Effects of spinal cord injury and hindlimb immobilization on sublesional and supralesional bones in young growing rats.

Both spinal cord injury (SCI) and hindlimb cast immobilization (HCI) cause reduction in maturation-related bone gain in young rats, but the effects of the two interventions on bone pathophysiology may be different. The objective of this study was to compare the effects of SCI and HCI on the sublesional/supralesional bones and bone turnover indicators in young rats. Forty male Sprague-Dawley rats (six-week-old) were randomized into four groups, with ten rats in each group. The groups were classified as follows: base-line control, age-matched intact control, HCI, and SCI groups. Bone tissues, blood, and urine samples were studied at 4 weeks after treatments. The tibial dry weights and ash weights in SCI were remarkably reduced by 7.5% (dry weights) and 8.2% (ash weights) compared with HCI. SCI rats showed lower areal bone mineral density in the proximal tibiae compared with HCI rats (- 14%). Cortical thickness and cortical area of the tibial midshaft in SCI were lower than HCI (- 23%, - 33% respectively). The bone surface/bone volume, trabecular separation, trabecular number, connectivity of the trabecular network, and structure model index of the proximal tibiae were remarkably different between SCI and HCI groups. In SCI tibiae, the mineralizing surface, mineral apposition rate, and surface-based bone formation rate were significantly higher than HCI groups (12%, 47%, and 29% respectively). In the compression test, the ultimate load, the energy of ultimate load, and Young's modulus of the proximal tibiae in SCI rats were significantly lower than HCI rats. The serum levels of osteocalcin and the urinary levels of deoxypyridinoline in SCI were higher than those in HCI. There were no significant changes in supralesional bones between SCI and HCI rats. SCI results in a rapid bone loss with more deterioration of trabecular microstructure and cortical bone geometric structure in sublesional bones. High bone turnover rate and low biomechanics strength were found in tibiae in SCI rats. This might be the result of the imbalance of bone resorption and bone formation induced by the impaired neuronal function.