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in Journal of the American Veterinary Medical Association


In collaboration with the American College of Veterinary Radiology

Open access
in Journal of the American Veterinary Medical Association



A 7.5-year-old 37.8-kg (83.2-lb) sexually intact male German Shepherd Dog (dog 1) and a 2.6-year-old 28.2-kg (62.0-lb) sexually intact male Dutch Shepherd (dog 2), both apprehension police dogs, were admitted for evaluation of left and right thoracic limb lameness, respectively.


In both dogs, signs of pain were elicited on palpation of the shoulder joint in the affected limb, and a distinct popping of the biceps brachii tendon (BT) was palpable on the craniomedial aspect of the affected joint on flexion and extension and was associated with moderate signs of pain. Biceps brachii tendon luxation (BTL) was diagnosed with dynamic musculoskeletal ultrasonography (both dogs) and MRI (dog 1).


Arthroscopic BT release by tenotomy was performed in both dogs. Lameness appeared to have resolved by 8 weeks after surgery and had not recurred by the last follow-up communications at 36 and 9 months after surgery for dogs 1 and 2, respectively. Both dogs successfully returned to their level of work performed before their injury.


Our findings for the dogs of the present report suggested that arthroscopic BT release could be considered a viable treatment option for BTL in dogs, including police dogs or other high-performance athletic dogs. Although our findings provided encouraging results, further research, best conducted with a multicenter prospective randomized study, would be needed to establish the most reliable treatment of BTL in high-performance athletic or working dogs.

Full access
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association


Objective—To determine whether oxidative stress could be induced in canine chondrocytes in vitro.

Sample—Chondrocytes obtained from healthy adult mixed-breed dogs.

Procedures—Harvested chondrocytes were maintained at 37°C with 5% CO2 for 24 hours. To assess induction of oxidative stress, 2 stimuli were used: hydrogen peroxide and a combination of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). To determine the effect of hydrogen peroxide, a set of chondrocyte-seeded plates was incubated with control medium alone or hydrogen peroxide (100, 200, or 300μM) for 24 hours. For inhibition of oxidative stress, cells were incubated for 24 hours with N-acetylcysteine (NAC; 10mM) before exposure to hydrogen peroxide. Another set of chondrocyte-seeded plates was incubated with control medium alone or with IL-1β (10 ng/mL) and TNF-α (1 ng/mL) for 24 hours. Supernatants were obtained for measurement of prostaglandin E2 production, and cell lysates were used for measurement of superoxide dismutase (SOD) activity and reduced-glutathione (GSH) concentration.

Results—Chondrocytes responded to the oxidative stressor hydrogen peroxide with a decrease in SOD activity and GSH concentration. Exposure to the antioxidant NAC caused an increase in SOD activity in hydrogen peroxide–stressed chondrocytes to a degree comparable with that in chondrocytes not exposed to hydrogen peroxide. Similarly, NAC exposure induced significant increases in GSH concentration. Activation with IL-1β and TNF-α also led to a decrease in SOD activity and increase in prostaglandin E2 production.

Conclusions and Clinical Relevance—Canine chondrocytes responded to the oxidative stress caused by exposure to hydrogen peroxide and cytokines. Exposure to oxidative stress inducers could result in perturbation of chondrocyte and cartilage homeostasis and could contribute to the pathophysiology of osteoarthritis. Use of antioxidants, on the other hand, may be helpful in the treatment of arthritic dogs.

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in American Journal of Veterinary Research