Advances in the Canine Cranial Cruciate Ligament, 2nd edition

(Wang) #1

42 Structure and Function


may not exhibit the same magnitude of sublux-
ation, as periarticular fibrosis often exists at the
time of complete CrCL rupture (Hayashiet al.
2004).
The cranial tibial subluxation occurring dur-
ing the stance phase of gait may be driven by
the quadriceps contraction, among other fac-
tors (Korvicket al. 1994; Tashmanet al. 2004).
In the dog, the moment across the joint is
flexor from ground contact until mid-stance,
and then extensor until the end of the stance
phase (Colborneet al. 2005). Quadriceps con-
traction at extended joint angles produces CrCL
strain, but in the CrCL-deficient stifle in flexion,
quadriceps contraction cannot load the CrCL or
cause tibial subluxation. Thus, during the swing
phase quadriceps activation on a flexed stifle
does not cause subluxation, suggesting that the
swing phase is CrCL-independent in the dog
(Korvicket al. 1994; Tashmanet al. 2004).
The CrCL is a passive restraint to exces-
sive internal tibial rotation, andex vivostudies
simulating weight-bearing demonstrated 14◦of
internal tibial rotation after CrCL transection
(Warzeeet al. 2001; Kimet al. 2009). Articular
surface geometry and lower tension in the lat-
eral collateral ligament with the stifle in exten-
sion were thought to have induced this axial
rotational malalignment (Warzeeet al., 2001,
Kimet al. 2009). Excessive peak internal rota-
tion in CrCL-deficient stifles, however, has not
been observedin vivo(Tashmanet al. 2004).
This suggests that the muscular forces about
the stifle, which have not been reproduced
in bench-top studies, are the primary stabiliz-
ers against abnormal axial rotation, and the
CrCL is a secondary rotational stabilizer at a
walk or trot. High-demand activities, however,
may generate higher axial torques that over-
come muscular compensation, and elicit abnor-
mal rotational stability in CrCL-deficient stifles.
Such investigations have yet to be performed in
the dog.
Joints and joint structures are complex sys-
tems whose components are interdependent on
one another and are constantly altering their
cellular and molecular mechanisms to maintain
and restore tissue homeostasis. In the stifle,
CrCL function is fundamentally important
in maintaining tissue homeostasis of other
structures such as the meniscus and cartilage.
In an attempt to maintain stifle function and


tissue homeostasis, these abnormal stresses on
compensating joint structures can then result
in their adaptation or their failure. This concept
has led to the idea that there is an envelope of
function or a range of loading that is compat-
ible with overall homeostasis. Loads above or
below this ‘zone of homeostasis’ may lead to
pathologic changes.In vivothree-dimensional
kinematic studies have shown that the dog has
little capability for eliminating cranio-caudal
instability via neuromuscular compensation to
stay in the ‘zone of homeostasis’ (Korvicket al.
1994; Tashmanet al. 2004; Anderst & Tashman
2009). In addition, bothex vivoandin vivostud-
ies have reported abnormal contact mechanics
and increased tangential shear loading caused
by femoro-tibial subluxation (Pozziet al. 2006;
Anderst & Tashman 2009). These alterations
in stifle biomechanics are likely an important
factor in osteoarthritis progression in the CrCL-
deficient stifle. Cranial tibial subluxation results
in a spatial shift of loading patterns to where
articular cartilage is unable to accommodate
these loads, inducing osteoarthritis (Andriacchi
et al. 2004) (Figure 5.3). Cartilage metabolism
is dependent on maintenance of the mechan-
ical stimuli that chondrocytes are adapted
for (Carteret al. 2004). Therefore, reduced or
increased loading of specific regions of the artic-
ular cartilage may trigger cartilage breakdown.
To prevent osteoarthritis, surgical treatment
of the CrCL-deficient stifle should aim at
restoring normal joint function. For an optimal
outcome, not only should cranio-caudal insta-
bility be restored but normal three-dimensional
kinematics and contact mechanics should be
obtained after surgical stabilization of the joint.
While aiming for normal joint biomechanics is
crucial when selecting surgical techniques for
stifle stabilization or CrCL repair, joint adapta-
tion should be taken in account when selecting
the treatment for the CrCL-deficient stifle. For
example, a dog with a chronic CrCL-deficient
stifle may be at a too-advanced adaptation
stage to allow significant improvement of its
joint biomechanics. In this case, arthroscopy or
arthrotomy and meniscal treatment, followed
by rehabilitation, may be selected over a stabi-
lization technique (Tiverset al. 2009). Further
work needs to be done to understand how
differences in stage of CrCL rupture may play a
role in treatment selection.
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