Ronald D. Montgomery

The Reharvested Central Third of the Patellar Tendon: A Histologic and Biomechanical Analysis

We assessed the histologic, mechanical, and structural properties of the reharvested central-third patellar ten don in greyhounds. Twelve dogs had the central third of the patellar tendon (5 mm) removed with corre sponding bone blocks from the patella and tibia; the remaining tendon defect was loosely closed. Six dogs were sacrificed at 6 months and six at 12 months, and the central third of the patellar tendon was harvested from both the operative and the contralateral control knees. Analysis of the structural changes in the ten dons revealed a significant increase in thickness for reharvested tendons at both 6 and 12 months when compared with controls. The entire residual tendons were narrower at 6 months and were shorter at 12 months compared with controls. Mechanical testing showed that the average failure load, ultimate tensile strength, strain at failure, and average modulus for the reharvested central third of the patellar tendon were significantly less than that of controls at both 6 and 12 months. Analysis of collagen fiber size by electron microscopy revealed a significant increase in collagen fiber diameter at 6 months (135 ± 41 nm versus 49 ± 4 nm) but no difference between the operative limbs and controls at 12 months. The reharvested bone- patellar tendon-bone complex does not have the same properties as the primary patellar tendon graft up to 1 year after harvest in a canine model, and its use for revision cruciate ligament reconstruction must be care fully reexamined.

The Effects of Aggressive Notchplasty on the Normal Knee in Dogs

We assessed the possible association between an aggressive intercondylar notchplasty and histopathologic, radiographic, and gait changes to the knee. Three groups of six adult greyhounds were observed for 6 months. Group I dogs had a sham operation. Group II dogs had a 4-mm notchplasty of the lateral femoral condyle where it articulates with the lateral tibial spine. Group III dogs had a 7- to 8-mm notchplasty of the lateral femoral condyle to simulate the long-term effects of an overly aggressive notchplasty. Force plate gait analyses were not significantly different for any dogs at 3 and 6 months. Histopathologic studies (hematoxylin and eosin and safranin O stains) revealed notchplasty area remodeling with a thin layer of lamellar bone covered by fibrous connective tissue. Both Group II and III dogs had significant loss of lateral femoral condyle and trochlear groove articular surface proteoglycans. The radiographic notch width index remained unchanged throughout the study for Group I; the indexes increased immediately after surgery in Groups II and III because of the notchplasty, but after 6 months these values returned to near-preoperative measurements. An aggressive intercondylar notchplasty caused articular cartilage histopathologic changes at 6 months consistent with those found in knees with early degenerative arthritis. Significant refilling of a non-impinged notchplasty occurred by 6 months after surgery. Our results raise concern about the effects of aggressive intercondylar notch widening in humans.

Total Hip Arthroplasty for Treatment of Canine Hip Dysplasia

Cemented THA is an established procedure for treating arthropathies of the hip in large, healthy mature dogs. CHD with secondary osteoarthritis is the most common indication. Although comparative studies between THA and excision arthroplasty have not been reported, our experience with both procedures and studies in the literature support THA as the best available treatment for crippling degenerative joint disease secondary to CHD in large, mature dogs. Negative aspects of the procedure include high cost, the potential of significant complications, and the sophisticated surgical technique required. Improvements in patient selection, design of implants, surgical technique, and postoperative care have decreased the incidence of complications and improved the success rate to over 90%. However, concerns in human applications about cement disease and the desire to increase the functional life of the prosthesis have renewed interest in cementless systems. Advantages of cementless THA are fixation via bony ingrowth and avoidance of problems associated with PMMA. Important technical aspects of cementless THA relate to optimal fit and fill so that the prosthesis is stable, bone ingrowth is promoted, and weight-bearing forces are transferred to the proximal femur physiologically. Problems recognized with cementless systems include fissure fracture, bone resorption, and excessive motion between the implant and bone. Currently, investigations are being conducted to develop prosthetic materials that more closely match the stiffness of bone, stem designs that provide optimal fit and maintain normal strain patterns in the bone, and coating materials that promote permanent fixation by bone ingrowth. Early clinical results in humans and research results in dogs have been encouraging but have not withstood the test of time. Results of cementless techniques must be compared to the standards set by cemented THA over the last 20 years in humans and the last 10 years in dogs.

Mucopolysaccharidosis-like phenotype in feline Sandhoff disease and partial correction after AAV gene therapy

Sandhoff disease (SD) is a fatal neurodegenerative disease caused by a mutation in the enzyme β-N-acetylhexosaminidase. Children with infantile onset SD develop seizures, loss of motor tone and swallowing problems, eventually reaching a vegetative state with death typically by 4years of age. Other symptoms include vertebral gibbus and cardiac abnormalities strikingly similar to those of the mucopolysaccharidoses. Isolated fibroblasts from SD patients have impaired catabolism of glycosaminoglycans (GAGs). To evaluate mucopolysaccharidosis-like features of the feline SD model, we utilized radiography, MRI, echocardiography, histopathology and GAG quantification of both central nervous system and peripheral tissues/fluids. The feline SD model exhibits cardiac valvular and structural abnormalities, skeletal changes and spinal cord compression that are consistent with accumulation of GAGs, but are much less prominent than the severe neurologic disease that defines the humane endpoint (4.5±0.5months). Sixteen weeks after intracranial AAV gene therapy, GAG storage was cleared in the SD cat cerebral cortex and liver, but not in the heart, lung, skeletal muscle, kidney, spleen, pancreas, small intestine, skin, or urine. GAG storage worsens with time and therefore may become a significant source of pathology in humans whose lives are substantially lengthened by gene therapy or other novel treatments for the primary, neurologic disease.