18/OA

Question 1

What is the definition of osteoarthritis (OA)?

Answer 1

A disease of the whole joint involving articular cartilage, subchondral bone, ligaments, capsule, synovial membrane, and periarticular muscles; results from the body’s failed attempt to repair damage caused by abnormal/excessive joint loading.

Question 2

What are the two main types of OA and their causes?

Answer 2

Primary (idiopathic, age-related with no known cause) and secondary (post-traumatic, infection, metabolic, or developmental disorders).

Question 3

Which factors influence OA prevalence?

Answer 3

Definition used (radiographic vs symptomatic), age (increases with age), country (lower hip OA in Asia), and sex (women > men for knee/hand).

Question 4

Which joints are most often affected by OA?

Answer 4

Knee > hand > hip; also feet and spine.

Question 5

What is the global burden of OA?

Answer 5

~250 million people affected worldwide; 3.9 million Canadians (13.6% over 20 years old).

Question 6

What does the cartilage of synovial joints consist of?

Answer 6

Hyaline cartilage made of chondrocytes, collagen, proteoglycans, and water; functions to resist compression, absorb shock, and reduce friction.

Question 7

What is the role of chondrocytes in cartilage?

Answer 7

Maintain the extracellular matrix and repair damaged cartilage.

Question 8

What are the main components and functions of cartilage ECM?

Answer 8

Collagen resists tension, proteoglycans/glycosaminoglycans resist compression, water enables nutrient transport and shock absorption.

Question 9

What happens to cartilage in early OA?

Answer 9

Fibrillation, vascular invasion, increased water, altered collagen, clustered chondrocytes, enzyme increase, and imbalance between repair and breakdown.

Question 10

What happens to cartilage in late OA?

Answer 10

Deep fissures, blood vessel invasion, cartilage replaced by bone/fibrocartilage, decreased water, chondrocyte loss, and enzymatic breakdown.

Question 11

What are the microscopic changes seen in OA cartilage?

Answer 11

Loss of collagen organization, decreased proteoglycans, hypertrophic chondrocytes, and microcracks.

Question 12

What is the function of subchondral bone?

Answer 12

Acts as a shock absorber; composed of calcified cartilage and compact bone, highly vascularized with nerve fibers.

Question 13

What changes occur in subchondral bone in OA?

Answer 13

Increased vascularity, sclerosis, cysts, and osteophyte formation; imbalance between bone formation and resorption.

Subchondral bone sclerosis: subchondral bone becomes abnormally thick and hardened

cysts = kystes = fluid-filled sacs that develop in the bone beneath the joint cartilage

osteophytes = excroissance osseuse

Question 14

What are common radiographic findings in OA?

Answer 14

Joint space narrowing, subchondral sclerosis, cysts, and osteophytes—most often in the medial knee compartment.

Question 15

What changes occur in the synovium during OA?

Answer 15

Synovial thickening, fibrosis, edema, increased hyaluronic acid, cartilage/bone debris, and imbalance of destructive vs inhibitory molecules.

Fibrosis: development of fibrous connective tissue in response to an injury.

Question 16

What changes occur in the meniscus in OA?

Answer 16

Collagen disruption, degenerative tears, vascularization, and increased collagen synthesis near tear sites.

Question 17

How are the joint capsule and ligaments affected in OA?

Answer 17

May show edema, fibrosis, or laxity; collagen remodeling and altered mechanical properties.

Question 18

What structures are responsible for pain in OA?

Answer 18

Innervated tissues—synovium, capsule, bone, tendons, ligaments; pain may be nociceptive, neuropathic, or central.

Question 19

What is nociceptive pain?

Answer 19

Injury/inflammation at a joint

Question 20

What is neuropathic pain?

Answer 20

Structural changes in joint innervation/nerve changes from peripheral

Question 21

What is central pain?

Answer 21

Enhanced descending pain pathways/loss of descending antinociceptive pathways

Question 22

How does OA affect muscles?

Answer 22

Muscle atrophy, reduced strength, decreased activation, and increased co-contraction around the joint.

Question 23

How does OA affect range of motion (ROM)?

Answer 23

ROM decreases as OA progresses, correlating with disease severity and disability.

Question 24

How does OA impact proprioception?

Answer 24

OA → joint tissue damage → altered sensory receptor input → impaired joint position sense (proprioception)

Question 25

How does OA affect physical function and participation?

Answer 25

Decreased activity levels, reduced physical function, and limited participation in social/leisure activities.

Question 26

What are the most common clinical signs and symptoms of OA?

Answer 26

Pain, morning stiffness, crepitus, swelling, instability, weakness, fatigue, and reduced ROM.

Question 27

How is OA clinically diagnosed?

Answer 27

Based on symptoms and physical exam using standardized criteria (e.g., EULAR and ACR criteria for knee OA).

Question 28

What are the main risk factors for developing OA?

Answer 28

Age, sex, obesity, joint injury, malalignment, high-impact activity, genetics, and occupation.

Question 29

How does mechanical loading relate to cartilage health?

Answer 29

Moderate loading maintains cartilage; excessive or abnormal loading leads to degeneration.

Question 30

What are 'altered articular contact forces' in OA?

Answer 30

Changes in intensity and area of cartilage loading cause biochemical and mechanical degeneration of joint tissues.

Question 31

What are the treatments for knee OA according to OARSI guidelines?

Answer 31

Core: Education, land-based exercise (strength, cardio, balance, yoga, tai chi), and weight management. Level 1A: Topical NSAIDS Level 1B: NSAIDS, aquatic exercise, gait aids, self-management Level 2: Injections, CBT w/ exercise

Question 32

What are the treatments for hip OA according to OARSI guidelines?

Answer 32

Core: Education, land-based exercise (strenght, cardio, balance) Level 1A: NA Level 1B: NSAIDS, mind-body exercise, self-management, gait aids Level 2: weight management

Question 33

What is the evidence for exercise in OA management?

Answer 33

Improves pain and function (small–moderate effect); benefits are similar across exercise volumes.

Question 34

What is neuromuscular exercise (GLAD/NEMEX programs)?

Answer 34

Structured exercises to improve joint control, strength, and function in hip/knee OA. 2-3 sets of 15 reps

Question 35

How do knee braces and heel wedges help OA?

Answer 35

Valgus braces or lateral wedges shift load from medial to lateral compartment; evidence of benefit is mixed.

Question 36

What are the effects of weight loss on knee OA?

Answer 36

Combined diet + exercise yields greatest improvements in pain, function, and inflammation reduction.

Question 37

What is the effectiveness of manual therapy for OA?

Answer 37

May reduce pain short term but offers no additional long-term benefit beyond exercise.

Question 38

How does cognitive behavioral therapy (CBT) or PCST help OA patients?

Answer 38

Improves coping and function when combined with exercise; focuses on pacing, problem solving, and reframing pain.

Question 39

How is hand OA managed?

Answer 39

Education, orthoses, assistive devices, and exercise; short-term improvement in pain and function.

Question 40

What surgical options exist for OA?

Answer 40

Arthroscopy (limited use), osteotomy, resurfacing, or joint replacement (hip, knee, thumb) for advanced disease. ## Footnote *Arthroscopy* (ahr-THROS-kuh-pee) is a procedure that uses a fiber-optic camera to diagnose and treat joint problems. An *osteotomy* is a surgical procedure where a bone is cut to change its alignment, length, or shape. *Resurfacing*: surgeon reshapes and caps the femoral head (ball) with a metal prosthesis instead of removing it entirely

Question 41

What are key physical therapy takeaways for OA management?

Answer 41

Core treatments are education, exercise, and weight loss; personalize care and address pain sensitization.