Diagnosis:  Cranial cruciate ligament failure due to age and 
obesity.

Cranial cruciate ligament failure due to advancing age (primary stimulus) 
appears to be a gradual process during which the ligament stretches, probably tears and 
then eventually fails.  Increasing body size is considered a factor that exacerbates this 
degeneration of the ligament.  Early in the process of failure, the joint will become unstable 
and osteoarthritic change may be initiated. In this particular case we did not see 
radiographic evidence of osteoarthritis, although radiographic changes are not usually 
evident until some time after osteoarthritic changes have begun (osteophytes, bone 
remodeling, bone lysis). Since the reverse can occur as well (osteoarthritis leading to 
cruciate ligament failure) we would expect to see moderate to severe osteoarthritis 
radiographically if osteoarthritis was the primary stimulus for the cruciate weakening.  
Additionally the lameness most likely would have been mild with sudden worsening had 
osteoarthritis been first.  

Radiographically we saw an increase in space between the lateral condyle of the 
distal femur and the cranial aspect of the lateral tibia, which can be explained by a possible 
tear  (partial or full) in the cranial cruciate ligament.  (This increase in space could also be 
misleading if positioning is not correct). The cruciate ligament is attached to a crescent 
shaped fossa on the caudal aspect of the medial side of the lateral femoral condyle and some 
fibers are attached to the caudolateral aspect of the of the intercondylar fossa. The ligament 
extends distad across the joint in a craniomedial direction and attaches to the cranial 
intercondylar area of the tibia.  There are actually 2 functional components of the cranial 
cruciate:  1) the smaller spiral part originates on the craniodorsal aspect of the femoral 
insertion and extends to the craniomedial aspect of the tibial insertion and is called the called 
the cranial medial band. This remains taut in flexion and in extension.  The bulk of the 
cruciate ligament is made up of a shorter but straighter portion known as the caudolateral 
band. This part is taut in extension and loose in flexion. The primary function of the 
cruciate ligament is to limit cranial displacement of the tibia, control internal rotation of the 
tibia on the femur and to prevent hyperextension of the joint. From this, it is logical to say 
that if the cruciate is partially or fully torn, especially in the more proximal portion of the 
ligament near the femoral attachment we would expect to see displacement on the more 
lateral side of the joint in an AP radiograph.  This may also explain when the joint space 
appears decreased on the medial aspect (loss of attachment laterally may cause increase 
compression medially. We do not know this for sure as this may be due to positioning that 
we see this radiographic change).  We speculate that there may be secondary meniscal 
damage as well due to change in the compressive forces. This can only be ascertained with 
surgery. The anatomical attachment also explains why we would see cranial displacement 
of the tibia upon manipulation (cranial drawer response) when there is a tear. 

	A fold of highly vascular synovial membrane covers the cruciate ligaments. 
Cranially, the synovial membrane is continuous with the infrapatellar pad.  
Paraligamentous vessels branching from the main vessels in the synovial membrane 
penetrate transversely into the liagmentous tissue and anastamose with longitudinally 
arranged endoligamentous vessels.  This interconnecting system of vessels provides an 
abundant blood supply to all areas of the ligament except the central core of the ligament.  
This extensive blood supply would explain synovial effusion w/ hemorrhage when the 
cruciate is torn either partially or fully.  The increase in joint fluid is evidenced with 
palpation as well as radiographically.  The slight hypoalbuminemia on the blood work is 
probably due to the hemorrhage within the joint and the leukocytosis is most likely due to 
this as well.   Usually on synovial fluid analysis you will see a poor mucin clot associated 
with inflammation (trauma) but effusion from recent trauma is diluted with plasma diasylate 
but no enzyme degradation has occurred.  In such cases, the quality of the clot remains 
normal.  We suspect that the synovial fluid is there fore the result of recent trauma.  
Ligaments are also rich in nerve supply, which may play an important role in joint pain 
when injured.

The clinical problem may not become evident until the ligament completely fails and 
by then usually osteoarthritis is severe.   Some cases may present with lameness before 
total failure or there may be acute total failure due to trauma, which we believe may be 
happened in BonnieÕs case.  Eventual total failure is associated with MILD 
TRAUMA, not the type of injury expected to tear a normal ligament surface) which 
causes changes in the cruciate. Although acute cruciate ligament rupture without any 
underlying conditions does occur, it is thought the majority of lesions are the result of 
chronic degenerative changes in the ligaments themselves.  Lesions seen on histopath 
associated with cruciate ligament degeneration include abnormal basophilic staining of 
collagen fibers, cells arranged in columns with pyknotic nuclei and cytoplasmic vacuoles, 
fibrillated collagen fibers, focal thickening of the intimae of the endoligamentous blood 
vessels and in some cases, gross thickening of blood vessel walls with total obliteration of 
the lumen. Repeated minor stresses can result in progressive DJD of the stifle. These are 
frequently bilateral which may explain why we are able to palpate mild cranial drawer on 
the right side as well. The changes in the right ligament may not be as severe as those in the 
left at this time.  These stresses are compounded in the obese animal.  As joint changes 
develop, the cruciate ligaments begin to degenerate and undergo alterations in their 
microstructure.  The collagen fibrils become hylanized and the tensile strength of the 
ligaments is reduced, making the ligaments more susceptible to damage from minimal 
trauma. These changes have been associated with the aging process and may explain the 
fact that most cruciate injuries are seen in animals older than 5 years.