Abstract
Spinal cord injury (SCI) has a huge impact on the individual, society and the economy. Though advances in acute care resulted in greatly reduced co-morbidities, there has been much less progress preventing long-term sequelae of SCI. Among the long-term consequences of SCI is bone loss (osteoporosis) due to the mechanical unloading of the paralyzed limbs and vascular dysfunction below the level of injury. Though osteoporosis may be partially prevented via pharmacologic interventions during the acute post-injury phase, there are no clinical guidelines to treat osteoporosis during the chronic phase. Thus there is need for scientific advances to improve the rehabilitative approaches to SCI-related osteoporosis. Recent advances in application of a new technology, functional electrical stimulation, provide a new and exciting opportunity to improve bone metabolism and to provide mechanical strain to the paralyzed lower limbs sufficient to stimulate new bone formation in individuals with SCI. The purpose of this minireview is to delineate our current understanding of SCI-related osteoporosis and to highlight recent literature towards its prevention and treatment.
Highlights
Spinal cord injury (SCI) has a huge impact on the individual, society and the economy
Though advances in acute care resulted in greatly reduced co-morbidities in the initial few years following a spinal cord injury, there has been much less progress preventing medical complications associated with SCI in the long-term
The general consensus is that SCI-related bone loss occurs in 2 phases: 1) a rapid, acute phase characterized by increased bone resorption that plateaus somewhere between 18-24 months post-injury and 2) a chronic phase, characterized by inhibition of bone formation with ongoing bone loss that is more gradual in nature [24,25,26,27]
Summary
There are no clinical guidelines for the prevention or reversal of SCI-related osteoporosis. The efficacy of bisphosphonate treatment appears to be limited to only within the acute phase (< 1 year) of injury [48]. This may be related to the fact that though bisphosphonates reduce bone resorption, they have limited effect on bone formation [49]. The ongoing discussion suggests that bone loss in individuals with SCI may be partially prevented via pharmacologic interventions, notably during the acute post-injury phase, current pharmacologic treatments do not appear to be capable of reversing bone demineralization. A recent, emerging theme in the literature is the utility of novel, nonpharmacologic paradigms that are designed for individuals with SCI to prevent and reverse the bone loss due to prolonged immobility
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