Hypothesis 1: chronic cranial cruciate ligament degeneration Damage to the cranial cruciate ligament is the primary focus of the diagnostic workup since the left stifle demonstrates a positive cranial drawer sign, a test that is indicative of a partial or complete cranial cruciate ligament rupture. In addition to this test result, there is no palpable pain or abnormality in the patella, collateral ligaments of the stifle or the hip joint. Although the cranial drawer of the right stifle was reported as <2mm, this is considered normal and will not be investigated further. However, an obese large-breed dog is predisposed to degenerative joint disease and other joint injury so the owner should be observant of any gait changes in the future. The cranial cruciate ligament deteriorates with age. As a dog ages, the ligament loses fibroblasts and chondrocytes become the predominant cell. Therefore, the structural integrity of the collagen in the ligament is lost. With chronic degeneration, the ligament first stretches as it loses its integrity, then it partially tears before becoming completely torn. As the ligament becomes weak, minor trauma can precipitate its rupture. Obesity exacerbates the degenerative process due to the excessive stress being placed on the cranial cruciate ligament from the additional weight. The cranial cruciate ligament is responsible for preventing the weight-bearing forces from thrusting the tibia cranially, so any additional weight makes this task harder. Osteoarthritic changes begin early on in the degenerative process and will be evident by the time the cranial cruciate ligament finally ruptures. However, the cruciate rupture speeds up the progression of osteoarthritis. The osteoarthritic changes are the result of the abnormal stress placed on the stifle joint from obesity, excessive exercise, and the abnormal movement caused by cranial cruciate ligament laxity. The stress causes the death and damage of articular chondrocytes. Damaged chondrocytes release cytokines into the joint, which attract leukocytes. These white blood cells, mainly neutrophils, release lysosomal enzymes, generating superoxide radicals. This perpetuates the cartilage degradation and inflammation. The inflammatory response also increases the permeability of the synovial vasculature, resulting in joint effusion. The cytokines also cause the release of prostaglandins, which are responsible for the painful response to movement and palpation of the stifle. Damaged chondrocytes also release metalloproteases, which act to alter the collagen/proteoglycan structure. This leads to the loss of proteoglycans and allows the articular cartilage to absorb water and swell. The abnormal biomechanics imposed on the joint by the swelling cartilage also contributes to the chondrocytes' death. Since the joint capsule is heavily innervated, any pressure placed upon it by the swollen articular cartilage will result in pain. The abnormal stress placed on the subchondral bone causes it to thicken and remodel, forming osteophytes. In an attempt to stabilize the joint, the fibrous joint capsule thickens. Medical meniscal injury is common after cranial cruciate ligament rupture. When this ligament ruptures, the abnormal tibial rotation places an excessive force on the meniscus from the femoral condyle. This occurs because the meniscus is immobile; it is fixed to the joint capsule. The additional compression and rotation placed on the meniscus tears its fibers. It is important to check for a medial meniscal injury during the cruciate repair because failure to repair the injury can decrease the prognosis after surgery due to exacerbation of osteoarthritis.