Diagnosis: canine hip dysplasia

	After reviewing the radiographs and the re-evaluated Ortalani sign, the 
preliminary diagnosis of hip dysplasia is confirmed.  There is substantial hip joint laxity, 
as indicated by the increased range of motion.  The radiographs show bilateral 
subluxation of the femoral head and no evidence of fractures.  The right and left 
acetabula have beginning osteophyte formation.  Also, both femoral heads are 
approximately 50% under their respective acetabula.  These radiographic changes 
indicate that this is a grade II hip dysplasia.  A grade II hip dysplasia is characterized by 
an obvious deviation from the norm, shallow acetabula, poor joint congruency and 50% 
subluxation.  Hip dysplasia also includes new bone formation on the craniodorsal margin 
of the acetabulum, as seen in this patient with the osteophyte formation.

	The pathophysiology of canine hip dysplasia revolves around the joint laxity 
resulting from congenital or developmental causes.  The joint laxity imposes abnormal 
stresses on the chondrocytes that results in their death.  Upon death or damage, the 
chondrocytes release cytokines and other inflammatory mediators.  These cytokines 
attract inflammatory cells.  Upom the arrival of the white blood cells, they release 
lysosomal enzymes that create superoxide radicals.  The toxins increase the cartilage 
degradation and promote inflammation.  The cytokines also induce the release of 
prostaglandins which increases the patientŐs pain perception.  Metalloproteases are also 
released from the damaged chondrocytes and articular cells.  These enzymes alter the 
collagen and proteoglycan structure.  The resulting loss of proteoglycans causes the 
articular cartilage to absorb water and swell.  The abnormal biomechanics resulting from 
the swollen cartilage cause cell death and perpetuates the inflammatory and degenerative 
cycle.