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The effects of spinal cord injury on bone loss and dysregulation of the calcium/parathyroid hormone loop in mice
Journal article   Open access   Peer reviewed

The effects of spinal cord injury on bone loss and dysregulation of the calcium/parathyroid hormone loop in mice

Tania Del Rivero and John R Bethea
Osteoporosis and sarcopenia, v 2(3), pp 164-169
Sep 2016
DOI: https://doi.org/10.1016/j.afos.2016.06.003
PMID: 30775482
url
https://doi.org/10.1016/j.afos.2016.06.003View
Published, Version of Record (VoR) Open

Abstract

Osteoporosis Bone Calcium Spinal cord injury Parathyroid hormone
To map the progression of osteoporosis following spinal cord injury in mice in specific areas and analyze changes in parathyroid hormone (PTH) and ion levels which could be responsible for overall bone loss. Spinal cord injury rapidly induces severe bone loss compared to other conditions, yet the cause of this bone loss has not been identified. Studies suggest the bone loss after injury is not solely due to disuse. To quantify bone loss we weighed individual bones and measured bone mineral density using dual energy X-ray absorptiometry at acute (1 week) and chronic (4 week) time points following a T9 contusion. An ELISA was used to measure blood PTH levels at 1 and 4 weeks after injury. Calcium and phosphate levels were also analyzed at 4 weeks following injury at the University of Miami pathology core. We observed a significant decrease in bone mineral density in hind limbs after an acute injury, and found this bone loss to progress over time. Furthermore, following chronic injury a decrease in bone mineral density is also observed in bones above the level of injury and in the total bone mineral density. We observed a significant decrease in parathyroid hormone levels in injured mice at the chronic time point, but not at the acute time point which suggests this could be involved in the global bone loss following injury. We also observed a significant increase in serum calcium levels following injury which could account for the imbalance of PTH levels.

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