Bone hyperemia precedes disuse-induced intracortical bone resorption

McCaig Centre for Joint Injury and Arthritis Research, Department of Surgery, University of Calgary, Calgary, Canada T2N 4N1 An in vivo model was used to determine whether bone hyperemia precedes increased intracortical porosity induced by disuse. Twenty-four adult male roosters (age 1 yr) were randomly assigned to intact-control, 7-days-sham-surgery, 7-days-disuse, and 14-days-disuse groups. Disuse was achieved by isolating the left ulna diaphysis from physical loading via parallel metaphyseal osteotomies. The right ulna served as an intact contralateral control. Colored microspheres were used to assess middiaphyseal bone blood flow. Bone blood flow was symmetric between the left and right ulnae of the intact-control and sham-surgery groups. After 7 days of disuse, median (±95% confidence interval) standardized blood flow was significantly elevated compared with the contralateral bone (6.5 ± 5.2 vs. 1.0 ± 0.8 ml · min 1 · 100 g 1 ; P = 0.03). After 14 days of disuse, blood flow was also elevated but to a lesser extent. Intracortical porosity in the sham-surgery and 7-days-disuse bones was not elevated compared with intact-control bones. At 14 days of disuse, the area of intracortical porosity was significantly elevated compared with intact control bones (0.015 ± 0.02 vs. 0.002 ± 0.002 mm 2 ; P = 0.03). We conclude that disuse induces bone hyperemia before an increase in intracortical porosity. The potential interaction between bone vasoregulation and bone cell dynamics remains to be studied. blood flow; bone loss; osteoclast; endothelial cell; vasoregulation