Diagnosis

Our diagnosis is rupture of the left cranial cruciate ligament with probable injury to the medial meniscus and degenerative joint disease.  The radiographs appear to show degenerative joint changes.  It is too soon after the traumatic incident for them to be secondary to the recent injury, so we believe the changes are most likely due to chronic instability in the joint.  While certain predisposing factors (see below) may cause some joint instability, it is generally not enough to induce degenerative changes.  These changes are most likely due to a partial rupture of the cranial cruciate ligament that just recently became an acute tear.  The partial tear might have occurred before the owner acquired the dog, since nothing is known about Bonnie's early life.  With healing of the initial tear, the lameness might have decreased so as to be unnoticeable as degenerative growths appeared to help correct the problem.  However, the weakened ligament was susceptible to further tearing over time (particularly due to the fact that Bonnie is overweight and goes on occasional jogs, which would strain the stifle joint), and was eventually entirely ruptured.

Pathophysiology
The cranial cruciate ligament is the primary restraint against cranial drawer motion and hyperextension of the tibia.  It also limits the internal rotation of the tibia by twisting against the caudal cruciate ligament, and prevents excessive varus and valgus motion of the tibia while in flexion.  Traumatic injury to the cranial cruciate ligament is most commonly due to a violent internal rotation of the leg.  As the internal rotation progresses, the cranial cruciate ligament is subject to injury from the caudomedial edge of the lateral femoral condyle as the condyle rotates against the ligament.  Another trauma induced cause of cranial cruciate rupture is a hyperextension of the stifle.  When this occurs, the roof of the intercondylar notch acts as a knife and transects the ligament.  Both of these injuries could have occurred while running the dog or while walking on the uneven terrain of the woods.

Other factors that might have predisposed Bonnie to cranial cruciate rupture are congenital malformations of bone or normal aging changes.  Abnormal conformation of the distal femur or proximal tibia could have decreased the fiber strength of the ligament.  There could have been a congenital narrowing of the intercondylar fossa, where the cranial cruciate ligament resides.  This might have increased tension between the ligament and surrounding bone, weakening the fiber of the ligament.  A normal aging change in all dogs is ligament deterioration especially in the central core due to decreased blood supple there.  There is a loss of fiber bundle organization and metaplastic changes of cellular elements which lead to loss of structural and material stiffness and strength.  This deterioration weakened the structure of the ligament making it easier for rupture to occur.  Intermittent episodes of the intensive physical activity coupled with the overweightness overloaded the structures in the stifle joint and weakened the ligaments. Cranial cruciate ligament injuries are more common in females than males and the incidence increases with ovariohisterectomy.  It was shown that in rats, OHE decreases elastin content and fiber diameter  in the hip joint.  This leads one to speculate that the lack of estrogen in a spayed female may cause a weakening of the fibers of the cranial cruciate ligament.

There is a significant likelihood that some of these factors are involved in the pathogenesis of the rupture since the other stifle joint appear to be unstable as well.  There was a drawer sign of 2mm in the right stifle, which falls at the high end of normal, but which also falls within the range of partial rupture.  This suggests that there is compromise of the right hind cranial cruciate ligament, but there has not been an inciting traumatic incident to cause a complete rupture and subsequent lameness.
	
The cruciate ligaments invaginate the joint capsule, so the joint capsule was probably compromised due to the rupture of the cranial cruciate ligament.  This damage to the joint caused release of cytokines from chondrocytes inducing surrounding cells to produce inflammatory products (prostaglandins and metalloproteinases).  The products produced by both the chondrocytes and the surrounding cells caused vasodilation of the capillaries causing them to leak fluid into the joint space, evidenced by the distension of the joint capsule.  The interleukens and prostaglandins also stimulate the pain receptors in the joint capsule eliciting pain and a reluctance to move.   

The menisci in the normal standing position transmit approximately 65 percent of the weight-bearing load. The medial meniscus is firmly bound to the tibial plateau by meniscal ligaments, whereas the lateral meniscus is relatively mobile. Since the menisci in the normal standing position transmit approximately 65 percent of the weight-bearing load and the strength of the menisci deteriorate with aging, correlating with loss of fiber bundle organization and metaplastic changes of cellular elements, abnormal pressure on the cranial cruciate ligament definitely would increase the weight-bearing load on the menisci. 

When cranial cruciate ligaments rupture, there is an increase in internal rotation of the tibia on the femur.  This causes the medial femoral condyle to place excessive twisting force on the relatively immobile medial meniscus. The twisting action may stretch and tear the medial meniscus or cause it to be crushed between the medial femoral condyle and the medial tibial condyle. Medial meniscal damage occurs in about 70-80 % of cranial cruciate ligament ruptures.  The menisci function in load transmission and energy absorption, help provide rotational and varus-valgus stability, lubricate the joint and render surfaces congruent.  A stifle valgus angulation deformity was seen on the video of Bonnie walking.  The hock seemed to be closer to the body with the toe pointed out.  This is probably due to the loss of medial stabilization due to both the cranial cruciate rupture and the damage to the medial meniscus.  The dog is also reluctant to go upstairs, this is probably because of the damage to the medial meniscus.  There is no more lubrication between the medial tibia and femur and in fact there may be bone against bone contact, causing pain and discomfort during flexion and extension.