Cranial cruciate ligament disease in the dog (Proceedings) - Veterinary Healthcare
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Cranial cruciate ligament disease in the dog (Proceedings)


CVC IN SAN DIEGO PROCEEDINGS


The most common cause of lameness on dogs in North America is partial or complete rupture of the CrCL. The annual economic impact of cranial cruciate ligament disease in dogs in the United States was estimated to be 1.2 billion dollars in 2003. Many surgical treatments have sought to restore stifle joint stability and minimize osteoarthritis through various techniques of replacing the ruptured ligament either inside the joint, or outside in an extracapsular method. The CrCL is composed of a craniomedial band (CrMB) and a larger caudolateral band (CLB). The CrMB is taut in flexion and extension, the CLB is taut in extension but lax in flexion. The CrCL functions to minimize internal rotation and hypertension of the stifle joint and prevent cranial translation of the tibial plateau relative to the femoral condyles.. Full extension of the stifle is limited by contact between the CrCL and the cranial intercondylar notch of the femur. Mechanisms of traumatic rupture of a normal CrCL include: internal rotation of the stifle in 20-50 degrees of flexion or forceful hyperextension. Tearing of the CLB alone (most likely from hyperextension) will not produce instability because the intact CMB is taut in both flexion and extension; no drawer motion will be present. Injuries caused by rotation or twisting are more likely to injure the CrMB, producing a small amount of drawer motion in flexion, but none in extension. Rupture occurs when the ultimate breaking strength of the ligament is exceeded which is estimated to be 4x the body weight of the dog.

There is no single cause of CrCL rupture in dogs. Acute trauma to a normal CrCL, which is the primary etiology of CrCL rupture in people, is a less common cause in dogs. Other factors that contribute to the degeneration and eventual rupture of the CrCL include anatomical factors, such as extreme tibial plateau angles (>35), narrowing of the intercondylar notch, and an extended standing angle of the stifle joint; hormonal influences, shown to be important in athletic girls; immune mediated disease processes, such as the production of anti-collagen antibodies or deposition of immune complexes; and heredity in that some breeds appear to be predispose dogs to CrCL rupture. The genetic basis for hereditability of a predisposition for CrCL rupture has been shown in Newfoundlands. They have an autosomal recessive mode of inheritance with a recessive allele frequency of 0.65 and partial penetrance (59%). There may be certain phenotypic expressions that predispose dogs to developing CrCL rupture. Hyperextension of the stifle joint increases the standing TPA, which places increased stress on the CrCL. In addition, the stifle joint shifts medial to the longitudinal axis of vertical load in dogs with a "cow-hocked" stance, which also places greater stress on the CrCL.

The pathogenesis of CrCL rupture involves the ligamentous changes that occur with disuse, and progressing age that weaken the integrity of the structure. The degenerative changes progress as the animal ages, but may be less severe in animals less than 15 kilograms in body weight. Degenerative changes associated with aging may account for 20-40% of dogs that eventually develop bilateral CrCL rupture. It has been postulated that the sedentary lifestyle of the typical middle-aged dog, compounded by obesity, may lead to diminished mechanical strength of the CrCL.

CrCL rupture has been identified in all breeds of dogs, but with a higher incidence in obese dogs. Rottweilers, Labrador retrievers, Newfoundlands, bull mastiffs, and chow chows appear to be at particular risk. Recent studies indicate that younger, larger, more active dogs may be predisposed to CrCL rupture. There is not a sex predilection for CrCL rupture, but there may be a slightly higher incidence in female spayed dogs. Although the strength of a dog's CrCL deteriorates with age, loss of fiber bundle organization and metaplastic changes of cellular elements in the CrCL may be pronounced at a young age in certain large-breed dogs.

Patients may present for acute CrCL injury, in which there may be subtle to non-weight bearing lameness of unknown origin. The lameness often improves somewhat within weeks, but then plateaus especially in dogs over 15 kg. These larger dogs may never return to pre-injury levels of activity and develop a second, acute lameness after meniscal injury. The lameness often resolves completely within 1-5 months in dogs less than 15 kg, although these dogs may also develop meniscal damage later. Chronic, mild lameness is associated with the development of degenerative joint disease. The acute lameness improves as any hemarthrosis resolves and fibrous proliferation of the periarticular tissue stabilizes the joint, there is an acute exacerbation of lameness as a result of a meniscal tear or progression of degenerative joint disease. Partial CrCL tears may be difficult to diagnose and present as a mild weight-bearing lameness associated with exercise that resolves with rest until degenerative joint disease sets in. As the ligament continues to tear, the joint becomes less stable and degenerative changes exacerbate the lameness until it no longer resolves with rest.


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Source: CVC IN SAN DIEGO PROCEEDINGS,
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