Effect of suspension on mouse bone microhardness

Abstract

Antiorthostatic (hindlimb) suspension of mice results in a considerable reduction of bone formation at the femur mid-diaphysis. Comparisons with appropriate control groups indicate that this reduction is attributable to the unloading aspect of the model, and not to physiological stress or changes in feeding. Microhardness measurements of bone are used to provide information on site-specific mineralization and structural properties. The microhardness of femora formed during suspension is significantly less than that formed in the bone of control mice. These differences are observed both along the endocortical (11%) and periosteal (8%) perimeters. The microhardness of bone formed prior to the experimental period ("extant bone") is not different in comparing suspended and control mice, and increased microhardness values for these areas are observed in comparison to baseline controls. Mice used to control for the physiological stress and feeding portions of the suspension model do not demonstrate reduced microhardness. Thus, the limb unloading effects of suspension, not the induced stress or feeding changes, cause a reduction in microhardness. As microhardness is positively related to mineralization in these bones, it appears that the reduced mineralization accompanying suspension unloading may contribute to compromised structural properties of the bone formed.