Biomechanics of the Normal and Cranial Cruciate Ligament-Deficient Stifle 41
activity (co-contraction). Co-contraction is con-
sidered an important mechanism in functional
adaptation in human patients with anterior cru-
ciate ligament rupture, but further research is
needed to understand its role in dogs.
The clinician needs to understand all the
motions in the stifle joint that are normally lim-
ited by the ligaments to perform and interpret
manual stress tests and correctly determine
the abnormality. The terminstabilityhas been
used to describe an abnormal motion that
exists in the joint due to a ligament injury.
The termlaxitysimply indicates increases in
motion or looseness, without providing any
direct indication of whether abnormal motion
occursin vivo. The goal of a comprehensive
stifle examination is to detect an increase in the
amount of motion (translation or rotation) or an
abnormal position (subluxation) to determine
the specific anatomic defect that is present.
The manual stress examinations are designed
to test only one or two motions at a time,
and therefore the diagnosis cannot be based
solely on the abnormal motion detected with
a single manual stress. The diagnosis requires
knowledge of stifle biomechanics, and which
ligaments limit each of the possible motions in
the stifle. Ultimately, the clinical examination
must be interpreted considering the stifle in
a six-degrees of freedom system, recognizing
that six possible motions may occur in three
dimensions.
Cranial cruciate ligament-deficient
stifle
The CrCL contributes to passive restraint of the
stifle by limiting cranial translation of the tibia
relative to the femur, excessive internal rota-
tion of the tibia, and hyperextension of the stifle
(Arnoczky & Marshall 1977).In vivokinematic
studies have demonstrated that most changes
after CrCL transection are noted in the stance
phase of the gait (Korvicket al. 1994; Tashman
et al. 2004). Approximately 10 mm of cranial tib-
ial translation is consistently observed and sus-
tained throughout stance. Femorotibial align-
ment is restored during the swing phase, and is,
therefore, largely unaffected by CrCLdeficiency
at a walk. The initial pattern of cranial transla-
tion progressively changes over time. Tashman
et al. (2004) demonstrated that by two years after
CrCL transection, the position of the tibia at the
terminal swing is shifted cranially by approx-
imately 5 mm (Figure 5.2). Thus, the decrease
in dynamic instability was considered to be an
indication of more persistent tibial subluxation
throughout the gait cycle, rather than a return
towards normal stifle kinematics (Tashmanet al.
2004). Thein vivoinvestigations by Tashman
et al. and Korvicket al. were performed in nor-
mal dogs with acute, experimental CrCL tran-
section. It is likely that stifles affected by nat-
urally occurring CrCL rupture in clinical dogs
10
15
20
25
30
-0.05 0 0.05 0.1 0.15 0.2
Cranial Translation (mm)
(A) Time (s) (B)
Pre-Treatment
2 Months
24 Months
10
15
20
25
30
-0.05 0 0.05 0.1 0.15 0.2
Cranial Translation (mm)
Time (s)
Pre-Treatment
2 Months
24 Months
Figure 5.2 Craniocaudal translation of the canine stifle during the stance phase of gait in cranial cruciate ligament
(CrCL) intact (A) and CrCL-deficient (B) dogs. Data represent baseline before CrCL transection or sham CrCL-transection,
2 months after surgery, and 24 months after surgery. Note that there are obvious changes in tibial translation after CrCL
transection, whereas there is relatively little laxity in the intact CrCL during locomotion. Over time, cranial translation of
the tibia becomes incrementally worse, suggesting that periarticular fibrosis does not provide much dynamic stability to
the CrCL-deficient stifle. Source: Tashmanet al. 2004. Reproduced with permission from John Wiley & Sons, Inc.