-11-1 Omorinishi, Ota-ku, Tokyo 143-8541, Japan | Department of Orthopaedic Surgery, Nara Medical University, 840, Shijyo-cho, Kashihara, Nara 634-8522, Japan | International Innovation Center, Kyoto University, Yoshida-Hon-machi, Sakyo-ku, Kyoto 606-8501, Japan
Note: [] Corresponding author: K. Hattori, Department of Orthopaedic Surgery, Nara Medical University, 840, Shijyo-cho, Kashihara, Nara 634-8522, Japan. Tel.: +81 744 22 3051; Fax: +81 744 25 6449; E-mail: hattori@naramed-u.ac.jp.
Abstract: Recent studies have reported that statins, inhibitors of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase, increase bone formation in osteoblasts in vitro, suggesting that statins may have a new therapeutic application in the treatment of osteoporosis. During the reparative phase of healing of bone fractures, bone marrow-derived mesenchymal stem cells differentiate into osteoblasts or chondrocytes to form callus. If statins also stimulate bone formation in bone marrow-derived mesenchymal stem cells they may have beneficial effects in the treatment of bone fractures. In this study, we assessed the effect of statins on bone formation in rat bone marrow-derived mesenchymal stem cells in vitro. The statins fluvastatin, simvastatin and pravastatin did not significantly enhance mineralization, alkaline phosphatase (ALP) activity and bone gra protein (BGP, osteocalcin). These findings suggest that statins do not increase bone formation in bone marrow-derived mesenchymal stem cells.
Keywords: Statins, bone marrow-derived mesenchymal stem cell, bone formation
