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  • Author or Editor: R. J. Todhunter x
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Objective—

To determine whether the composition of cartilage from the shoulder joints of dogs varied with the risk of developing canine hip dysplasia (CHD).

Design—

Observational study.

Animals—

12 skeletally mature (approx 1 year old) Labrador Retrievers.

Procedure—

Dogs were classified as having a low, moderate, or high risk of developing CHD on the basis of distraction indices. Cartilage was harvested from the craniolateral and weight-bearing regions of the humeral heads, and wet weight per unit area and dry, glycosaminoglycan, and fibronectin contents were determined.

Results—

Glycosaminoglycan and dry contents did not vary among risk groups. For cartilage from the craniolateral region of the humeral head, wet weight per unit area and fibronectin content increased as risk of developing CHD increased. Wet weight and fibronectin content of cartilage from the weight-bearing region of the humeral head did not vary among risk groups.

Clinical Implications—

Dogs that have a high risk of developing CHD are also more likely to develop osteoarthritis of the shoulder joint. The observed increases in wet weight per unit area and fibronectin content in cartilage from the craniolateral region of the humeral head in dogs at a high risk of developing CHD may be early signs of incipient osteoarthritis. (J Am Vet Med Assoc 1997;210: 1483-1485)

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objectives

To use lipopolysaccharide (LPS) to create synovitis in the midcarpal joint of ponies, and to assess the morphologic, histochemical, and immunohistochemical effects of synovitis on articular cartilage of the third carpal bone.

Animals

2- to 3-year-old ponies, 6 control (group 1) and 6 treated (group 2).

Procedure

Synovitis was induced in 1 midcarpal joint of group-2 ponies by intra-articular injections of LPS (0.02 μg/kg of body weight), morphine (0.1 mg/kg), and saline solution (group 2a) and morphine and saline solution alone in the contralateral midcarpal joint (group 2b). Articular cartilage sections and attached synovial membrane from the third carpal bones were examined by immunohistochemical distribution of interleukin 1β, tumor necrosis factor (TNF)-α, TNF receptors (P55, P75) and 3-B-3(–) epitopes, and by localization of proteoglycans (metachromatic staining). Proteoglycan extracts were assessed by metachromatic staining or western blotting and immunohistochemical staining, using anti-3-B-3 antibodies.

Results

Enhanced immunoreactivity for the cytokines and receptors was found in inflamed synovial membrane and noncalcified cartilage (group 2a more than 2b). Metachromasia of the noncalcified cartilage was greater in group-1 than in group-2a and group-2b specimens. In group 2a, chondrocyte hypertrophy and enhanced immunoreactivity for 3-B-3(–) epitope in areas of increased cytokine immunoreactivity suggested possible phenotypic change of the chondrocytes in response to synovitis. Immunohistochemical analysis by western blotting of proteoglycan extracts indicated strong 3-B-3(–) epitope immunolocalization in group-2a, weaker staining in group-2b, and barely detectable stain in group-1 specimens, which correlated with in situ immunolocalization.

Conclusions

Intra-articular administration of LPS may be used to induce a synovial environment conducive to increased immunoreactivity of interleukin 1β, TNF-α, and its receptors in equine synovial membrane and articular cartilage. These cytokines may be involved in the early phenotypic change of chondrocytes that is believed to occur in osteoarthritis and is characterized in this study by enhanced 3-B-3(–) epitope immunoreactivity and chondrocyte hypertrophy. (Am J Vet Res 1996;57:1080–1093)

Free access
in American Journal of Veterinary Research

Summary

Intra-articularly administered, long-acting corticosteroids are a beneficial treatment for many equine joint disorders because they alleviate inflammation and signs of pain, but they also exert detrimental effects on the biochemical composition and morphologic features of articular cartilage. Chondroprotective drugs have been shown to mitigate some of the deleterious effects of intra-articularly administered corticosteroids on articular cartilage of laboratory animals. Twenty-one ponies were assigned at random to receive 1 of 3 treatments in the right middle carpal joint. Group-1 ponies (n = 8) had methylprednisolone acetate (mpa; 0.2 mg/kg of body weight) and saline solution administered intra-articularly and im, respectively. Group-2 ponies (n = 9) received mpa (0.2 mg/kg) and polysulfated glycosaminoglycan (gag; 2 mg/kg). Group-3 ponies (control; n = 4) had saline solution administered intra-articularly and im. The corticosteroid or saline solution was injected into the right middle carpal joint on day 1. The im administered polysulfated gag or saline solution was administered at the same time, then was repeated every 3 days for 20 days. Ponies were euthanatized 21 days after initial injection by overdose of pentobarbital sodium.

The cartilage of younger ponies was significantly (P < 0.05) more responsive to the proteoglycan-depleting effects of mpa. Ponies < 10 years old of groups 1 and 2 had significantly (P < 0.05) lower gag content in the articular cartilage than did control ponies. Systemic treatment with polysulfated gag did not result in a protective effect against proteoglycan loss from the articular cartilage. Twenty-one days after mpa injection, difference in [35S]sulfate incorporation into proteoglycan, between either mpa-treated group and the control group, was not significant. There was an approximate tenfold increase in keratan sulfate concentration in synovial fluid from mpa-treated joints, compared with control joints. Chondroprotective effect of polysulfated gag on the basis of keratan sulfate release from the articular cartilage into the synovial fluid was not observed. Methylprednisolone acetate caused a decrease in the fibronectin content of articular cartilage, but there was no effect of polysulfated gag on the fibronectin content of mpa-treated articular cartilage.

Free access
in American Journal of Veterinary Research

Objective—

To determine whether onset of mineralization of the femoral and proximal tibial epiphyses and age at closure of the femoral and acetabular triradiate growth plates was different for Labrador Retrievers that were radiographically normal or that had canine hip dysplasia (CHD).

Design—

Cohort study.

Animals—

36 Labrador Retriever puppies.

Procedure—

Puppies were radiographed every other day from the time they were 8 to 10 days old until ossification of the femoral heads was apparent. Radiographs were then obtained weekly until puppies were 1 month old and then monthly until puppies were 8 to 12 months old. Age at which mineralization was first observed in the proximal and distal femoral and proximal tibial epiphyses and at which the femoral capital, triradiate acetabular, and distal femoral growth plates were no longer radiographically visible were recorded. Fifteen dogs were euthanatized and necropsied to determine whether dogs had CHD.

Results—

There were 26 radiographically normal left and right hip joints and 10 dysplastic left and right hip joints. Onset of mineralization of the proximal femoral epiphyses and of the right proximal tibial epiphysis was significantly later in dysplastic than in radiographically normal puppies. The left femoral capital growth plates closed significantly later in dysplastic than in radiographically normal joints, but other differences in growth plate closure were not detected.

Clinical Implications—

Endochondral ossification may be abnormal in dogs with CHD. The disease appears to affect multiple joints, even though it is most evident clinically in the hip joint. (J Am Vet Med Assoc 1997;210: 1458–1462)

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

We investigated whether stromelysin activity in the medium of canine articular cartilage explants is associated with proteoglycan degradation in these explants. Cartilage explants were treated with recombinant human interleukin 1α (rh-il-lα), lipopolysaccharide, or canine monocyte-conditioned medium. Proteoglycan synthesis and degradation were measured. Metalloproteinase activity (inhibitable by tissue inhibitor of metalloproteinase 2) in the culture medium was measured by use of fluorimetry with a quenched fluorescent substrate. Western blots of the medium were probed with polyclonal antibodies to human stromelysin, collagenase, and gelatinase.

Neither metalloproteinase activity nor proteoglycan degradation were inducible in canine cartilage explants treated with rh-ll-1α. However, proteoglycan synthesis was significantly (P < 0.05) decreased by concentrations of 10 and 100 ng of rh-il-1α/ml. Metalloproteinase activity in the medium accompanied proteoglycan degradation of cartilage treated with lipopolysaccharide and monocyte-conditioned medium. The metalloproteinase released into the medium was identified as prostromelysin by results of western blotting.

Free access
in American Journal of Veterinary Research

Summary

Nine dairy herds (mean size, 149 cows) with bulk-tank milk somatic cell counts of < 300,000 cells/ml and > 80% of cows with Dairy Herd Improvement Association linear somatic cell counts ≤ 4 were selected for study. Each herd was monitored for 12 consecutive months. Duplicate quarter-milk specimens were collected from each cow for bacteriologic culturing at beginning of lactation, cessation of lactation, and at the time of each clinical episode of mastitis. Streptococcus agalactiae was never isolated and Staphylococcus aureus was isolated from < 1% of all quarters. There were 554 episodes of clinical mastitis. During the year of study, the incidence rate of clinical mastitis varied from 15.6 to 63.7% of cows among the 9 herds. Mean costs per cow per year in herd for mastitis prevention were: $10 for paper towels, $3 for nonlactating cow treatment, and $10 for teat disinfectants. Mean cost associated with clinical mastitis was $107/episode. Approximately 84% ($90) of the costs attributed to a clinical episode were associated with decreased milk production and nonsalable milk. Costs of medication and professional veterinary fees per clinical episode varied Significantly among the 9 herds. Three of the herds did not have a veterinarian treat a clinical episode of mastitis during the year of study even though 2 of these herds had the first and third highest incidence rates of clinical mastitis. When calculated on a per cow in herd basis, mean costs of $40/cow/year were attributed to clinical mastitis. Our findings suggest that herds that have effectively controlled mastitis caused by contagious pathogens may still have substantial economic losses as a result of clinical mastitis and that losses and even rates of clinical mastitis may vary considerably among such herds.

Free access
in Journal of the American Veterinary Medical Association