Yuanzhen Peng1, Wei Zhao1, Yizhong Hu2, Fei Li3, X Edward Guo2, Dong Wang4, William A Bauman1,5,6, Weiping Qin7,8. 1. National Center for the Medical Consequences of Spinal Cord Injury, James J. Peters VA Medical Center, Bronx, NY, USA. 2. Department of Biomedical Engineering, Columbia University, New York, NY, USA. 3. Yantaishan Hospital, Yantai, Shandong, China. 4. Department of Pharmaceutical Sciences, College of Pharmacy, University of Nebraska Medical Center, Omaha, NE, USA. 5. Departments of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 6. Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 7. National Center for the Medical Consequences of Spinal Cord Injury, James J. Peters VA Medical Center, Bronx, NY, USA. weiping.qin@mssm.edu. 8. Departments of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA. weiping.qin@mssm.edu.
Abstract
STUDY DESIGN: Animal study. OBJECTIVE: This study examined how soon after spinal cord injury (SCI) bone loss occurs, and investigated the underlying molecular mechanism. METHODS: Eight-week-old male Wistar rats underwent complete transection of the thoracic spinal cord at T3-4 or sham operation (n = 10-12 per group). Blood, hindlimb bone samples, and bone marrows were collected at 2 and 7 days after SCI. RESULTS: The neurologically motor-complete SCI causes loss of bone mass and deterioration of trabecular bone microstructure as early as 2 days after injury; these skeletal defects become more evident at 7 days. These changes are associated with a dramatic increase in levels of bone resorption maker CTX in blood. Alternations of gene expression in hindlimb bone tissues and bone marrow cells at the first week after SCI were examined. Gene expressions responsible for both bone resorption and formation are increased at 2 days post-SCI, and the associated bone loss and bone deterioration are likely the result of higher levels of osteoclastic resorption over osteoblastic formation, as may be extrapolated from findings at molecular levels. CONCLUSIONS: Rapid bone loss occurs as early as 2 days after motor-complete SCI and interventions for inhibiting bone resorption and prompting bone formation should start as soon as possible after the injury to prevent bone loss.
STUDY DESIGN: Animal study. OBJECTIVE: This study examined how soon after spinal cord injury (SCI) bone loss occurs, and investigated the underlying molecular mechanism. METHODS: Eight-week-old male Wistar rats underwent complete transection of the thoracic spinal cord at T3-4 or sham operation (n = 10-12 per group). Blood, hindlimb bone samples, and bone marrows were collected at 2 and 7 days after SCI. RESULTS: The neurologically motor-complete SCI causes loss of bone mass and deterioration of trabecular bone microstructure as early as 2 days after injury; these skeletal defects become more evident at 7 days. These changes are associated with a dramatic increase in levels of bone resorption maker CTX in blood. Alternations of gene expression in hindlimb bone tissues and bone marrow cells at the first week after SCI were examined. Gene expressions responsible for both bone resorption and formation are increased at 2 days post-SCI, and the associated bone loss and bone deterioration are likely the result of higher levels of osteoclastic resorption over osteoblastic formation, as may be extrapolated from findings at molecular levels. CONCLUSIONS: Rapid bone loss occurs as early as 2 days after motor-complete SCI and interventions for inhibiting bone resorption and prompting bone formation should start as soon as possible after the injury to prevent bone loss.
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