Hypothesis 1: Trauma-induced cranial cruciate ligament tear

Injuries to the cranial cruciate ligament are one of the most commonly encountered abnormalities 
in the canine stifle. The constant mechanical stress imposed on the ligament predisposes it to 
injury. The acute onset of the lameness (within 1 week) and history of a very active lifestyle lead 
to exercise-induced trauma as the likely cause of disease. A six year-old dog may have age 
related factors that predispose the animal to an injury of this type, including changes in collagen 
with loss of strength and stiffness. In addition, this animal is markedly overweight, which also 
contributes to the likelihood of injury.  

The cranial cruciate ligament is comprised of craniomedial and caudolateral bands, which have 
different insertion points on the tibial plateau. The ligament serves several functions: limiting 
cranial translation of the tibia relative to the femur, limiting internal rotation of the tibia, and 
preventing hyperextension of the stifle joint. There are two mechanisms that explain an injury to 
the CCL and the accompanying loss of the preceding functions. Ligament injury is most 
commonly associated with violent internal rotation of the leg. When this occurs, the cranial and 
caudal cruciate ligaments tightly wind around themselves. As internal rotation progresses, the 
cranial cruciate ligament is vulnerable to injury from the caudomedial edge of the lateral femoral 
condyle as the condyle rotates against the ligament A second theory behind CCL tear involves 
hyperextension of the stifle. Hyperextension occurs when a running animal abruptly fixes the 
tibia (i.e. steps into a hole) while the rest of the animal continues forward. In a hyperextended 
state, the roof of the intercondylar notch (of the femur) may act as a knife and transect the 
ligament. 

The resultant trauma and instability induces an inflammatory response, including the release of 
cytokines from the chondrocytes, leading to destruction of the proteoglycan and collagen network 
of the articular cartilage by metalloproteinases. Exposed collagen from the torn ligament also 
elicits an autoimmune response, which increases the intra-articular inflammation. The effusion 
detected in the stifle joint on physical exam is due to intra-articular hemorrhage (ligament tear) as 
well as inflammatory vasodilation and neutrophil migration to the site of injury. The swelling 
produces the distention of the joint capsule on either side of the patellar ligament present in this 
animal. This distention will limit joint laxity and stop the hemorrhage within the stifle. The 
release of inflammatory mediators, such as bradykinin, as well as distention of the fibrous joint 
capsule will activate nociceptors and induce pain in the dog.

The presence of a 4-5 mm cranial drawer sign while under sedation is diagnostic for cranial 
cruciate ligament rupture. The initial absence of a cranial drawer sign was likely due to patient 
apprehension and muscle contraction. In this case, a complete tear of the ligament, as opposed to 
a partial tear, is more likely to result in a positive cranial drawer test. A partial tear involving the 
caudolateral band alone will not produce instability because the intact craniomedial band is taut in 
both stifle flexion and extension; therefore no cranial drawer sign would be detected. If a partial 
tear involving the craniomedial band occurs, the joint would remain stable in extension, but 
would be lax in flexion as the caudolateral band is also lax during flexion of the joint. Only 
complete rupture involving both bands of the ligament would result in a cranial drawer sign 
apparent on both extension and flexion.

Concurrent injury to other structures within the stifle joint is possible, particularly meniscal tear, 
which can be a direct result of the instability produced by a CCL rupture. Fifty to sixty-percent of 
dogs with complete tear of the ligament also sustain injury to the medial meniscus. Patella 
luxation is unlikely based on the orthopedic exam, and a caudal cruciate ligament rupture would 
present normal at the walk, but lame after strenuous exercise and therefore is unlikely. The 
collateral ligaments as well as the straight patellar ligament were normal on orthopedic exam.