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 language | English |
|---|---|
| Pages (from-to) | 369-376 |
| Number of pages | 8 |
| Journal | Journal of Musculoskeletal Neuronal Interactions |
| Volume | 16 |
| Issue number | 4 |
| Publication status | Published - 1 Dec 2016 |
| Externally published | Yes |
Keywords
- Bone growth
- Bone Metabolism
- Endochondral ossification
- Neurotrauma
- Osteoporosis
Cite this
}
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 journal › Article › Research › peer-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.
KW - Bone growth
KW - Bone Metabolism
KW - Endochondral ossification
KW - Neurotrauma
KW - Osteoporosis
UR - http://www.scopus.com/inward/record.url?scp=85007387108&partnerID=8YFLogxK
M3 - Article
C2 - 27973389
AN - SCOPUS:85007387108
VL - 16
SP - 369
EP - 376
JO - Journal of Musculoskeletal Neuronal Interactions
JF - Journal of Musculoskeletal Neuronal Interactions
SN - 1108-7161
IS - 4
ER -