Improved Fracture Healing in Patients with Concomitant Traumatic Brain Injury: Proven or Not?

Hofman, Martijn; Koopmans, Guido C; Kobbe, Philipp; Poeze, Martijn; Andruszkow, Hagen; Brink, Peter R.; Pape, Hans-Christian

doi:10.1155/2015/204842

Cited by 57 publications

(68 citation statements)

References 133 publications

(169 reference statements)

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“…Though several studies have reported enhanced callus volumes post-TBI 18 19 20 21 22 , the nature of callus formation following TBI is not well established. Several researchers have speculated that the enhanced callus volumes post-TBI may represent a form of heterotopic ossification about the fracture site 16 17 31 32 33 . We observed no gross morphological differences in healing calluses between multitrauma and fracture-only mice using high resolution μCT and histology, however the contribution of heterotopic ossification to an enhanced callus formation response cannot be ruled out.…”

Section: Discussionmentioning

confidence: 99%

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Closed head experimental traumatic brain injury increases size and bone volume of callus in mice with concomitant tibial fracture

Brady

Grills

Church

et al. 2016

Sci Rep

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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.

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Section: Discussionmentioning

confidence: 99%

“…Paradoxically, TBI has been associated with stimulation of osteogenesis, with heterotopic ossification (i.e. the formation of bone in soft tissues) and enhanced callus formation described in TBI patients for several decades 13 14 15 16 17 . Despite these associations the relationship between TBI and fracture healing remains poorly understood.…”

mentioning

confidence: 99%

Closed head experimental traumatic brain injury increases size and bone volume of callus in mice with concomitant tibial fracture

Brady

Grills

Church

et al. 2016

Sci Rep

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“…The increase in glutamate levels occurs several minutes after the primary trauma, peaks in about 10 minutes and stays increased for several days [45,64]. Excitotoxicity also causes calcium influx and overload [67,68], resulting in cellular damage due to several mechanisms (i.e. activation of destructive calcium-dependent proteases, oxidative stress, mitochondrial impairment and transition pore formation, and apoptotic events) [51,53,62,[69][70][71].…”

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

“…Modulating these inflammatory cells by changing their phenotype from pro-inflammatory to anti-inflammatory would likely promote therapeutic effects on TBI [42,59,98]. Additionally, peripheral injuries of the multi-injured patient may increase circulating levels of many of the inflammatory cytokines worsening TBI outcomes [13,68].…”

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Regner¹,

Meirelles²,

Simon³

2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

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Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Understanding the pathophysiology of TBI is crucial for the development of more effective therapeutic strategies. At the moment of the traumatic impact, transfer of kinetic forces causes neurologic damage; this primary injury triggers a secondary wave of biochemical cascades, together with metabolic and cellular changes, called secondary neural injury. These areas of ongoing secondary injury, or areas of "traumatic penumbra," represent crucial targets for therapeutic interventions. This chapter is focused on the interplay between progression of parenchymal injury and the neuroprotective and neurorestorative processes that are emerging and developing subsequently to traumatic impact. Thus, we emphasized the role of traumatic penumbra in TBI pathogenesis and suggested a crucial contribution of the neurovascular units (NVUs) and paracrine effects of exosomes and miRNAs in promoting neurological recovery.

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“…In contrast, TBI seems to be positively correlated with osteogenesis [7][8][9]. However, this association has not been found in all studies [10,11]. Furthermore, potential pathophysiological mechanisms for TBI-related impact on osteogenesis seem to be multifactorial (humoral, hormonal and cellular) and are far from clear [7,12,13].…”

Section: Introductionmentioning

confidence: 96%

Risk factors of non-union in intramedullary stabilized diaphyseal long bone fractures: identifying the role of fracture stabilization strategies and concomitant injuries

Hofman

Andruszkow

Heyer

et al. 2020

Eur J Trauma Emerg Surg

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Purpose Concomitant chest injury is known to negatively affect bone metabolism and fracture healing, whereas traumatic brain injury (TBI) appears to have positive effects on bone metabolism. Osteogenesis can also be influenced by the timing of fracture stabilization. We aimed to identify how chest injuries, TBI and fracture stabilization strategy influences the incidence of non-union. Methods Patients with long bone fractures of the lower extremities who had been treated between 2004 and 2014 were retrospectively analysed. Non-union was defined as fracture healing not occurring in the expected time period and in which neither progression of healing nor successful union is expected without intervention. Diverse clinical and radiological parameters were statistically analysed using the Statistical Package for the Social Sciences (SPSS). Results The total number of operations before consolidation was an independent predictor (odds ratio [OR] = 6.416, p < 0.001) for the development of non-union in patients with long bone fractures. More specifically, patients treated according to the damage control orthopaedics (DCO) principle had a significantly higher risk of developing a non-union than patients treated according to the early total care (ETC) principle (OR = 7.878, p = 0.005). Concomitant chest injury and TBI could not be identified as influencing factors for non-union development. ConclusionOur results indicate that the number of operations performed in patients with long bone fractures should be kept as low as possible and that the indication for and the timing of DCO treatment should be meticulously noted to minimize the risk of non-union development.

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Improved Fracture Healing in Patients with Concomitant Traumatic Brain Injury: Proven or Not?

Cited by 57 publications

References 133 publications

Closed head experimental traumatic brain injury increases size and bone volume of callus in mice with concomitant tibial fracture

Closed head experimental traumatic brain injury increases size and bone volume of callus in mice with concomitant tibial fracture

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Risk factors of non-union in intramedullary stabilized diaphyseal long bone fractures: identifying the role of fracture stabilization strategies and concomitant injuries

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