Objective—To evaluate cartilage thickness of the talus (especially at sites predisposed to osteochondrosis dissecans [OCD]) in growing and adult dogs not affected with OCD. Sample—Tarsocrural joints from cadavers of 34 juvenile (approx 3 months old) and 10 adult dogs. Procedures—Tarsal cartilage thickness was examined via a stereophotography microscopic system. Articular cartilage thickness was determined at 11 locations on longitudinal slices of the trochlear ridges and the sulcus between the ridges and at 2 locations in the cochlea tibiae. Cartilage thickness was measured at the proximal, proximodorsal, dorsal, and distal aspects of the trochlear ridges; proximodorsal, dorsal, and distal aspects of the trochlear sulcus; and craniolateral and caudomedial aspects of the cochlea tibiae. Differences within a joint and between sexes were evaluated. Results—Mean cartilage thickness decreased from proximal to distal in juvenile (lateral trochlear ridge, 1.52 to 0.41 mm; medial trochlear ridge, 1.10 to 0.40 mm) and from proximal to dorsal in adult (lateral trochlear ridge, 0.41 to 0.34 mm; medial trochlear ridge, 0.33 to 0.23 mm) dogs. Cartilage was thickest at the proximal aspect of the lateral trochlear ridge in both groups. Differences in proximodorsal, dorsal, and distal aspects of the ridges were not evident. Conclusions and Clinical Relevance—Healthy tarsocrural joints did not have thicker cartilage in sites predisposed to development of OCD. Evaluation of affected tarsocrural joints is necessary to exclude influences of cartilage thickness. These data are useful as a reference for distribution of cartilage thickness of the trochlea of the talus in dogs.

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 at postoperative week 17, this effect was significant (P < 0.05). This may be related to decreased turnover of KS in articular cartilage attributable to stall confinement and late increase in turnover related to exercise. Seventeen weeks after surgery, synovial fluid from exercised, medicated ponies had significantly (P < 0.05) higher KS content than did fluid from exercised, nonmedicated ponies. This indicated that exercise, when combined with medication, 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 joints, medication with PSGAG may have decreased either release of KS from the articular cartilage into the synovial fluid or inhibited synthesis of KS. Concentration of KS in synovial fluid was not related clearly to the development of osteoarthritis in these ponies. Exercise or medication did not affect plasma KS concentration, and synovial fluid and plasma KS concentrations were not correlated. Data indicated that KS concentration in plasma and synovial fluid may be increased in acute, marked, generalized articular cartilage catabolism and that KS turnover in cartilage of joints with large osteochondral defects was affected by intra-articular PSGAG and postoperative exercise.

Combined blood pool and delayed images produced by use of 99mTc-methylene diphosphonate (99mTcMDP) were evaluated as an objective measurement of the response of equine joints with osteochondral defects to postoperative exercise and intra-articularly administered polysulfated glycosaminoglycan (PSGAG). Osteochondral defects (approx 2.4 X 0.9 cm) were induced arthroscopically in the dorsodistal radial carpal bones of 18 ponies. These ponies were randomized (while balancing for age [range 2 to 15; median, 5.0; mean, 5.1 years]) to 2 treatment groups. Nine ponies were assigned to be exercised, and 9 were stall-rested. Six ponies in each group were administered PSGAG (250 mg) in 1 joint (medicated) and lactated Ringer's solution (LRS) in the contralateral joint. The 3 remaining ponies in each group were administered LRS in both joints (nonmedicated). Medication was given at surgery, then weekly for 4 weeks. The exercise protocol (begun at postoperative day 6 and conducted twice daily) started with 30 minutes walking (approx 0.7 m/s), and, by postoperative month 3, the ponies were being walked for 15 minutes and trotted (approx 1.6 m/s) for 25 minutes. Simultaneous dorsal images of both carpi were made 2 to 3 minutes after IV administration of 99mTcMDP (blood pool image) and 90 to 120 minutes later (delayed image). Scintimetry, in counts per minute per pixel per millicurie, was done before, and at 1, 2, 4, 8, 10, 13, and 17 weeks after surgery, prior to euthanasia. Radionuclide uptake on blood pool images decreased faster than that on delayed images, in which uptake remained high for 17 weeks. This indicated that bone was metabolically active for at least 17 weeks after surgery. Exercise significantly (P < 0.05) decreased uptake on the blood pool images of medicated joints up to 1 month after surgery. Thus, exercise (in the presence of PSGAG) probably had a transient, beneficial effect on soft tissues of the joint. Exercise, without PSGAG, promoted increased bone remodeling, because the highest uptake on delayed images was observed in exercised, nonmedicated ponies up to 3 months after surgery. This was consistent with development of osteoarthritis in these ponies. Medication alone stimulated bone remodeling, and data indicated that an identical effect may take place in contralateral LRS-injected joints, because of systemic circulation of the drug. However, the combination of exercise and medication appeared to moderate the independent effects of each. The combination of exercise and medication in individual joints resulted in notably (P < 0.05) decreased bone remodeling. Medication caused a decrease in bone remodeling in exercised ponies, indicating a protective effect against development of osteoarthritis.

A circular (5.5 mm diameter) full-thickness cartilage defect was created on the medial ridge of the talus in 12 skeletally mature dogs. In 6 dogs, the articular surface of the lesion was repaired, using an osteochondral graft obtained from the ipsilateral manus. The graft (digit I, first phalanx, distal articular surface and diaphysis) was contoured to obtain a press fit in the drilled talar recipient site. In 6 dogs, the lesion was not treated and healed by fibrous tissue replacement. Functional assessment (lameness, hock range of motion, joint stability, joint crepitus, and mid-femoral muscle circumference) was completed before surgery and at postoperative weeks 2 through 20. Radiographic assessment (periarticular soft tissue width, joint space width, osteophyte formation, and graft incorporation) was completed before surgery and at postoperative weeks 0, 6, 12, and 20. To facilitate histologic assessment, tissues were stained with toluidine blue and H&E. Histologic assessment of the articular surface on the surgically treated talus, ipsilateral tibia, and contralateral talus was completed, using a modification of the Mankin grading system. Subchondral bone was examined to assess graft viability and incorporation. Analysis of the ordinal data was completed, using a Mann-Whitney rank sum test. All dogs were fully weight bearing by postoperative week 7. Dogs without grafts had significantly (P = 0.036) better clinical function at postoperative week 6. Significant difference in functional assessment was not evident at postoperative week 20. Immediate postoperative radiographic assessment revealed significant (P = 0.005) difference between nongrafted and grafted groups. Significant difference was not observed at postoperative week 6, 12, or 20. All grafts appeared radiographically incorporated by postoperative week 12. All grafts restored joint surface congruity, whereas 3 of 6 nongrafted lesions had poor articular congruity. Of 6 grafts, 4 partially retained normal hyaline cartilage, resulting in significantly (P = 0.014) lower Mankin grades. Significant histologic differences between groups were not apparent when the apposing tibia and control talus were examined. Talar reconstruction by use of a phalangeal osteochondral graft is a viable surgical procedure. These data indicate that normal articular and subchondral architecture are more closely approximated by osteochondral reconstruction than by fibrous tissue repair.

Using biodegradable pins, sternal cartilage autografts were fixed into osteochondral defects of the distal radial carpal bone in ten 2 to 3-year-old horses. The defects measured 1 cm2 at the surface and were 4 mm deep. Control osteochondral defects of contralateral carpi were not grafted. After confinement for 7 weeks, horses were walked 1 hour daily on a walker for an additional 9 weeks. Horses were euthanatized at 16 weeks. Half of the repair tissue was processed for histologic and histochemical (H&E and safranin-O fast green) examinations. The other half was used for the following biochemical analyses: type-I and type-II collagen contents, total glycosaminoglycan content, and galactosamine-to-glucosamine ratio. On histologic examination, the repair tissue in the grafted defects consisted of hyaline-like cartilage. Repair tissue in the nongrafted defects consisted of fibrocartilaginous tissue, with fibrous tissue in surface layers. On biochemical analysis, repair tissue of grafted defects was composed predominantly of type-II collagen; repair tissue of nongrafted defects was composed of type-I collagen. Total glycosaminoglycan content of repair tissue of grafted defects was similar to that of normal articular cartilage. Total glycosaminoglycan content of nongrafted defects was 62% of that of normal articular cartilage (P < 0.05). Repair tissue of all defects was characterized by galactosamine-to-glucosamine ratio significantly (P < 0.05) higher than that of normal articular cartilage. These results at 16 weeks after grafting indicate that sternal cartilage may potentially constitute a suitable substitute for articular cartilage in large osteochondral defects of horses.

We compared the frequency and severity of osteochondrosis lesions in young Thoroughbred horses with cervical stenotic myelopathy (CSM) vs that in clinically normal Thoroughbreds of the same age. All lesions of the cervical vertebrae and appendicular skeleton were classifiedhistologically as osteochondrosis or nonosteochondrosis and were measured for severity. Minimal sagittal diameter was significantly smaller in horses with CSM from C2 through C6; no difference was detected at C7. Severity of cervical vertebral osteochondrosis was greater in the horses with CSM, however frequency was not different. Frequency and severity of nonosteochondrosis lesions were not different in cervical vertebrae or appendicular skeleton. Frequency and severity of appendicular skeleton osteochondrosis lesions were both greater in horses with CSM. Osteochondrosis and nonosteochondrosis lesions were more severe on facets at sites of compression than on facets at noncompressed sites in horses with CSM. However, compression was also observed at sites with no articular facet lesions. The association of widespread osteochondrosis and spinal canal narrowing with CSM suggests CSM may represent a systemic failure in the development or maturation of cartilage and bone.

To investigate whether arthrographic findings had any prognostic value with respect to treatment and outcome of bilateral osteochondrosis, shoulder arthrograms (n = 80) from 40 dogs with bilateral lesions were evaluated. Arthrography was performed, using 1.5 to 4 ml of a 25% solution of meglumine-sodium diatrizoate, with admixture of 0.2 mg of epinephrine. A shoulder with signs of pain and lameness was surgically treated. The contralateral shoulder was treated conservatively, and the final outcome was compared with the arthrographic findings. In 37 dogs, signs of lameness and pain were associated with a loose cartilage flap and, in 3, with a detached cartilage flap. In 2 dogs, admitted with bilateral lameness, a loose cartilage flap was detected in both shoulders. Of 12 dogs with a detectable loose cartilage flap in the contralateral shoulder joint, 6 became lame 2 to 4 months after initial surgical intervention and needed bilateral surgery. In the contralateral joint, development of thick articular cartilage over the subchondral defect or a detached cartilage flap lodged in the caudal pouch of the shoulder joint was a favorable prognostic sign. Such dogs had no signs of lameness on the contralateral side during a follow-up period that ranged from 1 to 7 years.

Six scapulohumeral joints (3 normal joints and 3 joints with radiographic evidence of osteochondrosis) underwent conventional magnetic resonance (MR) imaging and MR scapulohumeral arthrography to evaluate delineation of the articular cartilage. The MR arthrography was performed, using 5 ml of 500 micromolar gadopentetate dimeglumine (Gd-DTPA) as a contrast medium. Delineation of normal articular cartilage and cartilage defects was less accurate after intra-articular administration of Gd-DTPA. Therefore, it was concluded that MR arthrography with Gd-DTPA is unrewarding for evaluation of osteochondrosis lesions.

A matched case-control study was conducted to evaluate dietary components and exercise patterns as potential risk factors for osteochondritis dissecans in dogs. A telephone interview, with a standard questionnaire and protocol, was used to collect data on dietary intake of calories and nutrients and on the usual amounts and types of exercise of each dog. Thirty-one dogs with osteochondritis dissecans and 60 controls were matched on the basis of breed, sex, and age. Using a conditional logistic regression model, high dietary calcium, playing with other dogs, and drinking well water (rather than city water) were associated with increased risk of osteochondritis dissecans. Feeding of specialty dry dog foods was associated with decreased risk.

Thirty-six of 50 young equids examined at necropsy for gross pathologic and histopathologic evidence of osteochondrosis were determined to have lesions characteristic of this disorder in the distal joints of the tarsus. Abnormalities ranged from retained endochondral cores underlying undisturbed articular cartilage surfaces to clefts, subchondral osseous cyst-like lesions, and cartilage ulceration. Our findings supported the conclusion that osteochondrosis may cause spavin in the juvenile equid.