Osteochondral tissue includes articular cartilage, calcified cartilage, subchondral bone and trabecular bone. Injury to these tissues is common in several species, including horses and man. Injuries in horses include osteochondral fragmentation, osteochondral fracture, subchondral bone sclerosis and osteoarthritis. The role of subchondral bone in these diseases is controversial both in humans and horses. This project was established to investigate the effects of loading on subchondral tissues in horses by clinical and histologic methods. Results from this study will provide objective information on the response of subchondral bone to loading.

The first part of this study (Chapter 2) was designed to develop an ex vivo model of loading the carpal joints in order to evaluate the effects of loading on subchondral bone. The forelimbs from 12 horses were acquired from necropsy samples. One limb of each pair was loaded in an MTS machine as either a whole limb or carpal joint preparation, and the other limb of each pair served as an unloaded control. Limbs were cycled for 50,000 cycles under displacement control. Force transmitted through the limb and third metacarpal bone strain were evaluated and compared between loading schemes. All intercarpal joints were then dissected and the third carpal bones removed. One-cm osteochondral sections were then collected and evaluated for microdamage. Although whole limbs lost force quickly compared to carpal joint preparations, third metacarpal bone strain increased throughout the 50,000 cycles. However, third metacarpal bone strain decreased in the carpal joint preparations. Whole limbs had significantly greater diffuse-staining microdamage in the subchondral bone compared to their respective control limbs, but no differences existed between loaded and unloaded carpal joint preparations. Therefore, the resistance of the soft tissues in the whole limbs may have led to increases in third metacarpal bone strain, possibly increasing fatigue damage within that bone and the third carpal bone.

In the second part of the study, subchondral bone in the carpal and metacarpophalangeal joints of 6 horses that were exercised on a high-speed treadmill for 6 months were compared to that of hand-walked control horses by clinical imaging and histologic techniques. Treadmill exercised horses were more lame than hand-walked horses at the end of the study. Treadmill exercised horses had few radiographic signs of osteochondral damage, but did have greater uptake of radioisotope in the metacarpophalangeal joints, and greater areas of high density in the subchondral area of the third metacarpal condyles, as demonstrated by CT Osteoabsorptiometry, compared to hand-walked controls. Treadmill-exercised horses also had significantly more non-viable osteocytes in the subchondral bone of the radial carpal bone, the third carpal bone and the third metacarpal condyle than hand-walked horses. The radial carpal bones from treadmill exercised horses had more bone in the subchondral area than those from hand-walked horses. The third carpal bones of treadmill exercised horses had higher amounts of diffuse-staining microdamage in the subchondral plate and trabecular areas compared to those from handwalked horses. The third metacarpal bones of treadmill exercised horses had more bone area in the subchondral area, and more bone area and more oxytetracycline label in the trabecular area than hand-walked horses.

Overall, loading of the osteochondral area by either ex vivo or in vivo methods lead to changes in subchondral bone, including increased microdamage increased bone production and osteocyte death. Many of these responses (cell death and microdamage) may be initiating events in the normal response of subchondral bone to loading, but it is difficult to determine the point at which normal responses become pathologic.