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To assess both the humoral and neuronal impacts of TBI on fracture healing, we created a novel rodent model which combined a TBI with a concomitant long bone fracture either ipsilateral (same side) or contralateral (opposite side) to the brain lesion (Fig. Polytrauma injuries were compared to both TBI and fracture only. Blood and spleen were collected to evaluate systemic inflammation.TBI were produced in the right hemisphere following a craniotomy using an electromagnetic-controlled cortical contusion impactor (CCI) (Fig. Fracture callus and brain tissue were collected for histological processing and quantification.Polytraumatic injuries, specifically long bone fracture and traumatic brain injury (TBI), frequently occur together.Clinical observation has long held that TBI can accelerate fracture healing, yet the complexity and heterogeneity of these injuries has produced conflicting data with limited information on underlying mechanisms.To effectively understand how these complex longitudinal factors work together to drive overall healing response we then integrated all outcome measures into a multidimensional principal component analysis (PCA).
Schematic of experimental design and protocol is described in Materials and Methods.(A) The TBI only group included TBI without tibia fracture, the ipsilateral polytrauma group included TBI with ipsilateral tibia fracture, the contralateral polytrauma group included TBI with contralateral tibia fracture, and the fracture only group included tibia fracture without TBI.All assessments were performed at three time points, 5, 10 and 14 days post-injury (n = 5–6/group). (C) The representative radiographic image of closed transverse tibia shaft fracture.In the fracture gap, periosteal progenitor cells differentiate into chondrocytes and generate a provisional cartilaginous matrix that gives rise to bone indirectly by endochondral ossification (days 5–14).Two recent preclinical studies support evidence for accelerated fracture healing with TBI.