Honors College Thesis
 

Voluntary alcohol consumption in male rhesus macaques suppresses cancellous bone remodeling

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  • Background: Chronic heavy alcohol consumption is a risk factor for bone fracture. Using a non-human primate model of voluntary alcohol self-administration, we have recently shown that alcohol consumption suppresses intracortical bone remodeling. The current study extends this investigation to asses the effect of alcohol consumption on cancellous bone mass, architecture, and formation in lumbar vertebrae. Methods: Following a 4-month induction period, male rhesus macaques (n=5) voluntarily self-administered water or alcohol (4% w/v) for 22h/d, 7d/wk for a total of 12 months. Control animals (n=4) consumed an isocaloric maltose-dextrin solution. Tetracycline hydrochloride was administered orally 17 and 3 days prior to sacrifice to label mineralizing bone. The response to alcohol in lumbar vertebrae was evaluated using densitometry, microcomputed tomography, and histomorphometry. Results: Monkeys in the alcohol group consumed an average of 2.0 ± 0.2 (mean ± SE) g/kg/d of ethanol, resulting in an average blood ethanol concentration of 67± 9 mg/dl. However, average consumption and blood ethanol concentration varied widely from day to day, as well as from subject to subject. Significant differences in lumbar vertebrae 1-4 bone area, bone mineral content, and bone mineral density were not detected with treatment. Significant differences in cancellous bone architecture (bone volume/tissue volume, trabecular thickness, trabecular number, and trabecular spacing) were likewise not detected with treatment. However, bone formation rate/bone perimeter and bone formation rate/tissue area were lower in the alcohol-consuming monkeys compared to controls (46.5 ± 9.5 versus 23.0 ± 5.9 %/y and 20.6 ± 3.5 versus 9.6 ± 2.3 %/y, respectively). Conclusions: These results suggest that chronic alcohol consumption reduces cancellous bone formation in lumbar vertebrae. Key Words: Computed tomography, bone histomorphometry, non-human primate, DXA
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  • This work was supported by NIH grants AA022454 (to UTI) and AA109431, AA13510, and OD11092 (to KAG).
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