Antiorthostatic (hindlimb) suspension of mice results in a considerabl
e reduction of bone formation at the femur mid-diaphysis. Comparisons
with appropriate control groups indicate that this reduction is attrib
utable to the unloading aspect of the model, and not to physiological
stress or changes in feeding. Microhardness measurements of bone are u
sed to provide information on site-specific mineralization and structu
ral properties. The microhardness of femora formed during suspension i
s significantly less than that formed in the bone of control mice. The
se differences are observed both along the endocortical (11%) and peri
osteal (8%) perimeters. The microhardness of bone formed prior to the
experimental period (''extant bone'') is not different in comparing su
spended and control mice, and increased microhardness values for these
areas are observed in comparison to baseline controls. Mice used to c
ontrol for the physiological stress and feeding portions of the suspen
sion model do not demonstrate reduced microhardness. Thus, the limb un
loading effects of suspension, not the induced stress or feeding chang
es, 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 co
mpromised structural properties of the bone formed.