Hypothesis two:  Immune-mediated disorder

An unknown antigen, often microbial, stimulates the immune system, resulting in 
systemic production of IgM antibody and altering native IgG.  The IgG/Anti IgG 
and the antigen/IgM complexes then become fixed in synovial tissue, and are 
linked with complement. Neutrophils are 
chemotactically attracted to the site, engulf the complexes, die in the joint 
and release 
enzymes, resulting in inflammation.  	Inflammatory mediators, such as 
cytokines and prostaglandins, are responsible for causing pain, as well as 
upregulating epithelial expression of adhesion molecules, and causing 
chondrocytes to produce more degradative enzymes. Pannus formation also occurs 
with this process, causing erosion of underlying cartilage. Over time, all of 
this causes the affected joints to erode, causing deformity. 
	This degeneration, coupled with the formation of subchondral cysts often 
present in this disease, cause joint remodeling. The joint remodeling could 
ultimately interfere with the patellar ligaments, resulting in luxation.
 	Clinical signs typically appear in small and toy breeds during early 
adulthood.