70 Etiopathogenesis of Cruciate Ligament Rupture
7.5
5.0
2.5
0.0
30 30
Knee joint flexion (°)
90 90
Greyhound Labrador Retriever
* **
*
**
CC Laxity (mm)(Mean+/– SEM)
p = 0.04 p^ = 0.04
Figure 8.5 Cranio-caudal (CC) laxity testing in
Greyhounds (n=11) and Labrador Retrievers (n=11) at
100 N with the joint in 30◦and 90◦of flexion. Source:
Comerfordet al. 2005. Reproduced with permission from
John Wiley & Sons, Inc.
75
50
25
0
Greyhound Labrador Retriever
Expression of
pro-MMP–2 (% std)
(Mean+/– SEM)
p = 0.02
Figure 8.6 Levels of pro-MMP-2 (% inactive zymogen)
in Labrador Retriever and Greyhound cranial cruciate
ligaments. Source: Comerfordet al. 2005. Reproduced
with permission from John Wiley & Sons, Inc.
Greyhounds (Figure 8.7). This implies the
presence of partially degraded collagen triple
helices in Labrador CrCLs. Increased collagen
degradation, as indicated by the high levels of
MMP-2, is consistent with the thermal proper-
ties of the collagenous matrix of the Labrador
CrCL, as well as the increased stifle joint laxity
within this breed. Interestingly, gender or body-
weight did not correlate significantly with any
of the mechanical, biochemical, or thermal anal-
yses in this study.
Conclusions
Differences in cruciate ligament metabolism
(ACL and CrCL) indicated by greater MMP-2
expression and collagen denaturation are
100
75
50
25
0
Greyhounds Labrador Retrievers
Enthalpy (J/g collagen)
(Mean+/– SEM)
p = 0.05
Figure 8.7 The enthalpy of denaturation (J/g collagen)
of the differential scanning calorimetry thermograms from
Labrador Retriever and Greyhound cranial cruciate
ligaments. Source: Comerfordet al. 2005. Reproduced
with permission from John Wiley & Sons, Inc.
consistent with identified mechanical proper-
ties in guinea pigs and dogs. The ligaments
examined in these studies had no apparent
pathology and, therefore, the changes identi-
fied may be intrinsic to ligament metabolism.
This may be related to genetics (influencing
factors such as stifle joint morphology), and
may account for the differing breed predisposi-
tion to CR within these two species. Therefore,
subtle changes in cruciate ligament metabolism
and its influence on joint mechanics may play a
role in canine CrCL, and possibly human, ACL
rupture.
References
Amiel D, Chu CR, Lee J. Effect of loading on
metabolism and repair of tendons and ligaments.
Repetitive motion disorders of the upper extrem-
ity. S Gordon, Blair, SJ, Fine, LJ, eds. Rosemount,
IL, American Academy of Orthopaedic Surgeons,
- pp. 217–230.
Amis AA, Dawkins GP. Functional anatomy of the
anterior cruciate ligament. Fibre bundle actions
related to ligament replacements and injuries.
J Bone Joint Surg Br 1991;73:260–267.
Anderson-MacKenzie JM, Quasnichka HL, Starr RL,
et al. Fundamental subchondral bone changes in
spontaneous knee osteoarthritis. Int J Biochem Cell
Biol 2005;37:224–236.
Barrett JG, Hao Z, Graf BK, et al. Inflamma-
tory changes in ruptured canine cranial and
human anterior cruciate ligaments. Am J Vet Res
2005;66:2073–2080.
Benjamin M, Ralphs JR. Fibrocartilage in tendons and
ligaments – an adaptation to compressive load.
J Anat 1998;193:481–494.