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Introduction

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A significant decline in hip and knee region bone mineral density (BMD) occurs after motor complete spinal cord injury (SCI) which leads to a lifetime increased risk of lower extremity fragility or low trauma fracture.  Preserving bone mass and maintaining bone architecture are crucial to decrease the risk of lower extremity fragility fractures.  Within the first few days following SCI there is an increase in excreted calcium (known as hypercalciuria) that is 2-4 times that of individuals without SCI who are confined to prolonged bed rest (Bauman & Spungen 2001) and reflects excessive bone resorption.  Longitudinal studies also highlight a higher rate of hypercalcemia (excessive calcium in the blood) for people after SCI that reflects rapid bone mineral loss in the first 4-6 months that slows for the remainder of the first year post-injury (Hancock et al. 1980; Frey-Rindova et al. 2000).  Early studies also suggest that bone mineral density (BMD) stabilizes by 1-2 years after SCI (Griffiths et al. 1976; Hancock et al. 1980; Garland et al.1992) at 25-50% below that of able-bodied peers in the hip and knee region.  Other investigations support a continual loss of bone mass with time since injury (Demirel et al. 1998; Bauman et al. 1999; Eser et al. 2005) and suggest that lower extremity bone mineral homeostasis is not reached.

The immediate and excessive loss of bone mass post-SCI is believed to result from a decrease in mechanical loading as a result of reduced or complete loss of muscle function and/or weight-bearing activities.  Autoimmune, neural, vascular, hormonal and nutritional changes may also negatively affect bone, but the relative contributions of these factors are unknown (Jiang et al. 2006).  The reader is referred to two recent review articles which characterize the regional changes in bone density and architecture (Jiang et al. 2006; Craven et al. 2008). Furthermore, an inadequate dietary calcium intake (Tomey et al. 2005) or insufficient vitamin D may contribute to the rate and severity of BMD decline (Bauman et al. 1995).  Aging and inactivity accentuate bone resorption further, resulting in site-specific decreases in bone mineral content (that is, trabecular bone experiences larger decreases in mineral content than cortical bone). Additionally, women with motor complete SCI experience regional declines in hip and knee region BMD during menopause that are greater than age-matched able-bodied women (Garland et al. 2001).  These changes in bone density and bone architecture all contribute to the increased risk of fragility fractures in people with SCI. Fractures after SCI often result in delayed union or non-union and/or complications of immobilization (DVT, pressure sore, cellulitis). These fractures are associated with an increase in direct and indirect medical expenses, as well as the individual’s morbidity and mortality.