Do traumatic brain injuries lead to accelerated fracture healing?

Introduction Fracture healing can be defined as the physiological restoration of bone tissue, structure and function. A common association seen in orthopaedic practice is accelerated fracture healing, with exuberant callus formation in patients, with concomitant head injuries. This review explores our current state of understanding of this relationship. Materials and methods EMBASE and MEDLINE searches (Search terms: “traumatic brain injury” AND “fractures”; “head injury” AND “fractures”; “traumatic brain injury” AND “fracture healing”; “head injury” AND “fracture healing”) were performed in January 2014. Further, the author canvassed the reference lists of selected articles and online search engines such as Google Scholar. Results Few studies have examined the relationship between traumatic brain injury (TBI) and accelerated fracture healing, with conflicting results. Studies, to date, have either been retrospective studies or analyses of case series with relatively small number of patients. In some studies control groups have been used, whereas in others, reference has been made to fracture healing norms in the general population. Discussion Several hypotheses have been put forth to explain the link between TBI and accelerated fracture healing. Traumatic brain injury leads to a release of interleukin-6, BMP and prolactin. Local alkalinity at the fracture site, secondary to hyperventilation, and the release of basic fibroblast growth factors result in enhanced callus formation, which may represent true callus or be a variant of heterotrophic ossification. Conclusion Studies on the effect of traumatic brain injury on accelerated fracture healing have yielded conflicting results. The author proposes a combined mechanism for this association. Further basic research and clinical work is needed to better define this relationship.