Hypothesis 2 - Osteochondritis dissecans of the Femoral Condyle

Endochondral ossification of the epiphyseal surface of long bones results in a surface of articular cartilage covering subchondral bone.  The articular cartilage acts to distribute focal compressive forces over the entire bone surface.  The epiphyses of the long bones begin as a cartilaginous template and this is transformed into bone by endochondral ossification.  Any dysfunction in this process is termed osteochondrosis.  This often results in a thickened articular cartilage, and areas of focal weakness.  Many etiologies have been hypothesized for this abnormality.  Too high a plane of nutrition, genetics, and hormonal disturbances are often implicated. 

There exist two common sequelae to this disease.  In joints where the main force is compressive, subchondral bone cysts may occur.  In joints where shear forces are more common, such as the stifle joint, osteochondritis dissecans is more likely.  Osteochondritis dissecans is a defect in the articular surface that results in a flap of cartilage separating from the underlying subchondral bone.  This cartilage may or may not be calcified, so the appearance of a "joint mouse" on radiographs is not guaranteed.  The accompanying inflammatory response causes joint effusion, stretching the fibrous joint capsule, resulting in pain and lameness.  The joint effusion also contains inflammatory mediators, which will chemically stimulate the nociceptors in the joint capsule.  Additionally, the exposed subchondral bone contains several nociceptors, which would be another source of pain and thus lameness. 

In this case, endochondrosis has been present all her life, resulting in a subclinical lameness.  Since Bonnie has not been bearing as much weight on that leg, enough muscle atrophy resulted to cause a positive cranial drawer. A flap separated from the subchondral bone acutely, causing this episode of lameness.  Trauma is not necessary for the flap to separate which correlates well with the absence of trauma in her history.  

Bonnie has many of the predisposing factors for OCD.  She is an obese Labrador retriever.  (Labs tend to show a higher incidence of OCD.)  Her genetic background is unknown, so we cannot look at her parents or siblings to see if they developed osteochondrosis.  In Bonnie's case, the likely precipitating factor would be her weight.  Even with normal movement, the forces that her joints are experiencing may increase to a pathologic level.  A large focal force on an area of increased retained cartilage could cause a fissure and thus a flap to form.  Bonnie's weight could possibly be exacerbated by hypothyroidism.  This hormonal disturbance causes a decrease in circulating thyroid hormone due to a decreased sensitivity to thyroid stimulating hormone.  A deficit in thyroid hormone would cause a decrease in basal metabolic rate causing weight gain and lethargy. 

To diagnose OCD, radiographs are necessary.  One looks for an irregular subchondral bone density, surrounded by a zone of increased bone density, increased joint fluid, and possibly the presence of a cartilaginous flap (if it is ossified).  Bloodwork would help rule out the possibility of hypothyroidism.  We would test the resting T3 and T4 levels as well as test T4 after administration of TSH.