Abstract
Previously reported fracture rates in patients with spinal cord injury range from 1% to 20%. However, the exact role of spinal cord injury in bone metabolism has not yet been clarified. In order to investigate the effects of serum leptin and bone mineral density on the healing of long bone fractures in men with spinal cord injury, 15 male SCI patients and 15 matched controls were involved in our study. The outcome indicated that at 4 and 8 weeks after bone fracture, callus production in patients with spinal cord injury was lower than that in controls. Besides, bone mineral density was significantly reduced at 2, 4 and 8 weeks. In addition, it was found that at each time point, patients with spinal cord injury had significantly higher serum leptin levels than controls and no association was found between serum leptin level and bone mineral density of lumbar vertebrae. Moreover, bone mineral density was positively correlated with bone formation in both of the groups. These findings suggest that in early phases i.e. week 4 and 8, fracture healing was impaired in patients with spinal cord injury and that various factors participated in the complicated healing process, such as hormonal and mechanical factors.
Highlights
Among humans who suffer from three major disorders, including adipose tissue decomposition, neuroendocrine alteration and abnormal skeletal remodeling, spinal cord injury (SCI) is a long-standing and pressing public health problem
This study demonstrated the effects of SCI on the relationships among serum leptin level, bone mineral density (BMD) and fracture healing in clinical patients
Serum leptin was significantly higher in the SCI group than that in the control group at all-time points after the operation and the peak serum leptin concentration in the SCI group occurred at 2 weeks., Previous studies demonstrated that SCI could result in direct damages, such as diffuse axonal injury, contusions and intracranial hematomas
Summary
Among humans who suffer from three major disorders, including adipose tissue decomposition, neuroendocrine alteration and abnormal skeletal remodeling, spinal cord injury (SCI) is a long-standing and pressing public health problem. Studies have focused on abnormal bone metabolism in patients with SCI [1,2]. As documented complications of SCI, reduction in bone mineralization and deterioration of skeletal microarchitecture occur predominantly in long bones of lower limbs [3,4]. Other studies have demonstrated that SCI may result in the rising of various hormones that significantly increase serum osteo-inductive factors, such as osteocalcin and leptin [5,6]. Discovered as a satiety factor regulating food intake and energy expenditure, Leptin is the circulating protein product of the obesity (Ob) gene, which is synthesized and secreted by adipocytes [7,8].
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