Infectious arthritis:
Infection is due through the inoculation of the synovial membrane of bacteria.  These 
bacteria cause an inflammatory reaction.  The colonization of bacteria elicit a biochemical 
insult causing a massive influx of neutrophils.  These neutrophils produce cytokines and 
free radicals that destroy the surround synovial membrane.  Bacterial contamination of the 
synovium causes inflammation, and promotes formation of fibrin, clotting factors, PMNs, 
and proteinaceous serous effusion into the joint.  The fibrin deposition inhibits synovial 
fluid penetration.  The bacteria lysozomal enzymes break down the cartilage matrix.  This 
cascade of events results in the loss of proteoglycan and collagen from the articular 
cartilage.  This event, coupled with mechanical trauma, leads to rapid cartilage destruction.  
In this case, possible etiologies for an infectious arthritis could be an extension of 
osteomyelitis, trauma, or hematogenous spread of bacteria via the peridontitis.    
Radiographic change is similar to any nonerrosive joint disease.  Early signs include 
synovial effusion, increase synovial mass, soft tissue swelling which is indicated by a 
distended joint capsule.  Animals with septic arthritis usually exhibit a marked unilateral 
lameness.  Onset of clinical signs may be acute or gradual.  With chronic septic arthritis, 
clinical signs include single or multiple limb lameness, with  subacute endocarditis, weight 
bearing lameness, reduced range of motion, crepitit, and joint swelling.  In this case, we 
had a non-weight bearing lameness.  However, we did have a weight bearing lameness 
post trauma.

Rheumatoid arthritis:
Occurs in small/toy breed dogs 8 months to 8 years of age.  It is accompanied by fever, 
malaise, anorexia and lymphadenopathy in earlier stages.  It is an erosive noninfectious 
inflammatory joint disease.  It is characterized by chronic, bilaterally symmetrical erosive 
destruction of the joints.  Etiology is unknown, but considered immune-mediated.  There is 
an altered native IgG or tissue debris that stimulates production of IgM.  These resultant 
immune complexes are deposited in the synovium and initiate an inflammatory response 
because  PMNs engulf the complexes, die in the synovium or joint, and release enzymes.  
This is followed by synovial cell proliferation, cartilage and subchondral bone destruction, 
joint swelling, and rupture of the collateral ligaments.  This results in a non-functional 
joint. Most affected dogs have a history of stiffness after rest and limping.  Radiographic 
changes include 6 of the following 9 diagnostic criteria: synovial effusion, joint capsule 
distension,  perichondral decreased bone opacity, subchondral bone destruction, cyst 
formation.  Perichondral osteolysis and erosion, narrowing of the joint space, decrease 
opacity of the epiphyses next to the infected joints, mushrooming of the ends of the 
metatarsals, and varying degrees of luxation/subluxation.  Diagnosis is also made by joint 
tap, with the presence of slight turbidity, yellow or pink color, decreased viscosity, 
10,000-40,000 Nucleated cells/mm (20-80% being PMNs). Immune tests can also be 
performed to check for rheumatoid factor.  They are positive in 25% of cases, with 1:8 or 
higher indicative of rheumatoid arthritis.  In this patient, we have a similar rupture of the 
collateral ligaments and bilateral lameness.

Osteoarthritis:
Defined as a disease characterized by joint pain, tenderness, decreased ROM, crepitace, 
occasional effusion, and varying degrees of inflammation without systemic effects.  Nearly 
all osteoarthritis is secondary to some type of trauma.  Abnormal forces exerted on cartilage 
result to damage of the cartilage matrix and chondrocytes.  This initiates a complex series of 
events that leads to deterioration of the joint.  Damages to the chondrocytes leads to 
increased catabolic and anabolic activity.  This leads to the release of inflammatory 
mediators such as cytokines and PGs that lead to the breakdown of proteoglycan and 
collagen.  Synovial macrophages move into remove the debris, the joint capsule begins to 
thicken, there is increased activity of synoviocytes.  Ultimately, the catabolic activity of the 
chondrocytes exceeds the rate of anabolism, which leads to degenerative changes.  
Subchondral bone is subjected to increased stress, and responds by thickening (sclerosis).  
Clinical signs include altered gait, joint swelling, crepitace (due to friction of thickened 
synovium and joint capsule as it moves over abnormal cartilage and osteophytes), 
decreased ROM (capsule fibrosis or pain associated with the motion of the joint), muscle 
atrophy, and pain (most predominant sign).


Degenerative Joint Disease is a noninflammatory non-infectious degeneration of articular 
cartilage accompanied by bone formation at the synovial margins with fibrosis.  Primary 
DJD is of unknown etiology.  Secondary DJD occurs in response to abnormalities that 
cause joint instability ie. Cranial cruciate ligament rupture, abnormal loading of articular 
cartilage, or in response to other joint disease ie. infection or immune mediated.