Introduction
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 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). Hypercalciuria results in excessive bone resorption (i.e., bone breakdown). Longitudinal studies also highlight a higher rate of hypercalcemia (excessive calcium in the blood) for people after SCI that reflects the rapid bone mineral loss in the first 4-6 months that slow for the remainder of the first-year post-injury (Hancock et al. 1979; Frey-Rindova et al. 2000). Early studies also suggest that BMD stabilizes by 1-2 years after SCI (Griffiths et al. 1976; Hancock et al. 1979; Garland et al. 1992) at 25-50% below that of non-disabled peers in the hip and knee region. Other investigations support a continual loss of bone mass with increases in time post-injury (Demirel et al. 1998; Bauman et al. 1999; Eser et al. 2005) suggesting that lower extremity bone mineral homeostasis is not reached.
The immediate and excessive loss of bone mass post-SCI is believed to result in part from the complete loss of voluntary muscle function and/or weight-bearing capability. 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 that 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; Miyatani et al. 2014) 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 (BMC), i.e. 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 is greater than age-matched non-disabled women (Garland et al. 2001). These changes in bone density and bone architecture 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 (e.g., deep vein thrombosis, pressure injuries, cellulitis). These fractures are associated with an increase in direct and indirect medical expenses, as well as an increase the individual’s morbidity and mortality.
