DIAGNOSIS: HIP DYSPLASIA


	PATHOPHYSIOLOGY

	The dog, a 9 month old Rottweiler, is being fed an appropriate large breed 
dog food but is allowed to eat free choice.  Abnormal growth of the bones 
contributing to the coxofemoral joint (hip dysplasia) can be attributed to extra 
nutrients consumed, allowing for an accelerated growth rate.  The muscles cannot 
develop and mature fast enough for the rapidly growing bones and thus cannot 
hold the femur into the acetabulum.  Without the head of the femur juxtaposed to 
it, the acetabulum cannot mold itself correctly to the femoral head.  This 
results in a poorly conformed coxofemoral joint.  This is supported by the 
results of the orthopedic exam, under sedation.  A positive Ortalani sign was 
recorded.  This reflects increased laxity because of poor articulation 
of the joint. All other findings of the orthopedic exam ruled out all other 
limbs and their joints, confirming our suspicion of the coxofemoral joint.

	Poor articulation can cause trauma to the dorsal acetabulum or to the 
articular cartilage of the femur, resulting in inflammation.  As the layers of 
the articular cartilage are damaged, the pro-inflammatory mediators (cytokines 
TNF-alpha and IL-1beta, prostaglandins, etc.) are released by synoviocytes.  
This may possibly follow the phagocytosis of collagen and proteoglycan fragments 
(released upon trauma to the cartilage).  In response to the inflammatory 
mediators, the synovial lining undergoes hypertrophy and hyperplasia, and is 
accompanied by increased synovial vasculature permeability.  Synoviocytes 
produce increased low quality fluid (increased volume, decreased viscosity).  
The subsynovial layer of the joint capsule will thicken, due to activity of 
fibroblasts.  The body is attempting to stabilize the joint, however, the 
increased fluid volume actually decreases joint stability and allows for 
luxation of the joint.  This subluxation stretches the fibrous joint capsule, 
causing additonal signs of pain and lameness.  This process of subluxation was 
evident upon review of the radiograph.  For example, there was less than 2/3 of 
the femoral head within the acetabulum.  Also, a bilateral widening of the joint 
space was appreciated. 

	The malalignment of the femur and acetabulum will cause further damage as 
the subluxation continues.  The subchondral bone of the femur and acetabulum 
eventually respond to the inflammation by thickening, which leads to decreased 
compliance of the tissue.  Eventually, the bone will remodel (osteophytes are 
produced).  Radiographs illustrated presence of osteophytes on the cranial 
effective acetabluar margin and possible remodeling of the femoral head.  
Remodeling of the bone adds to the severity of pain and clinical signs.