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Abstract
Concomitant traumatic brain injury (TBI) and long bone fracture are commonly observed in multitrauma and polytrauma. Despite clinical observations of enhanced bone healing in patients with TBI, the relationship between TBI and fracture healing remains poorly understood, with clinical data limited by the presence of several confounding variables. Here we developed a novel trauma model featuring closed-skull weight-drop TBI and concomitant tibial fracture in order to investigate the effect of TBI on fracture healing. Male mice were assigned into Fracture + Sham TBI (FX) or Fracture + TBI (MULTI) groups and sacrificed at 21 and 35 days post-injury for analysis of healing fractures by micro computed tomography (μCT) and histomorphometry. μCT analysis revealed calluses from MULTI mice had a greater bone and total tissue volume, and displayed higher mean polar moment of inertia when compared to calluses from FX mice at 21 days post-injury. Histomorphometric results demonstrated an increased amount of trabecular bone in MULTI calluses at 21 days post-injury. These findings indicate that closed head TBI results in calluses that are larger in size and have an increased bone volume, which is consistent with the notion that TBI induces the formation of a more robust callus.
Highlights
Model that requires craniotomy[18,19,20,21,22]
Few studies have investigated the effect of closed-skull traumatic brain injury (TBI) on fracture healing, here we have developed a novel mouse model that involved a closed-skull weight-drop TBI and concomitant tibial fracture
In this study we have shown that in mice subjected to closed-skull TBI, fracture calluses at day 21 were larger, had a greater bone volume, and displayed a higher mean polar moment of inertia when compared to calluses from fracture-only mice
Summary
Model that requires craniotomy[18,19,20,21,22]. Given that previous studies have demonstrated enhanced osteogenesis in distant skeletal sites following bone injury, possibly through release of osteogenic humoral factors via a process known as ‘systemic acceleration’[23], the craniotomy performed to administer the CCI most likely represents a confounding variable. Despite the fact that closed-skull brain injury is the most common form of TBI in humans[24,25], the bone healing response of rodents exposed to closed-skull TBI (i.e. without craniotomy) remains unclear. In order to further explore the effect of closed-skull TBI on fracture healing, we developed a novel combined trauma mouse model that involved a weight-drop TBI and concomitant tibial fracture
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