What's new in orthopedics? Part 2

The first World Veterinary Orthopedic Congress (WVOC), continued a recent trend in orthopedic circles of increased focus on the canine shoulder joint. Historically, most orthopedic texts have had a relatively short discussion of shoulder pathology. Few causes of forelimb lameness originating in the shoulder were recognized beyond luxations, osteochondritis dessicans, and, occasionally, ossification of the tendon of the biceps brachii muscle. The limiting factor was the state of diagnostic imaging techniques; what couldn't be palpated or seen on plain radiographs didn't exist! The advent of arthroscopy literally opened the doors to the recognition of a wide range of shoulder pathology.

Traditionally, where the tendon of the biceps brachii muscle was concerned, functional pathology was characterized by lameness and pain on hyperextension of the shoulder joint and on deep palpation of the bicipital groove, with the diagnosis being confirmed by radiographic detection of osteophytes or calcification in the area of the tendon of origin of the muscle. In terms of frequency of occurrence, pathology involving the tendon of the biceps brachii muscle follows only chronic luxation and osteochondritis dessicans as shoulder-related causes of forelimb lameness. Arthroscopy shows that changes in the tendon can cover a wide range of lesions from mild synovitis, to partial tears, to complete avulsions, and that only about one-third of cases have radiographically detectable calcification (1).

Traditional surgical management of chronic tenosynovitis of the biceps brachii muscle has involved transection of the tendon from its origin on the supraglenoid tubercle of the scapula and reattachment to the proximal extremity of the humerus with a screw and spiked washer. Information presented at the WVOC and at the 2001 Veterinary Orthopedic Society meeting suggested that transection of the tendon via arthroscopy, without reattachment, is sufficient to relieve symptoms and return the animal to normal function (2,3). Indeed, the suggestion is that, in some clinical cases, spontaneous rupture of the tendon may occur, resulting in resolution of the problem.

Arthroscopy has also assisted in identifying causes of forelimb lameness in most of the supporting structures of the shoulder, most commonly the medial glenohumeral ligament and the tendons of insertion of the supraspinatus, infraspinatus, and subscapularis muscles. Clinical evaluation of the integrity of these structures in the absence of arthroscopy may require sedation or general anesthesia. Maximal abduction of the forelimb at the shoulder joint and a “cranial drawer test,” as one would use in the stifle, gives the clinician a good appraisal of shoulder stability. Comparison with the contralateral joint gives an instant frame of reference (4,5,6). Most instabilities are chronic and will respond poorly to conservative management.

A few odds and ends from the WVOC are as follows: Saltar-Harris type IV fractures of the lateral humeral condyle, commonly seen in puppies, have a good prognosis for continued bone growth after surgical repair. In fact, there appears to be a statistically significant “overgrowth” of the affected humerus (1 to 6 mm), as compared with the contralateral humerus (bone overgrowth after femoral fracture is a well-recognized phenomenon in children). The increased humeral length did not affect gait or function, and occurred regardless of whether or not orthopedic implants crossed the distal humeral growth plate (7).

Administration of ketoprofen, 0.25 mg/kg bodyweight (BW), PO, q24h, provided significant relief of arthritic pain in 8 Labrador retrievers, as measured by force plate analysis (8). This dose represents 25% of the manufacturer's suggested dosage level. No additional increase in weight-bearing, as measured by the force plate, was observed when the dose was increased to 0.5 mg/kg BW or 0.75 mg/kg BW. No side effects were noted over the 30 days' duration of the study.

Arachidonic acid, an omega-6 polyunsaturated fatty acid (PUFA), is the predominant PUFA incorporated into cell membranes. In the face of active inflammation, it acts as a substrate in the production of cytokines and other inflammatory mediators. Competitive inhibition by omega-3 PUFAs in this process results in the production of different, generally less inflammatory, substances, and it has been postulated that the dietary supplementation of omega-3 PUFAs may thus have a beneficial effect in the decrease of inflammatory mediators in osteoarthritis. Investigators at the University of Georgia were able to show that omega-3 dietary supplementation for 3 mo before transection of the cranial cruciate ligament and subsequent stabilization of the joint decreased clinical and radiographic evidence of osteoarthritis, as compared with controls (9). The implications here are fascinating: if you own a breed predisposed to rupture of the cruciate ligament, hip dysplasia, or elbow dysplasia, should you supplement your dog's diet with omega-3 PUFAs? When should supplementation start? At what dose? Is there any benefit in such supplementation after the inflammation has occurred? Stay tuned!