The sensitivity of the skeleton to its mechanical loading environment can result in severe bone loss upon the removal of mechanical signals, a concern for patients confined to bedrest, suffering from spinal cord injuries or neuromuscular diseases, or exposed to microgravity. Considering that treatments such as pharmacologic agents are associated with side effects, and many loading and exercise regimes require weight bearing, a novel physical stimulus was developed, comprised of low-level accelerations that could be applied in the absence of weight bearing. Here, in a series of experiments, the hypothesis that low-level accelerations are anabolic and anti-catabolic to the skeleton was tested.

To determine the effects of these signals on healthy adult bone, the left tibiae of adult female C57BL/6J mice were subjected to acceleratory motions applied at 45Hz, either 0.3g or 0.6g, for lOmin/d, while the right tibiae served as contralateral controls. After 3wks, bone formation rates (BFR) and the percentage of mineralizing surface (MS/BS) of the trabecular metaphysis were significantly (p<0.05) greater in tibiae accelerated at 0.3g (+88% and +64%, respectively) than in their contralateral controls. At 0.6g, BFR and mineral apposition rate (MAR) was 66% and 22% greater (p<0.05) in accelerated tibiae. Bone morphology was altered only in the epiphysis, where cortical area (+8%) and thickness (+8%) were greater in the stimulated tibiae. These results suggest that low-level accelerations can be anabolic to the adult skeleton.

To further elucidate the skeletal response to low level accelerations and determine the influence of acceleration magnitude, BALB/cByJ mice were subjected to acceleratory motions applied at 45Hz, 0.6g for lOmin/d, while the right tibiae served as contralateral controls. After 3wk, MAR of metaphyseal trabecular bone in the accelerated tibiae was 20% greater (p<0.05) as compared to the contralateral controls, although there were no differences in bone resorptive activity or bone morphology. In contrast, application of accelerations at a greater magnitude, 2.5g, induced lower metaphyseal trabecular MAR (- 7%, p<0.04) than controls, indicating that bone’s response to these signals is sensitive to the acceleration magnitude.

To examine how accelerations can influence a skeleton subjected to a catabolic stimulus, acceleratory signals were delivered at 45Hz, 0.6g, for 20min/d to the left tibiae of hindlimb-suspended mice, while the right tibiae experienced disuse-only. After 3wk, metaphyseal trabecular BFR were significantly greater (+70%) in the accelerated tibiae, although there were no differences in bone resorption. These responses in cellular activity were associated with differences in bone morphology, as metaphyseal trabecular bone loss and trabecular thinning were significantly reduced in the accelerated tibiae (- 23% and -12%, respectively) as compared to the disuse-only tibiae.

Together, the results of these studies suggest that low-level accelerations can influence bone formation and attenuate bone loss induced by disuse. Furthermore, they introduce a unique physical stimulus that, if verified in clinical work, could be applied as a prevention or treatment regime for skeletons inflicted with unloading-induced osteoporosis.