Osteoarthritis: Etiology, Pathogenesis and Treatment

Posted by e-Medical PPT Tuesday, July 31, 2012
Typically affects people over the age of 50
A biologic process which effects cartilage with subsequent inflammatory component
Characteristically the major component of the clinical presentation is pain and decreased function
>75% of people over the age of 75 have x-ray evidence of disease
> 75% of people over the age of 85 are symptomatic
Probably affects 16-20,000,000 Americans

OA Biology
Slowly progressive disease
Primarily initially affects cartilage
Early cellular response: increased synthesis of proteoglycans and collagen followed by increased hydration
Then later inability to keep up with repair process and failure to replace proteoglycans and collagen
Consequent loss of cartilage, fissuring of cartilage, subchondral bone sclerosis and finally eburnation with “bone on bone”
Subsequent inflammatory response to cartilage effects
Clear synovial hypertrophy with consequent stimulus of inflammatory cytokines (IL-1 and TNF alpha have been shown to be elevated in the joint fluid)
But these effects are more local: little increase in CRP, few signs and symptoms of systemic inflammatory disease

Diagnosis of OA
By imaging
Presence of osteophytes (biologic evidence of an attempt to repair?)
Progressive joint space narrowing which is a surrogate measure of cartilage thinning
Now known not to be linear and some patients are rapid progressors while others are slow progressors or somewhere in between; how to predict which patient falls into which category
Increased sclerotic change in subchondral bone
When significantly progressive might reflect eburnation

Radiographic Features of the Knee in OA
Joint space narrowing
Marginal osteophytes
Subchondral cysts
Boney sclerosis
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