Advances in the Canine Cranial Cruciate Ligament, 2nd edition

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54 Etiopathogenesis of Cruciate Ligament Rupture


presence of fibrocartilagenous areas in both
breeds.
Elastin fibers, composed of an elastin core
and fibrillin containing microfibrils, are tradi-
tionally considered minor components of the
ligament ECM. The elastin content is high in
Greyhound CrCL, and is associated with histo-
logical signs of degeneration (Smithet al. 2014).
The appearance of oxytalan fibers (bundles of
microfibrils) in degenerative CrCL ECM may
reflect an adaptive or reparative response to
normal or increased loads (Smithet al. 2014).
These observations suggest that the forma-
tion of fibrocartilage is clearly not a disadvan-
tage to healthy racing Greyhounds, and cannot
be regarded as pathological degeneration in this
breed. Fibrocartilage would appear to protect
CrCLs in Greyhounds, but in high-risk breeds
it may be indicative of a mild degenerative
change that is a risk factor for ligament rupture.
It is currently unclear whether CrCL degener-
ation and transformation into fibrocartilage is
a key pathologic change that is an important
risk factor for eventual CrCL rupture in certain
breeds of dog. Elastin fibers may have an adap-
tive or reparative role secondary to normal or
increased loads.


Conclusions


Taken together, the current literature suggests
that progressive CrCL fiber tearing during the
development of stifle instability is associated
with histologic changes to the matrix that
include a loss of ligament fibroblasts and chon-
droid transformation of surviving cells. The
disruption of matrix collagen includes a loss
of crimp. Two central hypotheses have been
proposed regarding the initial mechanism that
leads to cruciate ligament degeneration and
then rupture: (1) A primary defect in the liga-
ment tissue itself or in the metabolism of the
cruciate ligaments that leads to fiber rupture
and eventual partial rupture, particularly of the
CrCL, with development of microinstability of
the stifle; and (2) a dysregulation of synovial
immune responses and the development of a
chronic synovitis that promotes cruciate liga-
ment degeneration, as ligament nutrition and
metabolism are related to synovial fluid phys-


iology. These hypotheses are discussed further
in other chapters in this section. Confirmation
that one or both of these hypotheses is correct
should be a focus of future work studying the
CR mechanism in the dog.

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