Modulation of appositional and longitudinal bone growth in the rat ulna by applied static and dynamic force.

Appositional and longitudinal growth of long bones are influenced by mechanical stimuli. Using the noninvasive rat ulna loading model, we tested the hypothesis that brief-duration (10 min/day) static loads have an inhibitory effect on appositional bone formation in the middiaphysis of growing rat ulnae. Several reports have shown that ulnar loading, when applied to growing rats, results in suppressed longitudinal growth. We tested a second hypothesis that load-induced longitudinal growth suppression in the growing rat ulna is proportional to time-averaged load, and that growth plate dimensions and chondrocyte populations are reduced in the loaded limbs. Growing male rats were divided into one of three groups receiving daily 10 min bouts of static loading at 17 N, static loading at 8.5 N, or dynamic loading at 17 N. Periosteal bone formation rates, measured 3 mm distal to the ulnar midshaft, were suppressed significantly (by 28-41%) by the brief static loading sessions despite normal (dynamic) limb use between the daily loading bouts. Static loading neither suppressed nor enhanced endocortical bone formation. Dynamic loading increased osteogenesis significantly on both surfaces. At the end of the 2 week loading experiment, loaded ulnae were approximately 4% shorter than the contralateral controls in the 17 N static and dynamic groups, and approximately 2% shorter than the control side in the 8.5 N static group, suggesting that growth suppression was proportional to peak load magnitude, regardless of whether the load was static or dynamic. The suppressed growth in loaded limbs was associated with thicker distal growth plates, particularly in the hypertrophic zone, and a concurrent retention of hypertrophic cell lacunae. Negligible effects were observed in the proximal growth plate. The results demonstrate that, in growing animals, even short periods of static loading can significantly suppress appositional growth; that dynamic loads trigger the adaptive response in bone; and that longitudinal growth suppression resulting from compressive end-loads is proportional to load magnitude and not average load.