Thirteen Standardbred horses were trained on a treadmill for 31 weeks as part of a larger study into the effects of overtraining. Synovial fluid was collected from the midcarpal joint at the start, and at seven, 15, 21, 26 and 30 weeks of training. Low grade signs of midcarpal joint disease developed in all horses during the last 16 weeks of the program. Synovial fluid leukocyte counts remained unchanged throughout the study, whereas total protein concentration and lactate dehydrogenase activity increased significantly with training. Sulfated glycosaminoglycan (GAGs) levels increased initially, but then decreased. Correlations between the clinical signs of joint disease and sulfated GAG levels were weak.
Synovial fluid sulfated GAGs were compared with other diagnostic variables for predicting the degree of articular cartilage damage in horses with midcarpal joint disease. Interpretation of radiographs was found to be the most accurate for the prediction of articular damage. Synovial fluid analysis was found to be of little value. There was no correlation between sulfated GAG concentration and articular cartilage damage, and no significant difference between sulfated GAG concentrations from horses with clinical evidence of joint disease and horses with no signs of joint disease trained on a treadmill.
Anatomical dissections of the midcarpal joint were performed on ten cadavers. The medial palmar intercarpal ligament (MPICL) was found to consist of four fibre bundles. The predominant orientation of these was proximodorsal to distopalmar. The lateral palmar intercarpal (LPICL) and dorsomedial intercarpal (DMICL) ligaments had a similar orientation but were simpler in structure. The alignment of these ligaments suggested that they resisted transverse forces across the midcarpal joint. Using a dorsal transverse displacement of 1.5 mm of the proximal row of carpal bones relative to the distal row of carpal bones, it was demonstrated that the palmar intercarpal ligaments provided 22.7% of the restraining force while only contributing 9% of the ligamentous cross sectional area.
A study of 32 racing horses presented with midcarpal joint disease confirmed the high frequency of MPICL tearing (51%). Enlargement of the DMICL was also common (33%). There was no correlation between the severity of signs of midcarpal joint disease and the severity of MPICL tearing. An inverse relationship was demonstrated between subchondral bone damage within the midcarpal joint, and MPICL tearing (R=-0.55). There was no association between DMICL enlargement and osteochondral damage. A postmortem study of 142 joints of horses with no history of midcarpal joint disease demonstrated that the frequency of MPICL tearing in racing horses was 91%. Severity of tearing of the MPICL increased significantly with age. Histopathological evidence of degeneration (loss of organisation of collagen fibres) was consistently observed in MPICLs of adult horses. These changes were not observed in unborn term foals, but were present from one month of age. Enlarged DMICLs had regular collagen arrangement, but discrete areas of fibrovascular infiltration were consistently observed.
The race records of 42 horses undergoing midcarpal joint carpal arthroscopy were examined. Using multiple regression the extent of subchondral bone damage was the best predictor of postoperative performance. The addition of the grade of MPICL tearing significantly improved the prediction of postoperative performance, whereas the inclusion of the extent of articular cartilage damage had no effect
