Humoral Factors Enhance Fracture-Healing and Callus Formation in Patients with Traumatic Brain Injury

2009 ◽  
Vol 91 (2) ◽  
pp. 282-288 ◽  
Author(s):  
Dieter Cadosch ◽  
Oliver P Gautschi ◽  
Matthew Thyer ◽  
Swithin Song ◽  
Allan P Skirving ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Fracture Healing ◽  
Callus Formation ◽  
Humoral Factors

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

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Martijn Hofman ◽  
Guido Koopmans ◽  
Philipp Kobbe ◽  
Martijn Poeze ◽  
Hagen Andruszkow ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Fracture Healing ◽  
Callus Formation ◽  
Scientific Evidence ◽  
Preclinical Studies ◽  
The Relationship ◽  
Callus Volume ◽  
Over Time

Over the last 3 decades, scientific evidence advocates an association between traumatic brain injury (TBI) and accelerated fracture healing. Multiple clinical and preclinical studies have shown an enhanced callus formation and an increased callus volume in patients, respectively, rats with concomitant TBI. Over time, different substances (cytokines, hormones, etc.) were in focus to elucidate the relationship between TBI and fracture healing. Until now, the mechanism behind this relationship is not fully clarified and a consensus on which substance plays the key role could not be attained in the literature. In this review, we will give an overview of current concepts and opinions on this topic published in the last decade and both clinical and pathophysiological theories will be discussed.

scholarly journals Accelerated Lower Leg Fracture Healing in Traumatic Brain Injury in Accordance With Increased Hematoma Formation

2021 ◽  
Author(s):  
Dong Woo Shim ◽  
Hyunjoo Hong ◽  
Kwang-Chun Cho ◽  
Se Hwa Kim ◽  
Jin Woo Lee ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Fracture Healing ◽  
Bone Healing ◽  
Open Fracture ◽  
Callus Formation ◽  
Lower Leg ◽  
Hematoma Formation ◽  
Lower Leg Fracture ◽  
Group 1

Abstract BackgroundTraumatic brain injury (TBI) has been known to accelerate bone healing. Many cells and molecules have been investigated but the exact mechanism is still unknown. We aimed to investigate the effect of TBI on fracture healing regarding accelerated hematoma formation.MethodsWe retrospectively investigated patients who were surgically treated for lower leg fractures and who showed secondary bone healing. Patients with and without TBI were divided for comparative analyses. Radiological parameters were time to bridging callus formation and the largest callus ratio during follow-up. Preoperative levels of complete blood count and chemical battery within 3 days from trauma were measured in all patients. Subgroup division regarding age, gender, open fracture, concomitant fracture and severity of TBI were compared.ResultsWe included 48 patients with a mean age of 44.9 (range, 17 – 78), of whom 35 patients (72.9%) were male. There were 12 patients with TBI (Group 1) and 36 patients without TBI (Group 2). Group 1 showed shorter time to callus formation (P < 0.001), thicker callus ratio (P = 0.015), leukocytosis and lymphocytosis (P ≤ 0.028), and lower red blood cell counts (RBCs), hemoglobin, and hematocrit (P < 0.001). Aging and severity of TBI were correlated with time to callus formation and callus ratio (P ≤ 0.003) while gender, open fracture, and concomitant fracture were unremarkable.ConclusionLower leg fractures with TBI showed accelerated bone healing and superior measurements associated with hematoma formation (lymphocytes, RBCs, hemoglobin, hematocrit). Promoted fracture healing in TBI was correlated with the enhanced proinflammatory state.Level of Evidence: Case control study; III

The Association Between Traumatic Brain Injury and Accelerated Fracture Healing: A Study on the Effects of Growth Factors and Cytokines

2020 ◽  
Vol 71 (1) ◽  
pp. 162-168
Author(s):  
Majid Mollahosseini ◽  
Hadis Ahmadirad ◽  
Reza Goujani ◽  
Hossein Khorramdelazad
Keyword(s):  
Traumatic Brain Injury ◽  
Growth Factors ◽  
Brain Injury ◽  
Fracture Healing

scholarly journals Leptin Mediated Pathways Stabilize Posttraumatic Insulin and Osteocalcin Patterns after Long Bone Fracture and Concomitant Traumatic Brain Injury and Thus Influence Fracture Healing in a Combined Murine Trauma Model

2020 ◽  
Vol 21 (23) ◽  
pp. 9144
Author(s):  
Anja Garbe ◽  
Frank Graef ◽  
Jessika Appelt ◽  
Katharina Schmidt-Bleek ◽  
Denise Jahn ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Fracture Healing ◽  
Bone Fracture ◽  
Long Bone ◽  
Mouse Strains ◽  
Leptin Deficiency ◽  
Long Bone Fracture ◽  
Trauma Model ◽  
Deficient Mice

Recent studies on insulin, leptin, osteocalcin (OCN), and bone remodeling have evoked interest in the interdependence of bone formation and energy household. Accordingly, this study attempts to investigate trauma specific hormone changes in a murine trauma model and its influence on fracture healing. Thereunto 120 female wild type (WT) and leptin-deficient mice underwent either long bone fracture (Fx), traumatic brain injury (TBI), combined trauma (Combined), or neither of it and therefore served as controls (C). Blood samples were taken weekly after trauma and analyzed for insulin and OCN concentrations. Here, WT-mice with Fx and, moreover, with combined trauma showed a greater change in posttraumatic insulin and OCN levels than mice with TBI alone. In the case of leptin-deficiency, insulin changes were still increased after bony lesion, but the posttraumatic OCN was no longer trauma specific. Four weeks after trauma, hormone levels recovered to normal/basal line level in both mouse strains. Thus, WT- and leptin-deficient mice show a trauma specific hyperinsulinaemic stress reaction leading to a reduction in OCN synthesis and release. In WT-mice, this causes a disinhibition and acceleration of fracture healing after combined trauma. In leptin-deficiency, posttraumatic OCN changes are no longer specific and fracture healing is impaired regardless of the preceding trauma.

scholarly journals Long Non-coding RNAs in Traumatic Brain Injury Accelerated Fracture Healing

2021 ◽  
Vol 8 ◽  
Author(s):  
Guoning Guo ◽  
Yajun Gou ◽  
Xingyu Jiang ◽  
Shuhong Wang ◽  
Ruilie Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Endothelial Cells ◽  
Brain Injury ◽  
B Cells ◽  
Fracture Healing ◽  
Differentially Expressed Genes ◽  
Differentially Expressed ◽  
Cellular Behavior ◽  
Cellular Behaviors ◽  
Non Coding Rnas

It is commonly observed that patients with bone fracture concomitant with traumatic brain injury (TBI) had significantly increased fracture healing, but the underlying mechanisms were not fully revealed. Long non-coding RNAs (lncRNAs) are known to play complicated roles in bone homeostasis, but their role in TBI accelerated fracture was rarely reported. The present study was designed to determine the role of lncRNAs in TBI accelerated fracture via transcriptome sequencing and further bioinformatics analyses. Blood samples from three fracture-only patients, three fracture concomitant with TBI patients, and three healthy controls were harvested and were subsequently subjected to transcriptome lncRNA sequencing. Differentially expressed genes were identified, and pathway enrichment was performed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. High-dimensional data visualization by self-organizing map (SOM) machine learning was applied to further interpret the data. An xCell method was then used to predict cellular behavior in all samples based on gene expression profiles, and an lncRNA–cell interaction network was generated. A total of 874 differentially expressed genes were identified, of which about 26% were lncRNAs. Those identified lncRNAs were mainly enriched on TBI-related and damage repair-related pathways. SOM analyses revealed that those differentially expressed lncRNAs could be divided into three major module implications and were mainly enriched on transcriptional regulation and immune-related signal pathways, which promote us to further explore cellular behaviors based on differentially expressed lncRNAs. We have predicted that basophils, CD8+ T effector memory cells, B cells, and naïve B cells were significantly downregulated, while microvascular endothelial cells were predicted to be significantly upregulated in the Fr/TBI group, was the lowest and highest, respectively. ENSG00000278905, ENSG00000240980, ENSG00000255670, and ENSG00000196634 were the most differentially expressed lncRNAs related to all changes of cellular behavior. The present study has revealed for the first time that several critical lncRNAs may participate in TBI accelerated fracture potentially via regulating cellular behaviors of basophils, cytotoxic T cells, B cells, and endothelial cells.

OSTEOGENIC EFFECTS OF TRAUMATIC BRAIN INJURY ON EXPERIMENTAL FRACTURE-HEALING

2006 ◽  
Vol 88 (4) ◽  
pp. 738-743 ◽  
Author(s):  
MATTHEW BOES ◽  
MICHAEL KAIN ◽  
SANJEEV KAKAR ◽  
FRED NICHOLLS ◽  
DENNIS CULLINANE ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Fracture Healing ◽  
Experimental Fracture ◽  
Experimental Fracture Healing

Does Traumatic Brain Injury Result in Accelerated Mandibular Fracture Healing?

2012 ◽  
Vol 70 (9) ◽  
pp. 2135-2142 ◽  
Author(s):  
Wei Huang ◽  
Zubing Li ◽  
Zhi Li ◽  
Rongtao Yang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Fracture Healing ◽  
Mandibular Fracture

Leptin’s effect on accelerated fracture healing after traumatic brain injury

2013 ◽  
Vol 35 (5) ◽  
pp. 537-544 ◽  
Author(s):  
Hua Yan ◽  
Hong-Wei Zhang ◽  
Paul Fu ◽  
Bao-Long Liu ◽  
Wen-Zhe Jin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Fracture Healing
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