Sung-Yen Lin1, Lin Kang2, Jian-Chih Chen3, Chau-Zen Wang4, Han Hsiang Huang5, Mon-Juan Lee6, Tsung-Lin Cheng4, Chi-Fen Chang7, Yi-Shan Lin8, Chung-Hwan Chen9. 1. Department of Orthopedics, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung City, Taiwan; Department of Orthopedics, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan; Orthopaedic Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan; Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. 2. Department of Obstetrics and Gynecology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan. 3. Department of Orthopedics, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Orthopedics, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. 4. Orthopaedic Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Orthopedics, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Physiology, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. 5. Department of Veterinary Medicine, National Chiayi University, Chiayi City 60054, Taiwan. 6. Department of Bioscience Technology, Chang Jung Christian University, Tainan, Taiwan; Innovative Research Center of Medicine, Chang Jung Christian University, Tainan, Taiwan. 7. Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan. 8. Orthopaedic Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan. 9. Department of Orthopedics, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung City, Taiwan; Department of Orthopedics, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan; Orthopaedic Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Orthopedics, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. Electronic address: hwan@kmu.edu.tw.
Abstract
BACKGROUND: Previously, we found that (-)-epigallocatechin-3-gallate (EGCG) enhanced osteogenic differentiation of murine bone marrow mesenchymal stem cells by increasing the mRNA expression of osteogenesis-related genes, alkaline phosphatase activity and eventually mineralization. We further found EGCG supplementation preserved bone mass and microarchitecture in female rats during estrogen deficiency in the proximal tibia and lumbar spine at least in part by increasing bone morphogenetic protein-2 (BMP2). BMP2 can enhance de novo bone formation. PURPOSE: In this study, we evaluate the effect of local EGCG application in de novo bone formation in bone defect healing. METHODS: Twenty-four rats aged 4 months were weight-matched and randomly allocated to 2 groups: defect control with vehicle treatment (control) and defect with 10 µM EGCG treatment (EGCG). Daily vehicle and EGCG were applied locally by percutaneous local injection 2 days after defect creation for 2 weeks. Four weeks after treatment, animals were sacrificed for micro-computed tomography (μ-CT) and biomechanical analysis. RESULTS: Local EGCG at femoral defect can enhance de novo bone formation by increasing bone volume and subsequently improve mechanical properties including max load, break point, stiffness, area under the max load curve, area under the break point curve and ultimate stress. CONCLUSIONS: Local EGCG may enhance bone defect healing via at least partly by the de novo bone formation of BMP-2.
BACKGROUND: Previously, we found that (-)-epigallocatechin-3-gallate (EGCG) enhanced osteogenic differentiation of murine bone marrow mesenchymal stem cells by increasing the mRNA expression of osteogenesis-related genes, alkaline phosphatase activity and eventually mineralization. We further found EGCG supplementation preserved bone mass and microarchitecture in female rats during estrogen deficiency in the proximal tibia and lumbar spine at least in part by increasing bone morphogenetic protein-2 (BMP2). BMP2 can enhance de novo bone formation. PURPOSE: In this study, we evaluate the effect of local EGCG application in de novo bone formation in bone defect healing. METHODS: Twenty-four rats aged 4 months were weight-matched and randomly allocated to 2 groups: defect control with vehicle treatment (control) and defect with 10 µM EGCG treatment (EGCG). Daily vehicle and EGCG were applied locally by percutaneous local injection 2 days after defect creation for 2 weeks. Four weeks after treatment, animals were sacrificed for micro-computed tomography (μ-CT) and biomechanical analysis. RESULTS: Local EGCG at femoral defect can enhance de novo bone formation by increasing bone volume and subsequently improve mechanical properties including max load, break point, stiffness, area under the max load curve, area under the break point curve and ultimate stress. CONCLUSIONS: Local EGCG may enhance bone defect healing via at least partly by the de novo bone formation of BMP-2.