Does traumatic brain injury result in accelerated fracture healing?

Morley, John; Marsh, Sarah; Drakoulakis, E.G.; Pape, Hans-Christian; Giannoudis, Peter V.

doi:10.1016/j.injury.2004.08.028

Cited by 65 publications

(53 citation statements)

References 11 publications

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“…The discovery of the concept that the CNS may control bone formation could have been based at the clinical observation of massive osteoneogenesis and heterotopic formation of bone in patients with head injury, [29][30][31] but was in fact based on the observation of leptin's anti-osteogenic effect after ICV application and the high bone mass phenotype in leptin-deficient obese (ob/ob) mice. 8 After this seminal contribution to the understanding of bone remodeling, the molecular basis and several aspects of the signaling cascade from brain to bone that involve the SNS 9 and the molecular clock 11 have been elucidated, and it has further been shown that through CART there is also a link to the regulation of bone resorption, 10 the other arm of bone remodeling.…”

Section: Discussionmentioning

confidence: 99%

Low turnover osteoporosis in sheep induced by hypothalamic‐pituitary disconnection

Beil

Oheim

Barvencik

et al. 2012

Journal Orthopaedic Research

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The hypothalamus is of critical importance in regulating bone remodeling. This is underscored by the fact that intracerebroventricular-application of leptin in ewe leads to osteopenia. As a large animal model of osteoporosis, this approach has some limitations, such as high technical expenditure and running costs. Therefore we asked if a surgical ablation of the leptin signaling axis would have the same effects and would thereby be a more useful model. We analyzed the bone phenotype of ewe after surgical hypothalamopituitary disconnection (HPD þ OVX) as compared to control ewe (OVX) after 3 and 12 months. Analyses included histomorphometric characterization, micro-CT and measurement of bone turnover parameters. Already 3 months after HPD we found osteopenic ewe with a significantly decreased bone formation (69%) and osteoclast activity (49%). After a period of 12 months the HPD group additionally developed an (preclinical) osteoporosis with significant reduction (33%) of femoral cortical thickness, as compared to controls (OVX). Taken together, HPD leads after 12 month to osteoporosis with a reduction in both trabecular and cortical bone caused by a low bone turnover situation, with reduced osteoblast and osteoclast activity, as compared to controls (OVX). The HPD-sheep is a suitable large animal model of osteoporosis. Furthermore our results indicate that an intact hypothalamo-pituitary axis is required for activation of bone turnover. ß

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Section: Discussionmentioning

confidence: 99%

Low turnover osteoporosis in sheep induced by hypothalamic‐pituitary disconnection

Beil

Oheim

Barvencik

et al. 2012

Journal Orthopaedic Research

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“…It is a complex cascade of events which involves local and systemic factors [7][8][9][10][11][12][13][14][15] . This healing response has been described in many terms as "heterotopic ossification" by Garland et al [16][17][18] , "hypertrophic callus" by Glenn et al [19] , "ossifying hematoma" and "calcifying hematoma" by Keronohan et al [20] . The studies published in literature so far are limited by small sample size.…”

Section: Discussionmentioning

confidence: 97%

“…Garland et al in his study of patients with TBI with diaphyseal tibial, femoral or forearm fractures showed no evidence of increased rate of bone healing. However there were no comparable control groups [16][17][18] . He also concluded that callus response at the fracture site was a form of heterotopic ossification.…”

Section: Discussionmentioning

confidence: 99%

Does accelerated bone healing associated with traumatic brain injury (TBI) occur in open fractures

Perumal¹,

Sp²,

Shankar³

et al. 2018

Int. J. Orthop. Sci.

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Aim: Accelerated bone healing has been frequently reported in patients with traumatic brain injury (TBI). However, all these reports are restricted to closed fractures and there is no literature of the effect of TBI in open fractures. Between 2011 and 2013, sixty six patients with TBI of whom thirty four had closed fractures (Group IA) and thirty two had open fractures (Group IIA) were compared with eighty patients without TBI of whom forty had closed fractures (Group IB) and forty had open fractures (Group IIB). The mean duration of follow up was 13 months. Time to fracture union and fracture healing response were compared in both groups. Though group IA patients had shorter time to union (27 weeks) compared to all other groups (IB-32 weeks, IIA-36 weeks, IIB-30 weeks), there was no statistical significance between the groups (P>0.05). However, the subset of patients who underwent craniotomy in Group IA (6) had significantly shorter time to healing (24 weeks, P=0.05) compared to other groups. Considering the fracture healing response (FHR), there was no statistical difference between groups. Accelerated callus response from FHR of 1.4 to 1.8 was observed in closed fractures for thirty six weeks, whereas this was seen only for eighteen weeks in open fractures. In our study of 146 patients, the beneficial effect of TBI on fracture healing was restricted to the subset of patients with closed fractures and those requiring craniotomy. There was no beneficial response in patients with open fractures.

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“…The results of experimental studies have established that growth factors and cytokines play an important role in fracture healing and repair of musculoskeletal tissue. [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] The objective of this prospective controlled study was to investigate the effect of spinal cord injury and concomitant long bone fractures on the serum level of growth factors and cytokines, rather than bone morphogenetic protein (BMP) growth factor.…”

Section: T I C L E I N F Omentioning

confidence: 99%

Growth factors and cytokines in patients with long bone fractures and associated spinal cord injury

Khallaf

Kehinde

Mostafa

2016

Journal of Orthopaedics

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Does traumatic brain injury result in accelerated fracture healing?

Cited by 65 publications

References 11 publications

Low turnover osteoporosis in sheep induced by hypothalamic‐pituitary disconnection

Low turnover osteoporosis in sheep induced by hypothalamic‐pituitary disconnection

Does accelerated bone healing associated with traumatic brain injury (TBI) occur in open fractures

Growth factors and cytokines in patients with long bone fractures and associated spinal cord injury

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