What’s new in orthopedics? Part 2

The 13th Annual Congress of the European Society of Veterinary Orthopedics and Traumatology, held September 7–10, 2006, in Munich, Germany, featured several presentations from the host country, including a cadaver study of extracapsular cranial cruciate ligament (CCL) repair in the dog. Researchers from the University of Leipzig formulated an in vitro study to examine the impact of passive cyclic stifle motion on extracapsular repairs. One of the frustrating, but inevitable, findings when rechecking stifles after extracapsular CCL repair is the return of some degree of drawer motion in the days and weeks after surgery. While this instability may not be associated with continued lameness, there are cases where repeat surgery is required. This study subjected stifles with transected CCLs that had been stabilized with an extracapsular repair to 50, 100, and 250 cycles of passive motion between 90 and 135 degrees, followed by a further 100 cycles of motion between 70 degrees and complete extension. A significant increase in drawer motion of 1.1 mm was noted after the 250 cycles of stifle motion (1). This increased by an additional 0.6 mm by the completion of the additional 100 cycles of more aggressive motion. The researchers characterized this experimental stifle motion, particularly the 45 degrees of passive motion used during the initial 250 cycles, as representative of restricted activity that a reasonable owner might permit the dog during the early postoperative period. They suggested that “conditioning” of the extracapsular repair with 250 cycles of passive stifle motion on the surgery table followed by retightening the implants might help reduce the amount of drawer motion that develops in the postoperative period (1).

Some dogs, particularly those of larger breeds, may have an accessory center of ossification at the caudal aspect of the glenoid cavity in the shoulder joint (2,3). Olivieri et al (2) describe the incomplete ossification of this area as infrequent, usually bilateral, and, often, an incidental finding, but a potential source of lameness in some dogs (2). Lameness may result from this loose fragment at the caudal extent of the scapulohumeral joint causing instability, inflammation, and synovitis (2,3). Ciliberto et al (4) attempted to determine the frequency of this finding and the age of radiographic ossification of the accessory caudal glenoid ossification center (ACGOC) in the rottweiler, one of the breeds most commonly affected by this condition. Forty-five dogs were radiographed beginning at an average age of just under 13 wk. Seven dogs (15.5%) had an ACGOC, and all had it bilaterally. In 6 of the cases, the ACGOCs were fused by 24 wk of age, as was the one in the right shoulder of the 7th dog. The ACGOC in the left shoulder was still unfused at 68 wk (4). It was concluded that about 15.5% of rottweilers have an ACGOC; the majority of which fuse by 24 wk of age. Centers that are found to be unfused after this age may represent an incidental finding, but they can be associated with chronic lameness. Arthroscopic removal of the ACGOC is the treatment of choice in such instances (3).

Palumbo et al (5) studied humeral condylar fractures and found that these fractures occurred in hunting dogs at nearly 3 times the rate in the rest of the canine population. This finding is not new, especially in spaniels, because of a genetic predisposition for poor vascular supply and incomplete ossification between the condyles (6). However, the biopsy and bone scan results from this study suggest that some of these fractures share common features with stress fractures. The investigators theorize that hunting dogs that are inactive, or confined for large portions of the year, and are then subjected to bursts of intense activity over uneven terrain may be prone to stress fracture and eventual complete fracture involving the humeral condyles (5).

With the advent of arthroscopic surgery, an increasing array of shoulder lesions have been recognized as causing clinical lameness. Medial shoulder instability, as differentiated from medial luxation, is one of these entities that can arise from disruption of the medial glenohumeral ligament or, less commonly, from disruption of the subscapularis tendon. Many treatments have been described for medial shoulder instability, including tendon translocaton techniques (7), ligament reconstruction (8), and thermal shrinkage of the joint capsule by arthroscopically guided radiofrequency (9). Tendon translocation has been shown to dramatically alter shoulder biomechanics (7), ligament reconstruction involves a complex surgical exposure and procedure (8), while questions have been raised about the long-term effectiveness and tissue damage associated with radiofrequency (10). A cadaver and clinical study of medial shoulder instability showed promising results from imbrication of the subscapularis tendon with 2 horizontal mattress sutures of polydiaxonone (11). The procedure was easy to perform and restored stability and good clinical function in 5 clinical cases. CVJ