Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
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J. Bone Miner. Res. · Feb 2014
Multicenter Study Clinical TrialMortality after lower extremity fractures in men with spinal cord injury.
In the United States, there are over 200,000 men with spinal cord injuries (SCIs) who are at risk for lower limb fractures. The risk of mortality after fractures in SCI is unknown. This was a population-based, cohort study of all male veterans (mean age 54.1; range, 20.3-100.5 years) with a traumatic SCI of at least 2 years' duration enrolled in the Veterans Affairs (VA) Spinal Cord Dysfunction Registry from FY2002 to FY2010 to determine the association between lower extremity fractures and mortality. ⋯ In fully-adjusted models, the association of incident lower extremity fracture with increased mortality was substantially greater in older men (age ≥50 years) for the entire cohort (HR, 3.42; 95% CI, 2.75-4.25) and for those with complete SCI (HR, 3.13; 95% CI, 2.19-4.45), compared to younger men (age <50 years) (entire cohort: HR, 1.42; 95% CI, 0.94-2.14; complete SCI: HR, 1.71; 95% CI, 0.98-3.01). Every additional point in the Charlson comorbidity index was associated with a 10% increase in the hazard of death in models involving the entire cohort (HR, 1.11; 95% CI, 1.09-1.13) and also in models limited to men with complete SCI (HR, 1.10; 95% CI, 1.06-1.15). These data support the concept that both the fracture itself and underlying comorbidities are drivers of death in men with SCI.
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J. Bone Miner. Res. · Feb 2014
Delayed bone regeneration is linked to chronic inflammation in murine muscular dystrophy.
Duchenne muscular dystrophy (DMD) patients exhibit skeletal muscle weakness with continuous cycles of muscle fiber degeneration/regeneration, chronic inflammation, low bone mineral density, and increased risks of fracture. Fragility fractures and associated complications are considered as a consequence of the osteoporotic condition in these patients. Here, we aimed to establish the relationship between muscular dystrophy and fracture healing by assessing bone regeneration in mdx mice, a model of DMD with absence of osteoporosis. ⋯ In addition, PLX3397 treatment of mdx mice, a cFMS (colony stimulating factor receptor 1) inhibitor in monocytes, partially rescued the bone repair defect through increasing cartilage deposition and decreasing the number of macrophages. In conclusion, chronic inflammation in mdx mice contributes to the fracture healing delay and is associated with a decrease in angiogenesis and a transient delay in osteoclast recruitment. By revealing the role of dystrophic muscle in regulating the inflammatory response during bone repair, our results emphasize the implication of muscle in the normal bone repair process and may lead to improved treatment of fragility fractures in DMD patients.