Histology of Cruciate Ligament Rupture 51(A)(B)700600
500400
300
200Cell Number Density (#/mm2 )Cell Number Density (#/mm2 )1005000400030002000100000
Intact*
***RupturedFusiform Phenotype
Ovoid Phenotype
Spheroid PhenotypeFusiform Phenotype
Ovoid Phenotype
Spheroid PhenotypeCrCL StatusCore RegionEpiligamentous
RegionIntact Ruptured
CrCL StatusFigure 6.3 Relationship of cell number densities to
cranial cruciate ligament (CrCL) rupture status in the core
(A) and epiligamentous (B) regions-of-interest.∗Columns
are significantly different from intact CrCL (P<0.05).
Source: Hayashiet al. 2003a. Reproduced with
permission from John Wiley & Sons, Inc.
thereby causing the collagen to have a longer
crimp length and a smaller crimp angle. These
findings also support the general hypothesis
that microinjury to the ligament from mechan-
ical overload may form an important part of
the mechanically induced signaling events that
orchestrate CrCL remodeling, and may be a key
factor in the mechanism that leads to gradual
CR over time.
Fibroblast viability and metabolism are dif-
ferent in young intact, aged intact, and rup-
tured CrCL (Hayashiet al. 2003b). Metabolically
active viable fibroblasts detected by a metabolic
marker, lactate dehydrogenase (LDH), were
seen in all intact and ruptured CrCLs. How-
ever, the number of nonviable cells in the core
region of ruptured CrCLs was greater than that
in intact CrCLs of young and aged dogs (Fig-
ures 6.6 and 6.7).
(A)(B)3.02.52.01.51.00.50.0100806040200Extracellular Matrix GradePercentage Birefringent Collagen**Intact Ruptured
CrCL StatusIntact Ruptured
CrCL StatusFigure 6.4 Relationship of extracellular matrix (ECM)
organization (A) and collagen birefringence (B) to cranial
cruciate ligament (CrCL) rupture status in the core
region-of-interest. CrCL were graded using a numerical
rating scale (1, highly organized fibrous tissue structure
with parallel alignment and dense packing of collagen
fibers; 2, partially disrupted organized fibrous structure of
collagen fibers; 3, total loss of organized fibrous structure
of collagen with homogenous appearance of the ECM).
Values represent the mean of five fields-of-view.
∗Columns are significantly different from intact CrCL
(P<0.05). Source: Hayashiet al. 2003a. Reproduced
with permission from John Wiley & Sons, Inc.Cruciate ligament adaptation
and repairThe CrCL is a hypovascular tissue and its vas-
cular distribution is not homogeneous (Hayashi
et al. 2011a). In a study describing vascular dis-
tribution in grossly intact canine CrCL using
immunohistochemical staining for two compo-
nents of blood vessels (factor VIII for endothe-
lial cells, and laminin for basement membrane),
vascular staining was sparsely identified