52 Etiopathogenesis of Cruciate Ligament Rupture
60504030201006040200(A)Crimp Angle (degree)(B)Crimp Length (μm)*#Intact Ruptured
CrCL StatusIntact Ruptured
CrCL StatusFigure 6.5 Relationship of crimp angle (A) and crimp
length (B) to cranial cruciate ligament (CrCL) rupture.
∗Significantly different from intact CrCL (P<0.05).
#Lower crimp angle compared with intact CrCL
(P<0.15). Source: Hayashiet al. 2003a. Reproduced
with permission from John Wiley & Sons, Inc.
throughout the entire CrCL. However, the
proximal portion of the CrCL appears to have
a greater number of vessels than the middle or
distal portions of the ligament. In a study deter-
mining the microanatomic vascular distribution
in ruptured canine CrCL using specific vascular
immunohistochemical staining, the ruptured
CrCL was more vascular than intact CrCL.
However, there was no difference in vascular
density between the torn end and the remaining
core area of the ruptured CrCL (Hayashiet al.
2011b) (Figure 6.8). It remains to be determined
whether this finding is associated with the
cause of CrCL rupture, or is a result of CrCL
rupture.
Ruptured CrCLs have significantly higher
amounts of immature collagen crosslinks, total
and sulfated glycosaminoglycans and water
(A)(B)Figure 6.6 Photomicrographs of longitudinal frozen
sections of ruptured cranial cruciate ligament (CrCL) from
a 6-year-old ovariohysterectomized Labrador Retriever
obtained via bright-light microscopy. Specimens were
stained histochemically for lactate dehydrogenase (LDH),
a marker of cell viability. (A) Periphery of the main axial
tissue component (core) region of the ruptured CrCL.
Note the parallel rows of fusiform and ovoid
LDH-positive ligament fibroblasts, with an organized
extracellular matrix (ECM) containing crimped collagen
fibers. (B) Central part of the core region of the ruptured
CrCL. Note the low number of ligament fibroblasts; many
cells are devitalized (no LDH staining) with a spheroid
phenotype (arrows). Most of the collagen fibrils within
the ECM have been disrupted. Scale bar= 50 μm. Source:
Hayashiet al. 2003b. Reproduced with permission from
the American Veterinary Medical Association.content (cartilage-like material), and concentra-
tion of pro-matrix metalloproteinase 2 (gelati-
nase), compared to those of the intact ligament
(Comerfordet al. 2004). These findings suggest
that the ECM of ruptured CrCLhas an increased
matrix turnover. Cartilage-like tissue is more
vulnerable to disruption under normal tensile
loading, and therefore CrCL degeneration with