225. OA

Question 1

What are the signs of OA?

Answer 1

• 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

Question 2

Incident OA vs. Progressive OA

Answer 2

Incident: new OA in healthy joint
Progressive: worsening of existing OA

Question 3

Incident OA Risk Factors

Answer 3

Age, W>M
Genetic
Obesity
Occupational
Elite Athletic Activity (NOT physical activity)
Local injury
Developmental abnormalities
Meniscal tear/extrusion (knee)

Question 4

Describe the abnormal repair process in OA

Answer 4

NOT degenerative joint disease
Metabolically active process of destruction and repair
New bone (osteophytes)
Synovial hyperplasia (thickening)
Capsular thickening
Initial increase in chondrocyte #/activity

Question 5

Natural History of OA

Answer 5

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)

Question 6

What are the 4 constituents of healthy cartilage?

Answer 6

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

Question 7

How does OA cartilage differ from healthy cartilage?

Answer 7

1. depleted aggrecans
2. disorganized collagen matrix, loss of type II collagen
3. H2O content initially increases due to aggrecan loss, but causes loss of stiffness

Question 8

Cytokines involved in cartilage synthesis and repair

Answer 8

IL-1, TNF-alpha

prostaglandins

Question 9

What is the role of MMPs in OA?

Answer 9

Enzymes in cartilage degradation
Made by synoviocytes and chondrocytes under influence of cytokines
Target for disease-modifying drug development

Question 10

Pathology of OA (cartilage, bone, synovium, capsule)

Answer 10

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

Question 11

Three phases of OA

Answer 11

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

Question 12

Joints most affected in primary OA

Answer 12

Hands: DIP, PIP, 1st CMC
Cervical/Lumbar Spine
first MTP in foot
Knee
Hip

Question 13

Generalized OA: Pattern of Joint involvement

Answer 13

Hands + at least one large joint
more common in middle age women
Multiple Heberden’s Nodes (DIPs)

Question 14

What is secondary OA?

Answer 14

OA in atypical joints (elbow, shoulder, ankle)

consider when premature onset and atypical site

Question 15

General clinical characteristics of OA

Answer 15

Gradual onset
Only few joints problematic at once
slow evolution change of sx/structure
Strong assoc with men over 40 and perimenopausal+ women

Question 16

Symptoms of OA

Answer 16

PAIN, aching
Early OA: sx worse with use, relieved by rest (opposite of inflammatory A)
Advanced OA: pain at rest and with use, night pain - sleep interference
Morning stiffness < 30 min
Stiffness after inactivity
Less pronounced swelling

Question 17

Physical exam findings of OA + Labs

Answer 17

Bony enlargement
Limitation of ROM
Crepitus
Malalignment
Mild inflammation, warmth, effusion
Labs: non-inflammatory synovial fluid analysis

Question 18

Radiographic Findings of OA

Answer 18

Focal Joint space narrowing
Osteophytes
Subchondral cysts/sclerosis
Loss of bone at joint surface (Bony attrition)

Question 19

Prognosis of OA

Answer 19

VARIABLE, varies person to person and joint to joint (does NOT always have to worsen)

Question 20

Non-pharmacologic tx of OA

Answer 20

Pt. Education (Coping, self-management)
PT/OT (exercise to preserve ROM, AoDL)
Weight Loss (MODIFIES DISEASE COURSE)

Question 21

Pharmacologic Tx of OA

Answer 21

Systemic: non-narcotic analgesic (acetaminophen), NSAIDS/Cox2-i’s, narcotics only for advanced OA

Local: intraarticular - unclear, corticosteriod

surgical: repair tissue is structurally unstable, consider total joint replacement only in advanced OA