370 Canine Sports Medicine and Rehabilitation
limit hyperextension, cranial tibial translation,
and internal rotation (Arnoczky & Marshall,
1977). The caudal cruciate is the primary restraint
against caudal tibial translation and also helps
limit internal rotation of the tibia (Arnoczky &
Marshall, 1977; Heffron & Campbell, 1978;
Kowaleski et al., 2012). The medial and lateral
collateral ligaments serve to limit internal and
external rotation.
The menisci are crescent‐shaped, cartilagi
nous tissues that partially divide the articular
surfaces of the joint (Figure 14.21). Menisci dis
tribute load during weight bearing and provide
structural integrity to the stifle as it undergoes
tension and torsion. The menisci also play an
important role in joint nutrition and lubrica
tion. Both menisci are anchored to the tibial
plateau. The medial meniscus has a firm attach
ment to the tibia and medial collateral ligament,
while the lateral meniscus has a loose attach
ment to the tibia and an additional attachment
to the femur. As a result, the medial meniscus
is more vulnerable to injury with cruciate
deficiency as it becomes trapped between the
condyle and plateau during subluxation.
Kinematics of the cranial cruciate‐
deficient stifle
While standing, the canine stifle is flexed, result
ing in continuous loading of the CCL. This load
varies depending on activity level and contrac
tion of various muscle groups. The sloping
articular surface of the tibia is called the tibial
plateau angle (TPA). TPA reference ranges
have been documented in four common canine
breeds, although this slope can vary signifi
cantly between individual patients (Guastella
et al., 2008). When the canine stifle is weight
bearing, the tibia is displaced forward, as the
femur slides down the slope of the tibia. The
steeper the angle present, the more significant
the resultant force acting upon the CCL.
Pathophysiology
Traumatic rupture of a healthy CCL is typically
caused by hyperextension and excessive inter
nal rotation. More often, CCL injuries occur
when normal force is exerted on an abnormal
or degenerative joint. Proposed underlying eti
ologies include biological and biomechanical
factors. Biological factors include development,
genetics, metabolic function, hormonal influ
ences, infection, immune‐mediated processes,
and appropriate cellular production and turnover.
Biomechanical components include muscular
function and forces, alignment, conformation,
movement, and joint contacts and pressures
(Morgan et al., 2010; Reif et al., 2002). Because
cranial cruciate disease is generally degenera
tive, a patient with a ruptured CCL in has a
(A) (B)
Meniscus - normal lateral
Meniscus - medial
Figure 14.21 (A) Normal lateral meniscus; note attachment to the tibia and femur. (B) Normal medial meniscus.
The curled edge is referred to as the “flounce sign” and is highly correlated with a normal meniscus.