225. OA Flashcards
What are the signs of OA?
- joint failure
- Hyaline articular cartilage loss (initially focal)
- thickening and sclerosis of subchondral bony plate
- outgrowth of osteophytes at joint margins
- articular capsule stretching
- mild synovitis
- weakness of muscle bridging joint
Incident OA vs. Progressive OA
Incident: new OA in healthy joint
Progressive: worsening of existing OA
Incident OA Risk Factors
Age, W>M Genetic Obesity Occupational Elite Athletic Activity (NOT physical activity) Local injury Developmental abnormalities Meniscal tear/extrusion (knee)
Describe the abnormal repair process in OA
NOT degenerative joint disease
Metabolically active process of destruction and repair
New bone (osteophytes)
Synovial hyperplasia (thickening)
Capsular thickening
Initial increase in chondrocyte #/activity
Natural History of OA
Compensated: joint remodeling keeps up with tissue loss (increase chondrocyte activity, new bone formation, capsular thickening for stability)
Decompensated: insult outweighs repair response (disease progression, sx, disability)
What are the 4 constituents of healthy cartilage?
Chondrocytes: cells to synthesize matrix, produce cytokines
ECM proteins: compose matrix
Aggrecans: proteoglycan macromLc’s, GAGs/hyaluronic acid for compressible stiffness
Type II Collagen: weave to constrain aggrecans, provide tensile strength
How does OA cartilage differ from healthy cartilage?
- depleted aggrecans
- disorganized collagen matrix, loss of type II collagen
- H2O content initially increases due to aggrecan loss, but causes loss of stiffness
Cytokines involved in cartilage synthesis and repair
IL-1, TNF-alpha
prostaglandins
What is the role of MMPs in OA?
Enzymes in cartilage degradation
Made by synoviocytes and chondrocytes under influence of cytokines
Target for disease-modifying drug development
Pathology of OA (cartilage, bone, synovium, capsule)
Cartilage: surface fibrillation/irregularity, full thickness defects down to bone, large areas damaged/lost, bare bone
bone: thickening/stiffening of subchondral plate, osteophytes at joint margins
Synovium: edematous and inflamed
Capsule: edema, fibrosis
Three phases of OA
Phase 1: ECM edema, microcracks on cartilage, focal chondrocyte loss/proliferation
Phase 2: microcracks deepen, vertical clefts form in cartilage, clusters of chondrocytes around clefts
Phase 3: fissures cause cartilage to break off into fragments, subchondral bone uncovered, subchondral cysts, mild synovitis, subchondral bone sclerosis
Joints most affected in primary OA
Hands: DIP, PIP, 1st CMC Cervical/Lumbar Spine first MTP in foot Knee Hip
Generalized OA: Pattern of Joint involvement
Hands + at least one large joint
more common in middle age women
Multiple Heberden’s Nodes (DIPs)
What is secondary OA?
OA in atypical joints (elbow, shoulder, ankle)
consider when premature onset and atypical site
General clinical characteristics of OA
Gradual onset
Only few joints problematic at once
slow evolution change of sx/structure
Strong assoc with men over 40 and perimenopausal+ women
