Stacked rectangular rosette strain gages were used to measure surface bone strain on the dorsomedial cortex of the third metacarpal bones in 6 adult Thoroughbred horses during treadmill exercise. The peak principal compressive and tensile strains, angle of the peak strains and strain rate during loading were calculated and compared with speed and gait. At speeds from 4 to 14 m/s loading on the metacarpus resulted in compression of the dorsomedial cortex. Tension only occurred consistently in 1 forelimb of 1 horse at the walk (2 m/s). The angle of peak compression was within 10° of the longitudinal axis of the bone, and the magnitude of compression was proportional to the speed of exercise. Mean maximum compressive strains in the 6 horses at 2 m/s were –668 µstrain, –1,204 µstrain at 4 m/s; –1,617 µstrain at 6 m/s; –2,127 µstrain at 8 m/s, and –2,533 µstrain at 10 m/s. Recordings from 3 horses gave a mean –3,206 µstrain at 12 m/s, and strains at 14 m/s approached –4,000 µstrain. Peak strains were similar in both forelimbs at the canter while strain rate tended to be higher in the leading forelimb.

Osteochondrosis is a condition involving defective endochondral ossification and retention of cartilage in subchondral bone. The pathophysiology of this condition is poorly characterized, but it has been proposed that the fundamental defect is failure of chondrocyte hypertrophy. The aim of the current study was to characterize phenotypic changes in chondrocytes associated with the initiation of osteochondrosis. Early lesions were induced in an equine model of osteochondrosis by feeding foals a high energy diet for 8 or 15 weeks. Lesions in articular‐epiphyseal growth cartilage were examined histologically and by quantitative PCR analysis of expression of a number of genes representative of pathways that regulate chondrocyte behavior during endochondral ossification. There were more cells present in clusters in the lesions compared to normal articular cartilage. Expression of matrix metalloproteinase‐13, type I collagen, type X collagen, and Runx2 mRNA was significantly greater in the lesions compared to normal cartilage from the same joint. Expression of vascular endothelial growth factor, type II collagen, connective tissue growth factor, aggrecan, Sox9, and fibroblast growth factor receptor 3 mRNA was not significantly different in lesions than in control cartilage. These observations suggest that osteochondrosis does not result from failure of chondrocytes to undergo hypertrophy. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27: 452–457, 2009