Mechanisms of osteoporosis in spinal cord injury

Abstract

SummaryOsteoporosis is a known complication of spinal cord injury (SCI), but its mechanism remains unknown. The pathogenesis of osteoporosis after SCI is generally considered disuse. However, although unloading is an important factor in the pathogenesis of osteoporosis after SCI, neural lesion and hormonal changes also seem to be involved in this process. Innervation and neuropeptides play an important role in normal bone remodelling. SCI results in denervation of the sublesional bones and the neural lesion itself may play a pivotal role in the development of osteoporosis after SCI. Although upper limbs are normally loaded and innervated, bone loss also occurs in the upper extremities in patients with paraplegia, indicating that hormonal changes may be associated with osteoporosis after SCI. SCI-mediated hormonal changes may contribute to osteoporosis after SCI by different mechanisms: (1) increased renal elimination and reduced intestinal absorption of calcium leading to a negative calcium balance; (2) vitamin D deficiency plays a role in the pathogenesis of SCI-induced osteoporosis; (3) SCI antagonizes gonadal function and inhibits the osteoanabolic action of sex steroids; (4) hyperleptinaemia after SCI may contribute to the development of osteoporosis; (5) pituitary suppression of TSH may be another contributory factor to bone loss after SCI; and (6) bone loss after SCI may be caused directly, at least in part, by insulin resistance and IGFs. Thus, oversupply of osteoclasts relative to the requirement for bone resorption and/or undersupply of osteoblasts relative to the requirement for cavity repair results in bone loss after SCI. Mechanisms for the osteoporosis following SCI include a range of systems, and osteoporosis after SCI should not be simply considered as disuse osteoporosis. Unloading, neural lesion and hormonal changes after SCI result in severe bone loss. The aim of this review is to improve understanding with regard to the mechanisms of osteoporosis after SCI. The understanding of the pathogenesis of osteoporosis after SCI can help in the consideration of new treatment strategies. Because bone resorption after SCI is very high, intravenous bisphosphonates and denosumab should be considered for the treatment of osteoporosis after SCI.

Leisure-time physical activity and diet quality are not associated in people with chronic spinal cord injury

“…Dietary fibre has an important role in managing neurogenic bowel 17 and bone-related nutrients are critical for a population already at increased risk for osteoporosis. 18 Both dietary fibre and calcium intakes have recently been found to be low in the SCI population. 19 Taken together, these results suggest that overall, communitydwelling adults with chronic SCI may be at increased risk for diet-related chronic conditions.…”

Raman Assessment of Bone Quality

“…In comparison to age-matched controls, a decrease in mineral (relative to the CH 2 band at 1450 cm À1 ) by greater than 20% in the femur and approximately 12% in the humerus was found in the SCI group. The decrease in mineral-to-matrix ratios after SCI could be attributed to changes in hormone levels, which have been known to regulate bone remodeling [33]. However, correlative data on hormone levels are lacking and the hormone responsible for the decrease in mineral-tomatrix ratios has yet to be determined.…”

Does Standing Protect Bone Density in Patients With Chronic Spinal Cord Injury?

“…Some authors argue that neurologic damage and hormonal alterations due to the SCI per se may be the causal factors in the loss of bone density rather than immobilization alone (1,6,7,9). The reason for their argument was the different nature of calcium excretion and response to physical activity in those patients.…”