Mader, Tara Lynn2013-12-192013-12-192011-08https://hdl.handle.net/11299/161787University of Minnesota M.A. thesis. August 2011. Major: Kinesiology. Advisor: Moira Anne Petit. 1 computer file (PDF); v, 18 pages.Chemokines are proposed to be involved with bone loss. The purpose of this study was to determine whether genetic elimination of C-C chemokine receptor 2 (CCR2) was protective of bone geometry and function. Ovariectomy and denervation were used as interventions to induce bone loss in mice with and without CCR2 (C57BL/6 wild type and CCR2-knockout (CCR2-/-) mice, respectively). Cortical geometry and trabecular morphology of tibial bones were determined using μCT analyses. Bone mechanical properties were calculated from load displacement curves using 3-point bending testing. Overall, the elimination of CCR2 had a minor protective effect on bone mechanical properties. CCR2-/- mice had bones slightly larger and stronger than C57BL/6 mice. In ovariectomized and denervated mice, CCR2-/- tibiae exhibited 5-18% greater cross sectional area, cross sectional moment of inertia, ultimate load, and stiffness than C57BL/6 tibiae indicating a resistance to intervention-induced bone loss in the CCR2-/- mice. Trabecular bone volume fraction and bone mineral density was 2-22% greater in CCR2-/- mice than C57BL/6 mice at both the epiphysis and the metaphysis. Additionally, periosteal diameter was protected in CCR2-/- mice but not in C57BL/6 mice with interventions. It is concluded that genetic elimination of CCR2 results in larger bones that are minimally protected under conditions of induced bone loss.en-USThesis or Dissertation