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Furthermore, the nervous system normally exerts control over the immune system, making the immunological consequences of central nervous system injury complicated.
Following fracture, a hematoma forms immediately to stop the bleeding, contain debris, and activate a pro-inflammatory response that initiates repair; in the mouse this process occurs from roughly days 3–5 post-fracture.
Taken together, our results suggest that a contralateral bone fracture and TBI alter the local neuroinflammatory state to accelerate early fracture healing.
Clinical studies remain conflicted on the evidence for this phenomenon, partly due to heterogeneous injury patterns and the complex clinical treatment of these polytrauma patients.
Moreover, pathophysiological changes that occur as a result of polytrauma are rarely studied and there remains no consensus on how TBI may alter fracture healing at a mechanistic level.
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.
In this study, our goal was to focus on the earlier stages of fracture repair, days 5–14 post- injury, that are responsible for establishing healing patterns in order to provide more insight to the factors that may drive altered fracture response following combined bone and brain polytrauma.