Hypothesis 2:  Acute cranial cruciate ligament injury

	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.

	
Injury during strenuous exercise has been shown to cause cranial cruciate 
ligament rupture.  "Bonnie" certainly experiences activity that puts excessive 
force on her joints due to her body weight.  The cranial cruciate is responsible 
for limiting tibial rotation and stifle hyperextension.  It neutralizes the 
compressive forces that act to move the tibia cranially, but the tibia is only 
kept in place if the cranial cruciate is intact.  An acute injury to the cranial 
cruciate can occur if the dog suddenly rotates the femur externally when the 
stifle is flexed and bearing the dog's weight.  This sudden movement causes the 
internal rotation of the tibia and exceeds the breaking strength of the 
ligament.  The internal rotation causes the cranial cruciate to twist and it may 
become damaged on the femoral condyle.  Therefore, this twisting movement breaks 
the collagen fibers within the cruciate and the tibia is now free to move 
cranially (the cranial drawer sign).  Excessive force can also be placed on the 
cranial cruciate when the stifle is hyperextended.  This can occur if the dog 
suddenly stops running and the tibia is held in place while the rest of the body 
continues moving.
	Once the cruciate has ruptured, there is intra-articular hemorrhage and 
effusion causing pain.  The joint capsule, which is heavily innervated (hence 
the pain), will eventually limit the effusion and hemorrhage since its capacity 
for distension is limited.  The ruptured ligament retracts and fans out and will 
attain a "mop-end" appearance.  Osteophytes develop with time in an effort to 
stabilize the joint.

	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.

	A fracture the bone containing the insertions of the cranial cruciate 
ligament can also cause the clinical signs of cranial cruciate ligament rupture 
since the ligament no longer has the structural integrity to prevent the tibia 
from being pushed cranially by the forces of weight-bearing and muscle tension.  
This type of fracture is known as a fracture-luxation injury.  A fracture occurs 
as a result of force being placed on the bone that exceeds its stress capacity.  
As the bone absorbs the excess force, it breaks.  Once the bone fractures, the 
healing process begins with inflammation incited by necrotic dead bone in the 
fracture site.  Lysosomal enzymes released by the damaged osteocytes destroy the 
bone matrix while the acute phase proteins cause coagulation leading to a 
hematoma at the fracture site.  The components in the hematoma include 
macrophages, lymphocytes and fibroblasts, which eliminate the dead bone while 
promoting angiogenesis.  Osteoclasts also remove dead bone.  During the repair 
phase, the hematoma becomes organized as the macrophages initiate fibroplasias.  
Osteoprogenitor cells move into the fracture site from the medullary cavity and 
periosteum while new blood vessels migrate in from the surrounding soft tissue.  
A callus eventually bridges the fracture and the cartilage is mineralized and 
then transformed into bone.  This remodeling phase could take years after the 
initial trauma before it is completed.