Mechanical Stress by Spasticity Accelerates Fracture Healing After Spinal Cord Injury

Accelerated fracture healing in patients with spinal cord injuries (SCI) is often encountered in clinical practice. However, there is no distinct evidence in the accelerated fracture healing, and the mechanisms of accelerated fracture healing in SCI are poorly understood. We aimed to determine whether SCI accelerated fracture healing in morphology and strength, to characterize the healing process with SCI, and to clarify the factors responsible for accelerated fracture healing. In total, 39 male Wistar rats were randomly divided into healthy control without intervention, SCI only, fracture with SCI, botulinum toxin (BTX) A-treated fracture with SCI, and propranolol-treated fracture with SCI groups. These rats were assessed with computed microtomography, histological, histomorphological, immunohistological, and biomechanical analyses. Both computed microtomography and histological analyses revealed the acceleration of a bony union in animals with SCI. The strength of the healed fractures after SCI recovered to the same level as that of intact bones after SCI, while the healed bones were weaker than the intact bones. Immunohistology revealed that SCI fracture healing was characterized by formation of callus with predominant intramembranous ossification and promoting endochondral ossification. The accelerated fracture healing after SCI was attenuated by BTX injection, but did not change by propranolol. We demonstrated that SCI accelerate fracture healing in both morphology and strength. The accelerated fracture healing with SCI may be due to predominant intramembranous ossification and promoting endochondral ossification. In addition, our results also suggest that muscle contraction by spasticity accelerates fracture healing after SCI.