Hypothesis #1 (2/16/01)

Trauma occurred causing the lameness


The injury may be due to repeated trauma or it may be due to an acute episode.   
Certain 
breeds and faulty conformation may predispose the dog to stifle injury.  In this 
case the 
dog is a pomeranian which is predisposed to medial patellar luxation.

There are several conditions which may be caused by traumatic episodes in the 
dog:

Tibial tuberosity  avulsion may either be caused by one single traumatic episode 
or 
chronic episodes.  In  this case interference with the vasularity of the 
epiphyseal center 
leads to ischemia and necrosis and causes weakness and avulsion.  This is most 
common 
in growing puppies and most notably in greyhounds.  The injury occurs very near 
to the 
patella and is likely to cause stifle pain.

Traumatic luxation of the patella may occur in any breed at any age. The history 
usually 
relates an episode of pain followed by lameness. In some dogs a grade 1 luxation 
results, 
while other animals seem to have a much more severe problem. The traumatic 
incident 
causes the lateral joint capsule to be stretched and then tear and separate the 
fibers within 
the joint capsule.  The medial capsule then becomes contracted and thickened, 
restricting 
the patella in the medial luxated position.  A breed predisposition to patellar 
luxation may 
exacerbate this condition.
Trauma may also result in rupture to the patellar ligament also causing luxation 
of the 
patella.  The misplacement of the patella will eventually result in arthritic 
changes.
	
Injury to the cruciate ligament may also occur as a result of trauma.  Dogs 
predisposed to 
this injury are often overweight, large breed dogs, and will display a cranial 
drawer sign.
The most common mechanism of cranial cruciate ligament rupture is usually 
associated 
with a sudden rotation of the stifle with the joint in 20¡ to 50¡ of flexion. 
This may cause 
the cranial cruciate ligament to rupture in its midportion or, in the case of 
younger 
animals, to avulse a portion of its bony attachment.  Another mechanism of 
injury to the 
cranial cruciate ligament is hyperextension. Therefore, as the stifle is 
hyperextended, the 
cranial cruciate ligament is the first structure to be subject to injury. 
Rupture of the caudal 
cruciate ligament alone is rare and is usually associated with severe trauma or 
dislocation 
of the stifle joint. Rupture of either or both cruciate ligaments produces 
marked instability 
of the stifle joint, resulting in pain and lameness. This instability also leads 
to progressive 
degenerative changes within the joint.

Secondary osteoarthritis is almost always due to trauma as outlined above.  
There was 
damage to the condrocytes and/or cartilage matrix, which led to release of 
cytokines, 
resulting in inflammation.  The cytokines released from the damaged chondrocytes 
also 
decreased the ability of those condrocytes to produce normal proteoglycans and 
cartilage. 
An ultimately catabolic activity exceeds anabolic activity that leads depletion 
of the 
cartilage matrix and initiation of cartilage degradation.  The change in the 
cartilage 
matrix leads the swelling of the cartilage as a whole.  The swollen cartilage is 
unable to 
withstand concussive force and further damage to the condrocytes and cartilage 
matrix 
ensues.  As the cartilage is lost, the underlying articular surface degrades and 
there is an 
increased load over the focal areas of remaining cartilage and suncondral bone.  
As a 
whole the subcondral bone responds to the increase stress by thickening, which 
lead to 
decreased compliance and force absorption.  Any remaining cartilage then 
experiences 
more stress.  This whole process leads to a viscous cycle of joint damage and 
pain.