Advances in the Canine Cranial Cruciate Ligament, 2nd edition

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74 Etiopathogenesis of Cruciate Ligament Rupture


congenital stenosis who sustained an ACL tear
by non-contact means were found to be young,
with small ICN width index measurements
(Souryalet al. 1988). It is also thought that knee
laxity may contribute to ICN narrowing and
then result in further ACL impingement and
damage (Wadaet al. 1996).
To date, notch width (NW) or notch width
index (NWI) have been the parameters used to
determine the width of the human and canine
ICN. The shape of the notch is also thought
to be a critical factor in the role of the ICN in
ACL injury. ICN shapes have been described
as bell- or inverted U-shaped, A-shaped, or W-
shaped (wave/crest-shaped) (Andersonet al.
2001; Chen et al. 2016). In dogs, the ICN is
bell-shaped (Fitchet al. 1995). Normal ICNs
tend to be inverted U-shaped, whereas nar-
rower notches tend to more A- or W-shaped
(Andersonet al. 2001). The notch shape may also
change during life (Hirtleret al. 2016). Recent
studies have suggested that A-shaped notches
can predispose to ACL injury (Al-Saeedet al.
2013). It has also been suggested that determi-
nation of the notch shape index (NSI) (Tillman
et al. 2002; Genget al. 2016) may be a more use-
ful measurement, as it is a relative measure of
the notch width in a medial/lateral direction
to the notch height in the anterior/posterior
direction. A low NSI will cause the ACL to be
pushed into a smaller anterior outlet of the ICN,
with the joint in extension (Figure 9.1) (Till-
manet al. 2002). In a multivariate model of
knee joint geometry, gender-related differences
were found with regard to intercondylar notch
size and shape, with women having a narrower
notch and men having a smaller ACL volume
being predisposed to ACL injury (Sturnicket al.
2015).
Differences in the ICN and its width have
been investigated in normal and CrCL-deficient
stifle joints, as well as ‘at-risk’ stifle joints from
dog breeds with differing predispositions to
CR (Comerfordet al. 2006; Lewiset al. 2008;
Mostafaet al. 2009; Ragetlyet al. 2011). An
ex vivo study found that dogs at high-risk
for CR (Labrador and Golden Retrievers) had
smaller ICNs than dogs at a low-risk (Grey-
hounds) (Comerford et al. 2006). This study
hypothesized that smaller ICNs may cause lig-
ament impingement with associated cartilagi-
nous changes within the extracellular matrix


F

E

B

A

C

D

Figure 9.1 Measurements of the canine intercondylar
notch (ICN) (adapted from Fitchet al.1995). A, cranial
notch width; B, central notch width; C, caudal notch
width; D, condylar notch width; E, ICN height; F, femoral
condyle height. The cranial notch width index (NWI) is
A/D, the central NWI is B/D, and the caudal NWI is C/D,
the notch shape index (NSI) is B/E and ICN height index
is E/F). Source: Comerfordet al. 2006. Reproduced with
permission from Elsevier.

(ECM), leading to CrCL inflammation and
degeneration.
Cranial NWIs were significantly greater
in the low-risk breeds (e.g., Greyhounds),
compared to high-risk breeds (Retrievers)
(Comerfordet al. 2006). However, there was no
significant difference in the NSI between high-
and low-risk dog breeds (Figure 9.2). As part
of this study, the stifle joints of the three dog
breeds were placed in full extension and the
areas of the CrCLs impinged by the ICN were
marked and removed. Analyses of biochem-
ical parameters such as collagen content and
crosslinks, matrix metalloproteinases (MMPs),
tissue inhibitors of metalloproteinases (TIMPs)
and sulfated and total glycosaminosglycans
(GAGs) were then performed as previously
described (Comerfordet al. 2004). The expres-
sion of pro and active MMP2 was significantly
increased in CrCLs of the high-risk breeds,
compared to the low-risk breed, suggesting
increased collagen remodeling (Figure 9.3).
There were significantly more sulfated GAGs
in the impinged areas of the high-risk CrCLs,
compared to those of the low-risk breeds
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