Hypothesis #1 -- Trauma

One explanation for the right rear leg lameness revolves around trauma sustained 
from the fall 
from the bed one year ago. Damage to a multitude of anatomical structures in the 
stifle joint 
region could have produced the clinical signs of a weight bearing lameness and 
medial patellar 
luxation out of the trochlear groove.

Tearing or other damage to a ligament supporting the stifle joint could lead to 
lameness in the 
dog. The medial and lateral collateral ligaments are likely targets for 
traumatic ligament damage 
to the stifle joint. The primary injury, together with the inflammation and 
fibrosis involved in the 
healing of the ligament, could incite a weight-bearing lameness in this animal. 
A negative cranial 
drawer sign on the right leg makes a cranial cruciate ligament tear unlikely. 
However, medial buttress is present, and is often seen in chronic thickening of 
the medial cartilage and medial collateral ligament in the joint.
 
The patella is connected to the hind limb proper via 3 main ligaments: the 
patellar ligament, the 
medial femoropatellar ligament and the lateral femoropatellar ligament. The 
tendon of the 
quadriceps muscle also inserts on the patella, and contributes to its support. 
Damage to any of the 
3 ligaments due to trauma, and subsequent fibrosis of tissue upon healing, could 
lead to an 
unequal tension between the ligaments. In time this could lead to increased 
movement of the 
patella in a medial direction, presenting as luxation. Similarly, the quadriceps 
muscle could have 
sustained injury (i.e. tear, pull) when Titan fell off the bed, and when the 
tissue healed it did so in 
such a matter to change the relationship between the quadriceps tendon and its 
insertion on the 
patella. This type of injury would also lead to a weakening of the support 
structures for the 
patella, and may allow luxation. 

Another proposed scenario implicating trauma involves bone injury. The stifle 
joint is associated 
with both the distal femur and the proximal tibia. Fracture on either bone (in 
the areas 
communicating with the joint) and the changes that are associated with fracture 
repair could have 
compromised overall joint stability acutely, and progressed to further 
degenerative changes in the 
long run. More specifically, The femoropatellar ligament (both medial and 
lateral) attach to the 
respective med and lat epicondyles of the femur before inserting on the patella. 
A fracture 
involving one of the epicondyles might affect the support of the femoropatellar 
ligament, 
allowing patellar luxation. The patella lays along the medial and lateral 
trochlear grooves of the 
femur; trauma-induced fracture along the trochlea would most certainly affect 
the patella and its 
supporting ligaments. The patellar ligament inserts on the tibial tuberosity. 
Fracture and the repair 
process could alter the insertion of the ligament to an abnormal position, which 
could cause pain 
as well as a weaker connection to the patella.    

The absence of pain in the right rear leg upon physical exam of the stufle joint 
(as opposed to the 
left rear leg) also leads to the possibility of nerve damage in the area. Damage 
to one of the main 
pelvic limb nerves, such as the sciatic nerve, was not suspected due to the 
normal appearance of 
muscle integrity in the leg. One would expect to see muscle atrophy with severe 
damage to the 
sciatic nerve, the tibial nerve or the common perineal nerve. A more likely 
situation is that a 
small sensory nerve branch coming off of the common perineal nerve has been 
damaged. In this 
case nociceptor function would be compromised, and pain may not be detected upon 
manipulation of the joint. 

Finally, it is possible that the stifle joint capsule or cartilage was 
traumatized, and chronic degenerative changes have occurred since the initial 
injury. The stifle joint functions normally because of an intricate balance of 
cells that perform catabolic and anabolic functions, and trauma could have 
shifted this balance and results in a chronic non-weight bearing lameness in the 
right rear leg. The initial fall could have impacted the articular cartilage, 
damaging the chondrocytes in a focal area. Chondrocytes produce supportive 
collagen (types II and IX) and proteoglycans (compressive stress). Type II 
collagen is the primary collagen fibers, and type IX fibers cross type II fibers 
perpendicularly, forming a grid of fibers. Between these grids the proteoglycans 
reside and act as rigid springs, they give the collagen stiffness and help to 
maintain the shape of the cartilage. Proteoglycans are hydrophilic, and draw 
fluid in to fill the remaining space.

With cartilage trauma, the type IX collagen may be torn apart, allowing 
increased space between fibers, and more room for water to diffuse to the 
proteoglycans. The cartilage thickens and swells, and increased friction between 
two cartilage layers may cause fragments of collagen matrix to break off and 
float freely. Synovial macrophages detect these fragments and phagocytize them, 
and they release inflammatory mediators and cytokines, like IL-1, IL-6, TNF, and 
prostaglandin E. Cytokines like IL-1 inhibit chondrocyte synthesis of new 
cartilage and proteoglycans, and eventually cartilage breakdown exceeds 
synthesis. This abnormal cartilage can no longer withstand normal everyday 
stressors. Additional stress is placed on the subschondral bone, and causes 
thickening. This thickening leads to sclerosis of the tissue, the subchondral 
bone can't resist as much stress, and even more stress is placed on remaining 
cartilage. This results in eventual bone remodeling, and a progressive 
degeneration of the joint with a progressive lameness.

The periarticular tissues could have also been initially traumatized. The joint 
capsule consists of three layers, an inner synovial cell lining (produces 
hyaluronic acid, cytokines, PG's), a subsynovial connective layer, and an outer 
fibrous joint capsule. The outer fibrous joint capsule often incorporates other 
ligaments and adds to the strength of the joint. Trauma could have torn the 
fibrous capsule or supporting ligaments, and effectively stretched the support 
of the joint. The damages synoviocytes release cytokines and prostaglandins and other degradative enzymes. They also may decrease production of synovial fluid, leading to increased joint friction. The periarticular joint capsule is well innervated and vascular, and trauma to this area would certainly cause pain and subsequent lameness.