Cranial cruciate ligament (CrCL) rupture is the most common cause of hindlimb lameness in dogs. Treatment of CrCL injury is
an integral part of veterinary orthopedic practice, and represents a $1.23 billion/yr industry in the United States. With
training, diagnosis of CrCL rupture is often straightforward. However, the ideal treatment of CrCL injury is debated, and
no single procedure has emerged as clearly superior for returning dogs to normal function.
Anatomy and biomechanics
The stifle is stabilized by four primary ligaments: medial collateral, lateral collateral, cranial cruciate, and caudal cruciate.
The cranial cruciate ligament consists of two parts- the craniomedial band and the caudolateral part. Both parts originate
from the caudomedial aspect of the lateral femoral condyle, and course diagonally across the intercondyloid fossa to the cranial
intercondyloid area of the tibia, near the intermeniscal ligament. The craniomedial band is taut during all phases of the
gait, while the caudolateral part is taut only in extension of the stifle. The caudal cruciate ligament originates on the
lateral surface of the medial femoral condyle and runs caudodistally to the lateral edge of the popliteal notch of the tibia.
The function of the cranial cruciate ligament in stabilizing the stifle is threefold. It prevents cranial translocation of
the tibia relative to the femur (also known as cranial drawer or cranial tibial thrust), limits internal rotation of the tibia,
and prevents hyperextension of the stifle. Prevention of cranial tibial thrust is thought to be the most significant function
of the CrCL, The caudal slope of the tibial plateau relative to its long axis causes the CrCL to be under strain during normal
weightbearing. The absence of a CrCL results in cranial tibial thrust during the stance phase of the gait. Neutralization
of cranial tibial thrust (or cranial drawer) is the primary goal of most surgical techniques.
Additional support to the stifle joint is provided by the medial and lateral menisci.The menisci are semilunar fibrocartilagenous
discs that function in a hoop-stress mechanism to distribute force in the stifle joint. Cranially, the medial and lateral
menisci are both anchored to the tibial plateau. Caudally, the lateral meniscus is attached to the caudal intercondylar fossa
of the femur. In contrast, the medial meniscus is attached to the tibial plateau, just cranial to the tibial attachment of
the caudal cruciate ligament. Understanding this difference is critical to understanding the etiology of meniscal tears associated
with CrCL injury (see below).
Etiology and pathophysiology
Dogs with CrCL injury may present with acute onset lameness, however the injury is rarely of purely traumatic etiology. In
most cases, the damage to the ligament appears to be chronic, and the damaged ligament frequently exhibits lymphoplasmacytic
inflammation on biopsy. The injury is probably multifactorial, with causes including conformation, obesity, inactivity, aging,
hormone imbalance, and repetitive trauma. A ligament that has been weakened by these insults may then proceed to rupture from
normal or near-normal loads. Partial rupture is not uncommon, and in some cases a complete tear of only one portion (craniomedial
or caudolateral) of the ligament may occur. Due to the degenerative nature of most CrCL ruptures, a significant proportion
of dogs (20-40%) will proceed to injure the contralateral CrCL at some point during their life.
Pain and lameness with CrCL injury initially is due to instability of the stifle joint and stretching of the joint capsule.
With time, this initiates a cascade of events, including synovitis, hyaline cartilage degradation, degenerative joint disease
and periarticular fibrosis. In addition, tethering of the caudal pole of the medial meniscus to the tibia may cause this structure
to become crushed under the medial femoral condyle, as it is drawn forward during cranial tibial thrust.
Presentation and signalment
Cranial cruciate ligament rupture most commonly affects young to middle aged, large breed dogs. However, any breed dog may
be affected, and CrCL injury should be suspected and ruled out in any case of hindlimb lameness. Affected dogs may have a
variety of presentations, probably due to the multifactorial nature of the disease. They may be non-weightbearing, partially-weightbearing,
or occasionally non-ambulatory.
Probably the most common presentation is a dog that has a history of acute onset hindlimb lamenes with improvement, then recent
worsening of the lameness. These dogs may have had a partial tear that improved with rest, and then went on to rupture completely.
In contrast, some animals will present with a chronic progressive lameness, with no inciting event. These dogs often are progressing
due to worsening of osteoarthritis. They may also become acutely worse due to subsequent meniscal tear. Both of these presentations
typically exhibit positive cranial drawer and varying amounts of osteoarthritis and joint effusion on radiographs.