Sodium selenate treatment mitigates reduction of bone volume following traumatic brain injury in rats

R. D. Brady, B. L. Grills, T. Romano, J. D. Wark, T. J. O’Brien, S. R. Shultz, Stuart J. McDonald

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Objectives: Administration of sodium selenate to rats given traumatic brain injury (TBI) attenuates brain damage and improves long-term behavioural outcomes. We have previously provided evidence that TBI causes bone loss in rats, however the effect of sodium selenate treatment on bone quantity following TBI is unknown. Methods: Rats were randomly assigned into sham injury or fluid percussion injury (FPI) groups and administered saline or sodium selenate for 12 weeks post-injury. Femora were analysed using histomorphometry, peripheral quantitative computed tomography (pQCT) and biomechanical testing. Results: Distal metaphyseal trabecular bone volume fraction of FPI-selenate rats was higher than FPI-vehicle rats (41.8%; p<0.01), however, femora from selenate-treated groups were shorter in length (4.3%; p<0.01) and had increased growth plate width (22.1%; p<0.01), indicating that selenate impaired long bone growth. pQCT analysis demonstrated that distal metaphyseal cortical thickness was decreased in TBI rats compared to shams (11.7%; p<0.05), however selenate treatment to TBI animals offset this reduction (p<0.05). At the midshaft we observed no differences in biomechanical measures. Conclusion: These are the first findings to indicate that mitigating TBI-induced neuropathology may have the added benefit of preventing osteoporosis and associated fracture risk following TBI.

Original languageEnglish
Pages (from-to)369-376
Number of pages8
JournalJournal of Musculoskeletal Neuronal Interactions
Volume16
Issue number4
Publication statusPublished - 1 Dec 2016
Externally publishedYes

Keywords

  • Bone growth
  • Bone Metabolism
  • Endochondral ossification
  • Neurotrauma
  • Osteoporosis

Cite this

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title = "Sodium selenate treatment mitigates reduction of bone volume following traumatic brain injury in rats",
abstract = "Objectives: Administration of sodium selenate to rats given traumatic brain injury (TBI) attenuates brain damage and improves long-term behavioural outcomes. We have previously provided evidence that TBI causes bone loss in rats, however the effect of sodium selenate treatment on bone quantity following TBI is unknown. Methods: Rats were randomly assigned into sham injury or fluid percussion injury (FPI) groups and administered saline or sodium selenate for 12 weeks post-injury. Femora were analysed using histomorphometry, peripheral quantitative computed tomography (pQCT) and biomechanical testing. Results: Distal metaphyseal trabecular bone volume fraction of FPI-selenate rats was higher than FPI-vehicle rats (41.8{\%}; p<0.01), however, femora from selenate-treated groups were shorter in length (4.3{\%}; p<0.01) and had increased growth plate width (22.1{\%}; p<0.01), indicating that selenate impaired long bone growth. pQCT analysis demonstrated that distal metaphyseal cortical thickness was decreased in TBI rats compared to shams (11.7{\%}; p<0.05), however selenate treatment to TBI animals offset this reduction (p<0.05). At the midshaft we observed no differences in biomechanical measures. Conclusion: These are the first findings to indicate that mitigating TBI-induced neuropathology may have the added benefit of preventing osteoporosis and associated fracture risk following TBI.",
keywords = "Bone growth, Bone Metabolism, Endochondral ossification, Neurotrauma, Osteoporosis",
author = "Brady, {R. D.} and Grills, {B. L.} and T. Romano and Wark, {J. D.} and O’Brien, {T. J.} and Shultz, {S. R.} and McDonald, {Stuart J.}",
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Sodium selenate treatment mitigates reduction of bone volume following traumatic brain injury in rats. / Brady, R. D.; Grills, B. L.; Romano, T.; Wark, J. D.; O’Brien, T. J.; Shultz, S. R.; McDonald, Stuart J.

In: Journal of Musculoskeletal Neuronal Interactions, Vol. 16, No. 4, 01.12.2016, p. 369-376.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Sodium selenate treatment mitigates reduction of bone volume following traumatic brain injury in rats

AU - Brady, R. D.

AU - Grills, B. L.

AU - Romano, T.

AU - Wark, J. D.

AU - O’Brien, T. J.

AU - Shultz, S. R.

AU - McDonald, Stuart J.

PY - 2016/12/1

Y1 - 2016/12/1

N2 - Objectives: Administration of sodium selenate to rats given traumatic brain injury (TBI) attenuates brain damage and improves long-term behavioural outcomes. We have previously provided evidence that TBI causes bone loss in rats, however the effect of sodium selenate treatment on bone quantity following TBI is unknown. Methods: Rats were randomly assigned into sham injury or fluid percussion injury (FPI) groups and administered saline or sodium selenate for 12 weeks post-injury. Femora were analysed using histomorphometry, peripheral quantitative computed tomography (pQCT) and biomechanical testing. Results: Distal metaphyseal trabecular bone volume fraction of FPI-selenate rats was higher than FPI-vehicle rats (41.8%; p<0.01), however, femora from selenate-treated groups were shorter in length (4.3%; p<0.01) and had increased growth plate width (22.1%; p<0.01), indicating that selenate impaired long bone growth. pQCT analysis demonstrated that distal metaphyseal cortical thickness was decreased in TBI rats compared to shams (11.7%; p<0.05), however selenate treatment to TBI animals offset this reduction (p<0.05). At the midshaft we observed no differences in biomechanical measures. Conclusion: These are the first findings to indicate that mitigating TBI-induced neuropathology may have the added benefit of preventing osteoporosis and associated fracture risk following TBI.

AB - Objectives: Administration of sodium selenate to rats given traumatic brain injury (TBI) attenuates brain damage and improves long-term behavioural outcomes. We have previously provided evidence that TBI causes bone loss in rats, however the effect of sodium selenate treatment on bone quantity following TBI is unknown. Methods: Rats were randomly assigned into sham injury or fluid percussion injury (FPI) groups and administered saline or sodium selenate for 12 weeks post-injury. Femora were analysed using histomorphometry, peripheral quantitative computed tomography (pQCT) and biomechanical testing. Results: Distal metaphyseal trabecular bone volume fraction of FPI-selenate rats was higher than FPI-vehicle rats (41.8%; p<0.01), however, femora from selenate-treated groups were shorter in length (4.3%; p<0.01) and had increased growth plate width (22.1%; p<0.01), indicating that selenate impaired long bone growth. pQCT analysis demonstrated that distal metaphyseal cortical thickness was decreased in TBI rats compared to shams (11.7%; p<0.05), however selenate treatment to TBI animals offset this reduction (p<0.05). At the midshaft we observed no differences in biomechanical measures. Conclusion: These are the first findings to indicate that mitigating TBI-induced neuropathology may have the added benefit of preventing osteoporosis and associated fracture risk following TBI.

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SN - 1108-7161

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