Abstract
Spinal cord injury causes rapid, severe osteoporosis with increased fracture risk. Mechanical unloading after paralysis results in increased osteocyte expression of sclerostin, suppressed bone formation, and indirect stimulation of bone resorption. At this time, there are no clinical guidelines to prevent bone loss after SCI, and fractures are common. More research is required to define the pathophysiology and epidemiology of SCI-induced osteoporosis. This review summarizes emerging therapeutics including anti-sclerostin antibodies, mechanical loading of the lower extremity with electrical stimulation, and mechanical stimulation via vibration therapy.
MeSH terms
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Adaptor Proteins, Signal Transducing
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Bone Density
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Bone Density Conservation Agents / therapeutic use
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Bone Morphogenetic Proteins / metabolism
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Electric Stimulation Therapy
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Exercise Therapy
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Genetic Markers
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Humans
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Osteoporosis / epidemiology
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Osteoporosis / etiology*
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Osteoporosis / physiopathology
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Osteoporosis / prevention & control
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Osteoporotic Fractures / epidemiology
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Osteoporotic Fractures / etiology*
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Osteoporotic Fractures / physiopathology
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Osteoporotic Fractures / prevention & control
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Parathyroid Hormone / metabolism
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Risk Factors
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Spinal Cord Injuries / complications*
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Spinal Cord Injuries / physiopathology
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Vibration
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Vitamin D Deficiency / etiology
Substances
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Adaptor Proteins, Signal Transducing
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Bone Density Conservation Agents
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Bone Morphogenetic Proteins
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Genetic Markers
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Parathyroid Hormone
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SOST protein, human