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.