Exploring changes in bone mass in individuals with a chronic spinal cord injury.

People experience rapid bone loss shortly after a spinal cord injury (SCI), but the long-term bone changes are yet to be confirmed. This study showed that trabecular bone may have reached a steady state, whereas cortical bone continued to decline in people with a chronic SCI (mean time post injury: 15.5 ± 10 years). INTRODUCTION: (1) To explore changes in bone [primary measure: trabecular volumetric bone mineral density (vBMD); secondary measures: cortical vBMD, cortical thickness, cortical cross-sectional area (CSA), and polar moment of inertia] over 2 years in individuals with a chronic spinal cord injury (SCI). (2) To explore whether muscle density changes were potential correlates of the observed bone changes. METHODS: This study is a secondary data analysis of a prospective, observational study involving 70 people with a chronic SCI (≥ 2 years post injury). The study included 4 strata of participants with diverse impairments: (1) Paraplegia (T1-T12) motor complete American Spinal Injury Association Impairment Scale (AIS) A/B (n = 23), (2) Paraplegia motor incomplete AIS C/D (n = 11), (3) Tetraplegia (C2-C8) AIS A/B (n = 22), and (4) Tetraplegia AIS C/D (n = 14). Peripheral quantitative computed tomography scans were taken at the 4% (distal tibia), 38% (diaphyseal tibia), and 66% (muscle cross-sectional area) tibia sites by measuring from the distal to proximal tibia starting at the inferior border of the medial malleolus. The tibia sites were assessed annually over a span of 2 years. Comparisons were made using a paired-samples t test and simple linear regression was used to adjust for sex, time post injury, and bisphosphonate use. RESULTS: We observed no changes in trabecular vBMD at the 4% tibia site, but there was a statistically significant decline in cortical vBMD, cortical thickness, and CSA at the 38% tibia site. Changes in muscle density were not associated with the decreases observed in cortical bone. CONCLUSION: Our findings suggest that individuals with chronic SCI (mean duration of injury: 15.5 ± 10 years) may have reached a plateau in bone loss with respect to trabecular bone, but cortical bone loss can continue well into the chronic stages.

Exercise, muscle, and the applied load-bone strength balance.

A fracture occurs when the applied load is greater than the bone can withstand. Clinical practice guidelines for the management of osteoporosis include recommendations for exercise; one of the few therapies where the proposed anti-fracture mechanisms that include effects on both bone strength and applied loads, where applied loads can come in the form of a fall, externally applied loads, body weight, or muscle forces. The aim of this review is to provide an overview of the clinical evidence pertaining to the potential efficacy of exercise for preventing fractures in older adults, including its direct effects on outcomes along the causal pathway to fractures (e.g., falls, posture, bone strength) and the indirect effects on muscle or the muscle-bone relationship. The evidence is examined as it pertains to application in clinical practice. Considerations for future research are discussed, such as the need for trials in individuals with low bone mass or students that evaluate whether changes in muscle mediate changes in bone. Future trials should also consider adequacy of calorie or protein intake, the confounding effect of exercise-induced weight loss, or the most appropriate therapeutic goal (e.g., strength, weight bearing, or hypertrophy) and outcome measures (e.g., fracture, disability, cost-effectiveness).