Middle carpal cartilage explants from 4 horses with mild osteoarthritis involving that joint were maintained in tissue culture to test the effects of a polysulfated glycosaminoglycan (PSGAG) on proteoglycan synthesis and degradation. Cultures were exposed to 0.025 or 25 mg of PSGAG/ml for 48 hours, after which the medium was replaced with medium containing similar doses of PSGAG and 35S. Subsequently, the sulfated proteoglycan content of the medium and extracts of the explants was measured. Gel filtration chromatography was used to estimate the size and to purify the principal, large proteoglycan monomer, which was further characterized by digestion, using glycosidic enzymes. In a second experiment, explants were incubated with 35S for 48 hours, and were subsequently exposed to the same concentrations of the PSGAG for an additional 48 hours. The amount of remaining labeled proteoglycan was determined for culture medium and cartilage extracts. Gel filtration chromatography was used to assess the hydrodynamic size of the large proteoglycan monomer. Aliquots of proteoglycans from the second experiment were incubated in high-molecular weight hyaluronate and chromatographed to assess reaggregation. Polysulfated glycosaminoglycan caused a significant (P < 0.04) decrease in sulfated proteoglycan synthesis by cartilage explants. Radioactive proteoglycan content in explants labeled prior to exposure to PSGAG were similar. Large proteoglycan monomer size was similar in both experiments (median partition coefficient [K(AV)] = 0.40), and was not influenced by PSGAG treatment. Prelabeled explants exposed to hyaluronate and chromatographed under associative conditions had similar proportions of the radiolabel eluting as proteoglycan aggregate. Enzymatic digestion of newly synthesized large monomer revealed a mild dose-dependent increase in the proportion of keratan sulfate substitution on core protein. It was concluded that PSGAG in vitro, at the dosages evaluated, caused a decre.

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 osteochondral defect was made arthroscopically in 1 radial carpal bone of 2 ponies, and in 2 other ponies, chymopapain was injected into the radiocarpal joint to induce cartilage catabolism. Sequential and concurrent plasma and synovial fluid concentrations of KS were measured, up to 13 months 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 exercise and/or injected intra-articularly with 250 mg of polysulfated glycosaminoglycan (PSGAG). Medication was given at surgery, then weekly for 4 weeks. Blood samples were collected and synovial fluid was aspirated before surgery, when medication was given, and at postmortem examination (postoperative week 17). The KS concentration was measured in these fluids to determine whether changes in KS concentration indicated an effect of joint treatment. In experiment 1, the concentration of KS in synovial fluid was highest 1 day after joint injury, and the concentration in plasma peaked 2 days after joint injury. For ponies receiving chymopapain intra-articularly (generalized cartilage catabolism), a fivefold increase over baseline was observed in the concentration of KS in plasma (peak mean, 1.2 microgram/ml), and a tenfold increase over baseline in synovial fluid (peak mean, 2.0 mg/ml) was observed. On average, these maxima were threefold higher than values in fluids of ponies with 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 ponies at all postoperative times, and.

In recent years, exercise on a water treadmill has come to have great relevance in rehabilitation and training centres for sport horses. Its use exploits certain physical properties of water, related to the fundamental principles of hydrodynamics, such as buoyancy, viscosity, hydrostatic pressure, and water temperature. These properties together with deliberate specification of the depth of the water and the velocity of the treadmill provide a combination of parameters that can be varied according to the purpose of the rehabilitation or training programme, the disease to rehabilitate, or the healing phase. In the current article, kinematic adaptations to exercise on a water treadmill and the direct application of such exercise to the rehabilitation of superficial and deep digital flexor tendon and accessory ligament injuries and back and joint diseases are described.

A fourteen years old male oriental white stork from Korea Institute of Oriental White Stork Rehabilitation Research was presented to Veterinary Medical Center of Chungbuk National University with anorexia and lameness for 5 days. Bilateral intertarsal joint swellings were observed in physical examination. The radiographic findings indicated degenerative changes of joint cartilage and surrounding bones. In cytologic examination of synovial fluids, mononuclear leukocytic inflammation was identified. In blood films, a few fungal hyphae were observed and 2 fungal colonies were identified in blood culture on Sabroud dextrose agar.

Objective-To assess gait abnormalities associated with selective anesthesia of the suprascapular nerve (SSN) achieved by use of perineural catheterization and thereby determine the function of that nerve as it relates to gait in horses. Animals-3 adult horses with no preexisting clinically apparent lameness at a walk. Procedure-Each horse was anesthetized; the right SSN was exposed surgically for placement of a perineural catheter to permit delivery of 1 mL of 2% mepivacaine hydrochloride. Six hours after recovery from anesthesia, each horse was videotaped while walking (50-step data acquisition period) before and after administration of mepivacaine. Videotapes were reviewed and the proportion of abnormal steps before and after selective SSN anesthesia was assessed. A step was considered abnormal if a marked amount of scapulohumeral joint instability (ie, lateral luxation of the proximal portion of the humerus) was observed during the weight-bearing phase of the stride. Results-Clinically apparent gait dysfunction was detected in all 3 horses following perineural administration of the local anesthetic agent. Anesthesia of the SSN resulted in scapulohumeral joint instability as evidenced by consistent lateral excursion of the shoulder region during the weight-bearing phase of gait at a walk. The proportion of abnormal steps before and after SSN anesthesia was significantly different in all 3 horses. Conclusions and Clinical Relevance-These data support the role of the SSN in shoulder joint stability in horses and define SSN dysfunction as 1 mechanism by which the syndrome and gait dysfunction clinically referred to as sweeny may develop.

Objective-To evaluate whether additive genetic correlations existed between certain aspects of the radiographic appearance of the distal sesamoid (navicular) bones (RNB) or between RNB and other types of radiographic changes in the limbs of Hanoverian Warmblood horses. Animals-5,157 horses. Procedures-Quasi-linear and binary traits were defined by the appearance of canales sesamoidales (CSs) and the structure and contour of the forelimb navicular bones (NBs). Prevalences of osseous fragments in the metacarphophalangeal and metatarsophalangeal (fetlock) and tarsocrural joints and deforming arthropathy in tarsal joints were analyzed as binary traits. Genetic parameters were estimated by use of multivariate linear models. Results-Heritability estimates for the RNB traits ranged from 0.10 to 0.34. Additive genetic correlations among those traits were usually close to unity. Extensive radiographic changes in the NBs, including changes in CSs and alterations in structure and contour, had correlations with less distinct radiographic changes. Negative additive genetic correlations were observed between small numbers of short and conical CSs in the central portion of the distal border of the NB and osseous fragments and arthropathy, and between most types of radiographic findings in the NBs and osseous fragments in tarsal joints. Conclusions and Clinical Relevance-The genetic bases for different types of RNB were not identical. The detection of correlations between normal RNB and findings of short and conical CSs versus deformed CSs and structural and contour changes warrants further study. Genetically justified distinction between physiologic and pathologic NB changes will increase the efficiency of selecting against NBs with radiographically apparent alterations.

A 3-year prospective study of large-breed dogs (4 months to 3 years of age) was conducted to evaluate the influence of radiographic positioning and age on coxofemoral joint (hip) laxity, subjective hip score, and development of degenerative joint disease (DJD). The dogs (n = 142) were breeder- or client-owned and represented 14 breeds. With dogs under heavy sedation, hips were radiographed in the standard hip-extended position and in the new compression/distraction position at 4, 6, 12, 24, and 36 months of age. The standard hip-extended radiographic view was evaluated by 3 methods: subjective evaluation by a board-certified veterinary radiologist (WHR), according to the standard 7-point Orthopedic Foundation for Animals (OFA) scoring scheme (OFA/WHR); joint laxity quantitation, using the Norberg angle (NA) method; and subjective scoring by a veterinary orthopedic surgeon for radiographic evidence of DJD. The hips in the distraction radiographic view were evaluated for passive hip laxity, as measured by use of a unitless distraction index (DI). Results of the study indicated that at a specific age (4, 6, 12, 24, or 36 months), all methods of hip evaluation correlated with each other at a moderate level (P < 0.05). The strength of contemporaneous correlation tended to increase with age of evaluation. Longitudinally, the between-method correlations were usually significant (P < 0.05), but not at a sufficiently high level to permit reliable between-method prediction. Prospective intraclass (within-method) statistical analysis of the various hip-scoring methods indicated that DI was superior to NA and OFA/WHR in comparability of score over time. The intraclass correlation coefficient ranged from 0.55 to 0.91 for DI in contrast to 0.40 to 0.78 for NA, and 0.06 to 0.39 for OFA/WHR over the age intervals of the study. For reference, the highest Kappa of 0.39 for the subjective OFA/WHR scoring reflected a maximal level of agreement between time intervals, only slightly better than chance. The associated large error questions the predictive use of the 7-point, subjective hip-scoring scheme, particularly prior to the age of 2 years.

Using arthroscopic technique, identical diameter defects were created in the proximal articular surface of both intermediate carpal bones of 6 horses. One of each pair of defects was deepened to penetrate the subchondral plate. Removed cartilage was assayed for [35S] sulfate incorporation, total hexosamine content, and DNA content. Six weeks later, cartilage was harvested and similarly analyzed from the distolateral portion of the radius directly opposite the created lesions and the distomedial portion of the radius distant from the lesion. The repair tissue filling the full-thickness defect and the cartilage at the periphery of the partial-thickness lesion also were analyzed. There was a marked increase in synthetic activity (35S sulfate incorporation) opposite the full-thickness defect, compared with the cartilage opposite the partial-thickness defect. A marked decrease in glycosaminoglycan content in the cartilage opposite the full-thickness defect was found as compared with that opposite the partial-thickness defect. The repair tissue filling the full-thickness defect was highly cellular, high in synthetic activity, but low in glycosaminoglycan content. Insignificant changes occurred in the cartilage adjacent to the partial-thickness defect. On the basis of these results, we suggest that full-thickness defects at 6 weeks result in more detrimental change to the cartilage opposite it than do partial-thickness lesions of the same diameter.

Osteoarthritis (OA) of the metacarpophalangeal joint is the most common articular disease in polo ponies leading to early retirement. A biomarker that would discriminate between pathological and physiological changes secondary to exercise could be helpful in OA prevention. The aim of this study was to investigate the effects of polo training on synovial fluid biomarkers of inflammation and cartilage turnover in polo ponies of different skill levels. Synovial fluid samples were collected from metacarpophalangeal joints of polo ponies before and during the polo season (320 d). Nucleated cells, soluble protein, prostaglandin E2 (PGE2), glycosaminoglycans (GAG), and urea were measured. The main synovial fluid GAG are chondroitin sulphate (CS, ~25 μg/mL) and hyaluronic acid (HA, ~400 μg/mL). After a polo match, a transitory increase in protein and PGE2, but not CS and HA, occurred (expressed as urea ratio), returning to basal levels in 24 h. During the polo season, the number of synovial fluid nucleated cells was always in the normal range. Increases in protein and HA occurred during the initial 40 to 80 d, returning to basal levels afterwards. In contrast, in polo prospects the concentration of CS steadily increased during the season. Long-term follow-up revealed that the synovial fluid CS was significantly higher in polo ponies that developed joint diseases within 24 months following our study. In conclusion, CS seems to be an early marker of articular cartilage damage.

Three doses of sodium monoiodoacetate (MIA) were used to induce degenerative changes in articular cartilage in middle carpal joints of horses. Twelve young (2- to 5-year-old) horses, free of lameness, were randomly allotted to 3 groups. One middle carpal joint of each horse was injected with 0.9% NaCl solution (control joint). The contralateral middle carpal joint was injected with 0.09 mg of MIA/kg of body weight (group 1); 0.12 mg(kg (group 2); or 0.16 mg(kg (group 3). After MIA administration, horses were allowed ad libitum exercise in a 2-acre paddock for 12 weeks. At the end of the study, gross and microscopic tissue changes were evaluated and biochemical analyses of articular cartilage were done. Grossly, diffuse partial-thickness articular cartilage lesions were observed in group-2 (n = 2) and group-3 (n = 4) horses, but not in group-1 horses. Articular cartilage uronic acid content was significantly (P < 0.03) decreased in all MIA-injected joints, compared with controls. Articular cartilage matrix staining with safranin-O was decreased in 3 of 4 MIA-injected joints of group-1 horses and in all MIA-injected joints of group-2 and group-3 horses, compared with controls (P < 0.06). Microscopic degenerative changes in articular cartilage were not significantly different between MIA-injected and control joints in group-1 horses, but were increased (P < 0.06) in all MIA-injected joints of group-2 and group-3 horses, compared with controls. Qualitatively, decreased matrix staining and degenerative changes were more severe in group-3 horses. On the basis of articular cartilage gross and microscopic changes, as well as biochemical changes, 0.12 mg of MIA/kg injected intra-articularly was determined to induce moderate degrees of articular cartilage degeneration. This model of chemically induced articular cartilage injury could be useful for evaluating treatment effects of anti-arthritic drugs in horses.