OA Flashcards
Articular Cartilage Structure
- Superficial (squished and horizontal)
- Transitional
- Radial (more space and vertical)
- Calcified
Subchondral Plate
Fiber Alignment
Highly organized based on the patterns of surface motion and mechanical stress
Nutrition of Hyaline Cartilage
A neural, avascular, alymphatic
Diffusion for nutrition no removal of waste
Gets nutrition through the synovial membrane and cartilage matrix
Immature cartilage can receive nutrients from bone vessels prior to formation of calcified cartlilage
Cartilage and Immobilization: Non contact areas
Usually peripheral
Changes here first
Decreased staining intensity for gags (Safrinin O)
Loss of cells
Enlargement, clustering of cells
Finally degeneration (does not progress to deep layers)
“Starved to death”
Cartilage and Immobilization: Contact areas
“pressure necrosis”
Initially, cell proliferation and increased metabolic activity
Decreased proteoglycan (GAG) content
Eventual cell degeneration (slower than in non-contact areas but will progress to deep layers)
Infiltration of mesenchymal cells from marrow cavity with formation of fibrous tissues
Cartilage and load bearing
Load distribution more than load attenuation
The thicker the tendon the less the bony contact
Rate of Loading
Increased rate met by increased stiffness and
does not allow for adequate distribution of force
Impulse loading (high rate) is most damaging to articular cartilage
Cartilage also loaded in the tension and direction of loading relative to surface fibers is important.
Role of the Fibers
Physically contain proteoglycans and counteracts swelling pressure
Surface fibrillation allows escape of proteoglycans
Remaining proteoglycans can “spread out” and therefore hold more water
Role of Subchondral Bone
Primary shock absorber
Thickening of subchondral plate with increased stiffness
Cartilage gets “caught between a rock and a hard place”
Factors that increase joint stress: force
External loads
Body weight
Tight periarticular tissues
Loading rate
Joint instability
Abnormal forces
Muscle weakness or poor motor control
Exercise and OA
Strong Evidence!
Mostly a question of type and dose.
Muscle as shock absorber
“Normal” joint mobility (not hyper or hypo)
Muscle as a stabilizer to maintain normal motion
Anti-inflammatory effects an mechanotransduction
Hypomobility and OA
Chronically elevated contact pressure
Less motion and surface areas during dynamic movement
Shortening and thickening of capsular tissues
“Degenerative” process
Hypermobility and OA
Loss of normal ICR (instant center of rotation)
Cartilage stressed abnormally relative to surface fiber orientation
Excessive translation
Abnormal joint forces
Distraction
Compression
Shearing
Degenerative changes
