Abstract
Spinal cord injury (SCI) results in rapid, severe osteoporosis and an increased risk of lower extremity fractures. Despite the medical complications associated with these fractures, there is no standard of care to prevent osteoporotic fractures following SCI. Functional electrical stimulation‐ (FES‐) assisted rowing is a promising intervention to improve bone health in SCI because of its ability to generate a muscular contraction in conjunction with mechanical loading of the lower extremity long bones. Combination therapy consisting of FES‐rowing plus zoledronic acid (ZA) may be a superior treatment via inhibition of bone resorption and stimulation of new bone formation. We studied participants enrolled in a randomized clinical trial comparing FES‐rowing alone with FES‐rowing plus ZA to improve bone health in SCI. Volumetric CT scans at the distal femur and proximal tibial metaphyses were performed. Bone geometric properties (cortical thickness index [CTI], cortical compressive strength index [CSI], buckling ratio [BR], bending strength index) and mineral (cortical bone volume [CBV], cortical bone mineral density, cortical bone mineral content) indices were determined. In models adjusting for baseline values, we found that the CBV (p = 0.05 to 0.006), the CTI (p = 0.009), and the BR (p = 0.001) at both the distal femoral and proximal tibial metaphyses were greater in the ZA plus rowing group compared with the rowing‐only group. Similarly, there was a significant positive association between the total rowing work completed and the BR at the proximal tibia (p = 0.05). A subgroup analysis of the rowing‐only arm showed that gains in the CSI at the tibial metaphysis varied in a dose‐dependent fashion based on the total amount of exercise performed (p = 0.009). These findings demonstrate that the osteogenic response to FES‐rowing is dose‐dependent. Combination therapy with ZA and FES‐row training has therapeutic potential to improve bone quality, and perhaps reduce fracture risk at the most common fracture site following SCI. © 2019 The Authors. JBMR Plus Published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.
Highlights
Osteoporosis following spinal cord injury (SCI) is thought to be based primarily on the loss of mechanical loading that occurs after lower extremity paralysis.[1–3] Bone loss leads to fractures in up to 50% of individuals with SCI, with the majority of fractures occurring at the metaphyses of the proximal tibia and distal femur
Several animal and human studies have shown new bone formation based on functional electrical stimulation- (FES) alone.[20,21] Slowing of bone loss has been reported in response to Functional electrical stimulation- (FES-)cycling.[22]. The primary aim of this study was to test the osteoanabolic effects of a novel therapeutic exercise, either alone or in combination with an antiresorptive medication
Volunteers were ineligible for the study if they were actively being treated for epilepsy; actively using medications potentially affecting bone metabolism, including parathyroid hormone (PTH) and PTH analogs, bisphosphonates, androgenic steroids, estrogenic steroids, antiepileptics, lithium, or oral glucocorticoid; if they had a history of peripheral nerve compression or rotator cuff injury that limited the ability to exercise; uncontrolled diabetes; active renal disease; implanted defibrillator or pacemaker; an active grade 2 or greater pressure ulcer in a location that could be worsened with exercise; or if they had an active bone fracture or lower extremity contractures
Summary
Osteoporosis following spinal cord injury (SCI) is thought to be based primarily on the loss of mechanical loading that occurs after lower extremity paralysis.[1–3] Bone loss leads to fractures in up to 50% of individuals with SCI, with the majority of fractures occurring at the metaphyses of the proximal tibia and distal femur. Osteoporosis following spinal cord injury (SCI) is thought to be based primarily on the loss of mechanical loading that occurs after lower extremity paralysis.[1–3]. There is evidence suggesting that these drugs mitigate bone loss after SCI,(8–11) they do not stimulate new bone formation. There have been few therapeutic interventions shown to stimulate new bone formation, increase bone mass, improve bone microarchitecture, or improve bone strength after SCI.[12–14]. Because lower extremity paralysis is a contributing factor to disuse osteoporosis, reintroduction of mechanical loading may effectively stimulate bone regeneration. For individuals with SCI, functional electrical stimulation- (FES) rowing exercise may provide sufficient mechanical loading of the paralyzed lower limbs to stimulate bone formation. We conducted a clinical trial testing combination therapy with FES-rowing plus a bisphosphonate (zoledronic acid [ZA]) compared with FESrowing alone to improve bone in the paralyzed lower extremity. We hypothesized that gains with rowing would be dose-dependent, in that greater rowing work would yield greater gains in bone
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