Degenerative Joint Disease
	
It is probable that Bonnie is suffering from osteoarthritis.  The osteoarthritis is most likely secondary to some type of trauma. It is likely that the degenerative changes occurred either as a result of the vigorous exercises 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 occurring on normal cartilage.  
	Other sources of trauma include meniscal tears, OCD, and patellar luxation.  However OCD is probably unlikely considering Bonnie is six years old and OCD is seen primarily in young dogs. Patellar luxation is also unlikely because the orthopedic exam found that the patellas were correctly positioned and normal mobile. 
	Abnormal forces on normal cartilage are a common pathoetiology of secondary osteoarthritis.  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 furthers 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.
	Pain found upon manipulation of the stifle is characteristic of osteoarthritis.  Other findings such as joint effusion and distension of the joint capsule can be explained by the production of increased joint fluid and thickening of the joint capsule, respectively, which are characteristic of osteoarthritis.  Although these general physical exam findings can be explained by DJD, the finding of a positive cranial drawer on orthopedic exam is not characteristic of osteoarthritis alone.