Reduced bone mass accrual in mouse model of repetitive mild traumatic brain injury
Author(s) -
Hongrun Yu,
Jon E. Wergedal,
Charles H. Rundle,
Subburaman Mohan
Publication year - 2014
Publication title -
the journal of rehabilitation research and development
Language(s) - English
Resource type - Journals
eISSN - 1938-1352
pISSN - 0748-7711
DOI - 10.1682/jrrd.2014.04.0095
Subject(s) - traumatic brain injury , bone mineral , medicine , astrocytosis , endocrinology , brain size , peak bone mass , concussion , central nervous system , poison control , magnetic resonance imaging , osteoporosis , injury prevention , radiology , psychiatry , environmental health
Traumatic brain injury (TBI) can affect bone by influencing the production/actions of pituitary hormones and neuropeptides that play significant regulatory roles in bone metabolism. Previously, we demonstrated that experimental TBI exerted a negative effect on the skeleton. Since mild TBI (mTBI) accounts for the majority of TBI cases, this study was undertaken to evaluate TBI effects using a milder impact model in female mice. Repetitive mTBI caused microhemorrhaging, astrocytosis, and increased anti-inflammatory protective actions in the brain of the impacted versus control mice 2 wk after the first impact. Serum levels of growth regulating insulin-like growth factor 1 (IGF-I) were reduced by 28.9%. Bone mass was reduced significantly in total body as well as individual skeletons. Tibial total cortical density was reduced by 7.0%, which led to weaker bones, as shown by a 31.3% decrease in femoral size adjusted peak torque. A 27.5% decrease in tibial trabecular bone volume per total volume was accompanied by a 34.3% (p = 0.07) decrease in bone formation rate (BFR) per total area. Based on our data, we conclude that repetitive mTBI exerted significant negative effects on accrual of both cortical and trabecular bone mass in mice caused by a reduced BFR.
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