KERATAN SULFATE AS A MARKER OF ARTICULAR-CARTILAGE CATABOLISM AND JOINT TREATMENT IN PONIES

Keratan sulfate (KS) is a glycosaminoglycan, distribution of which is confined mostly to hyaline cartilage. As such, it is a putative marker of hyaline cartilage catabolism. In experiment 1, a focal osteochondr al defect was made arthroscopically in 1 radial carpal bone of 2 ponie s, and in 2 other ponies, chymopapain was injected into the radiocarpa l joint to induce cartilage catabolism. Sequential and concurrent plas ma and synovial fluid concentrations of KS were measured, up to 13 mon ths after induction of cartilage injury, to determine whether changes in KS concentrations reflected cartilage catabolism. In experiment 2, a large, bilateral osteochondral defect was made in the radial carpal bones of 18 ponies, which were subsequently given postoperative exerci se and/or injected intra-articularly with 250 mg of polysulfated glyco saminoglycan (PSGAG). Medication was given at surgery, then weekly for 4 weeks. Blood samples were collected and synovial fluid was aspirate d before surgery, when medication was given, and at postmortem examina tion (postoperative week 17). The Ks concentration was measured in the se fluids to determine whether changes in KS concentration indicated a n effect of joint treatment. In experiment 1, the concentration of KS in synovial fluid was highest 1 day after joint injury, and the concen tration in plasma peaked 2 days after joint injury. For ponies receivi ng chymopapain intra-articularly (generalized cartilage catabolism), a fivefold increase over baseline was observed in the concentration of KS in plasma (peak mean, 1.2 mug/ml), and a tenfold increase over base line in synovial fluid (peak mean, 2.0 mg/ml) was observed. On average , these maxima were threefold higher than values in fluids of ponies w ith osteochondral defects (focal cartilage disease). In experiment 2, nonexercised ponies had lower KS concentration (as a percentage of the preoperative concentration) in synovial fluid than did exercised poni es at all postoperative times, and at postoperative week 17, this effe ct was significant (P < 0.05). This may be related to decreased turnov er of KS in articular cartilage attributable to stall confinement and late increase in turnover related to exercise. Seventeen weeks after s urgery, synovial fluid from exercised, medicated ponies had significan tly (P < 0.05) higher KS content than did fluid from exercised, nonmed icated ponies. This indicated that exercise, when combined with medica tion, may increase KS release from articular cartilage. Synovial fluid from medicated joints of nonexercised ponies had significantly (P < 0 .05) lower KS concentration than did synovial fluid from nonmedicated joints of nonexercised ponies. This indicated that, in nonexercised jo ints, medication with PSGAG may have decreased either release of KS fr om the articular cartilage into the synovial fluid or inhibited synthe sis of KS. Concentration of KS in synovial fluid was not related clear ly to the development of osteoarthritis in these ponies. Exercise or m edication did not affect plasma KS concentration, and synovial fluid a nd plasma KS concentrations were not correlated. Data indicated that K S concentration in plasma and synovial fluid may be increased in acute , marked, generalized articular cartilage catabolism and that KS turno ver in cartilage of joints with large osteochondral defects was affect ed by intra-articular PSGAG and postoperative exercise.