Diagnosing cranial cruciate ligament pathology - Veterinary Medicine
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Diagnosing cranial cruciate ligament pathology
Not all dogs with cranial cruciate ligament pathology have palpable stifle instability. Here are a few examination skills and diagnostic tools to help you make an early diagnosis.


The periphery of each meniscus is attached to the joint capsule. The attachment of the lateral meniscus differs from that of the medial meniscus in three distinct ways: 1) the caudal margin of the lateral meniscus is less firmly attached to the joint capsule; 2) the lateral meniscus is not attached to the lateral collateral ligament, but the medial meniscus is attached to the medial collateral ligament; and 3) the caudal margin of the lateral meniscus is also attached to the femur with the meniscofemoral ligament. Only the peripheral 10% to 25% of each meniscus is supplied by a vascular network and innervated. The axial majority of the menisci is avascular and aneural and is nourished by diffusion of synovial fluid.

The femoral condyle is shaped similar to a rounded-off L that produces motion like a cam would as the stifle is fully extended.6 This shape varies among breeds; for example, a Welsh corgi has a considerably different distal femoral conformation than a Shetland sheepdog has. The proximal tibia consists of an articular plateau and a tibial tubercle. The tibial plateau has a natural caudal and distal slope that also varies.6


During weightbearing in the hindlimbs, ground reaction forces are resisted by contracting the extensor, or antigravity, muscles (quadriceps and gastrocnemius muscles). These combined forces across the stifle compress the femur against the caudal- and distal-sloped proximal tibial plateau. The slope of the tibial plateau converts this femorotibial compression into a cranially directed shear force called cranial tibial thrust.6 This shear force does not normally induce cranial tibial translation in healthy canine stifles because it is constrained by the intact cranial cruciate ligament with probable contribution by the pull of the hamstring muscles on the proximal tibia. The magnitude of the cranial tibial thrust is a function of external ground reaction forces, internal muscular forces, and the slope of the tibial plateau. When cranial tibial thrust exceeds the tensile strength of a healthy cranial cruciate ligament or a weakened, degenerative cranial cruciate ligament, the ligament completely or partially ruptures.


Rupturing or stretching the cranial cruciate ligament permits cranial tibial translation (classically evaluated with the cranial drawer test) and excessive internal rotation.3 The pathogenesis of cranial cruciate ligament tearing is typically the result of a complex interplay of pathologic processes. Essentially, a healthy cranial cruciate ligament ruptures if the ligament's breaking strength is exceeded, usually in association with traumatic or athletic injury. Because the cranial cruciate ligament is the primary constraint against stifle extension and internal rotation, events causing excessive internal rotation and hyperextension are probable mechanisms for pure traumatic rupture.7 However, such cases represent a minority of patients with cranial cruciate ligament pathology. More commonly, cranial cruciate ligament pathology is related to degenerative changes within the ligament that occur with age and disuse.8,9

During aging, a dog loses fibroblasts, converts surviving fibroblasts into chondrocytes, and loses collagenous matrix within the cranial cruciate ligament.8 These aging changes develop at younger ages in larger breeds compared with smaller breeds. Ruptured cranial cruciate ligaments harvested from medium- and large-breed dogs within 24 hours of the acute onset of lameness showed degenerative changes and unsuccessful attempts at repair.8 These changes predispose the cranial cruciate ligament to tearing, and this mechanism is called cranial cruciate disease.10 Such pathophysiologic understanding explains the relatively high frequency of dogs with unilateral cranial cruciate ligament pathology that eventually develop similar changes in the contralateral stifle. Immune-mediated and septic arthritis of the stifle may also predispose the cranial cruciate ligament to rupture.

It is commonly theorized that abnormal biomechanics associated with medial patellar luxation, malaligned skeletal conformations, or both predispose a dog to cranial cruciate ligament rupture. While scientific evidence for a causal relationship is lacking, clinical observations suggest the conditions may be associated. When patellar luxation and cranial cruciate ligament rupture coexist, surgical correction of each problem is typically indicated. Regardless of the underlying mechanism of the cranial cruciate ligament pathology, unchecked instability induces synovitis, cartilage degeneration, periarticular osteophytosis, and meniscal injury. Interestingly, in an experimental setting, when the stifle was stabilized immediately after cranial cruciate ligament excision, no gross or radiographic evidence of degenerative joint disease was noted.11 This observation suggests that early diagnosis and treatment may benefit patients.


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