Degenerative Joint Disease
	
It is probable that Bonnie is suffering from osteoarthritis in addition to a cranial cruciate ligament tear (see pathophysiology for CCL below).  The osteoarthritis is most likely secondary to some type of trauma.  Abnormal forces on normal cartilage is a common pathoetiology of secondary osteoarthritis.  It is likely that  the degenerative changes occurred either  as a result of the vigorous exercies  that Bonnie receives  or as a result of rupture/tear of her cranial cruciate ligament.    Either of these types of trauma fall under abnormal forces occuring on normal cartilage.  Other sources of trauma include meniscal tears, OCD, and patellar luxation. These abnormal forces would result in damage to the chondrocytes  and cartilage matrix which will eventually initiate a self perpetuating  pathway  of mechanical  and biochemical  changes.  
	Damage to the chondrocyte and cartilage matrix results in increased anabolic and catabolic activity of the chondrocyte.  This includes the breakdown of collagen and proteoglycan as well as the release of inflammatory mediators  such as prostaglandins and cytokines.  The degradation of proteoglycans  and collagen which provide compressive and structural strength to cartilage, respectively, leads to a compromised joint.    The breakdown products of these proteins are removed by synovial macrophages.  This results in a thickening of the joint  capsule.  The cartilage, as  it is now, can no longer withstand normal biomechanical forces thus any force applied to the articular surface will result in further damage to the cartilage and chondrocytes.    
The release of inflammatory mediators leads to inflammation and further cartilage damage.   The trauma causes chondrocytes to release cytokines such as interleukin 1 and 6, and tumor necrosis factor alpha.  These cytokines  stimulate other cells to produce additional inflammatory  products thereby perpetuating the pathway  of cartilage destruction.  Moreover, the cytokines  decrease the ability of the chondrocytes to produce normal cartilage and proteoglycans.    Eventually cartilage degradation will be initiated and the cartilage matrix will be depleted as the anabolic activity within the joint is exceeded by the catabolic activity .
	The degradation of articular  cartilage  results in an inability  of the cartilage to evenly  distribute  normal biomechanical  forces.   The inability to evenly distribute forces leads to increased stress over the remaining  articular cartilage  and underlying  subchondral bone.  The subchondral bone thickens  in response to this increased stress and in the process looses some of its compliance.   Due to the decreased  compliance of the subchondral bone  it can no longer absorb as much force could under normal conditions. This results in even more stress and thus further trauma to the overlying articular  cartilage.   This pathway is irreversible and self-perpetuating  to the point that cartilage degradation  is responsible for further cartilage degradation by the process described above.

CCL Hypothesis

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.  The primary rule out for this dog is a cranial cruciate rupture since this dog had a cranial drawer sign of 4-5mm.  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..  Bonnie could have placed her left hind leg into a ditch, abruptly fixing the tibia, while the rest of the body kept moving forward causing hyperextension.  Bonnie could also have stepped on an unstable branch, that then rolled out from under her causing the tibia to quickly rotate inward.  

While trauma is the most likely cause of this dog's cranial cruciate rupture, there are other factors that might have predisposed Bonnie to cranial cruciate rupture.  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.  This dog was probably also in poor physical condition with poor muscle development around the stifle.  While it went for 30-60 minute walks twice a day, we don't know how rigorous those walks were.  They might have involved multiple rest stops and actually been a very short distance.  The lack of muscle bulk did not protect the intra-articular structures of the stifle joint from excess stress.  The intermittent episodes of the intensive physical activity of three mile runs coupled with the overweight 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 might be unstable.  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.