Systemic Bone Loss Following Myocardial Infarctionin Mice

Myocardial infarction (MI) and osteoporotic fractureare leading causes of morbidity and mortality, and epidemiological evidence linking their incidence suggests possible crosstalk. MIcan exacerbate atherosclerosis through sympathetic nervous system (SNS) activation andβ3 adrenoreceptor-mediated release ofhematopoieticstem cells (HSCs), leading tomonocytosis.We hypothesized that this same pathwayinitiatessystemic bone lossfollowing MI, sinceosteoclasts differentiate from monocytes. In this study, MI was created with left anterior descending (LAD)arteryligation in 12-week-old male mice (n=24) randomized to β3 -adrenergic receptor antagonist (SR 59230A) treatment or no treatmentfor 10 days post-operatively.Additional mice (n=21, treated and untreated) served as un-operated controls. Bone mineral density (BMD), bone mineral content (BMC), and body composition were quantified at baseline and 10 days post-MIusing DXA; circulating monocytelevels were quantifiedandthe L5 vertebral body and femur were analyzed withmicro-computed tomography 10 days post-MI. We found that MI led tocirculating monocyte levels increases, BMD and BMC decreasesat the femur and lumbar spine in MI mice (-6.9% femur BMD,-3.5% lumbar BMD), and trabecular bone volumedecreases in MI mice compared to control mice. β3 -AR antagonist treatment appeared to diminish the bone loss response (-5.3% femur BMD, -1.2% lumbar BMD), though these results weresomewhat inconsistent. This article is protected by copyright. All rights reserved.