Osteoarthritis

Question 1

What age group experiences osteoarthritis?

Answer 1

Usually starts around age 50 with highest incidence after 70. Proteoglycan and collagen synthesis decreases with age.

Question 2

Who’s more affected by osteoarthritis? Men or women?

Answer 2

Men more often than women

Question 3

What are the cells that make the extracellular matrix of the cartilage?

Answer 3

Chondrocytes

Question 4

What is the function of cartilage?

Answer 4

Reduce friction and absorb shock

Question 5

What sort of joints does osteoarthritis affect?

Answer 5

Synovial joints - freely moving joints. Synovial fluid hydrates, oxygenates and feeds articular cartilage.

Question 6

Are there blood vessels or nerves in articular cartilage?

Answer 6

No - so insensitive to pain, can’t regenerate much and gets fed from synovial fluid.

Question 7

Cartilage is made of these protein core and polysaccharide chains called glycosaminoglycans (or GAG’s) that make up what..?

Answer 7

Proteoglycans

Question 8

What binds one proteoglycan to another to form a complex?

Answer 8

Hyaluronate binds them to form complexes and proteoglycans aggregates with collagen fibres

Question 9

How do GAG’s attract cations?

Answer 9

Negatively charged GAG’s attarct cations like Na+ and water which makes cartilage resilient and it also regulates synovial fluid movement within the cartilage because where Na+ goes, water follows.

Question 10

What two things break cartilage down?

Answer 10

1) Cytokines stimulate the synthesis of degradative enymes (that’s why there’s a lot of IL-1 in inflammed joints).
2) Matrix metalloproteinases breakdown collagen and inhibit proteoglycan production.

Question 11

What makes cartilage?

Answer 11

1) Growth factors like the insulin like growth factor (IGF-1) and the transforming growth factor (TGF - beta) which stimulate proteoglycan and collagen synthesis and activate proteinase inhibitors (inhibit degradative enzymes)

Question 12

Do genetics and environmental factors have anything to do with osteoarthritis?

Answer 12

Yes.

Question 13

What’s primary osteoarthritis?

Answer 13

It’s associated with aging. Accumulates with effects of wear and tear. Happens as the quantity and quality of proteoglycans in cartilage decrease with age.

Question 14

What is secondary osteoarthritis?

Answer 14

Happens because of wear and tear due to chronic or excessive joint stress, joint instability, or direct damage to cartilage. Example: obesity, occupational, repetitive use, athletes or sport injury, congenital - like leg length discrepency, abnormal gait d/t neuromuscular disease, neuropathy

Question 15

What are some hematologic disorders that cause osteoarthritis?

Answer 15

Hemophilia and hemochromatosis

Question 16

What are 5 steps that lead to the pathogenesis of OA?

Answer 16

1) Erosion of articular cartilage
2) subchondral sclerosis (scarring)
3) Formation of subchondral cysts
4) Formation of bone osteophytes
5) Secondary inflammation (mild synovitis)
(Damage, sclerosis, cysts, spurs, inflammation)

Question 17

What’s the hallmark sign of OA?

Answer 17

Loss of proteoglycans

Question 18

When do cytokines get released in response to joint injury or stress and activate proteinases?

Answer 18

When articular cartilage erodes.

Question 19

What happens as cartilage erodes?

Answer 19

It starts as proteoglycans are lost and collagen gets broken down. Worsens as proteoglycan and collagen synthesis can’t keep up with age. Cytokines get released due to join injury and then cartilage loses strength due to loss of collagen, and loss of resilience (loss of proteoglycans)

Question 20

What does the eroded cartilage look like?

Answer 20

Softened (chondromalacia), surface defects (rough appearance), superficial cracks (fibrillation), and progressive erosion to the underlying bone.

Question 21

What is subchondral sclerosis?

Answer 21

Thickening or hardening of the subchodnral bone. Cartilage is lost and so the bone is exposed. Bone rubs against bone. And bone remodeling increases density in this area (making it look more white on an Xray)

Question 22

What causes subchondral cysts to be formed?

Answer 22

Happens with advanced disease. Synovial fluid seeds into subchondral bone through microfractures. Trapped fluid forms cysts and increass pressure can cause pain.

Question 23

Where do osteophytes form?

Answer 23

At the edges of the articular surfaces in response to bone stress. They enlarge and deform joins which causes pain and limits movement. Example: bouchards nodules

Question 24

What are joint mice?

Answer 24

Pieces of cartilage and bone that break off into the synovial cavity

Question 25

What causes synovitis?

Answer 25

Usually chunks of cartilage and bone will be eaten by phagocytes but if they’re too big then they stay there and the body initiates an immune response to them. This causes inflammation and stretching of the joint capsule. THEN… cells in the synovial membrane release cytokines which stimulates the matrix metalloproteinase synthesis by chrondrocytes (viscious cycle)

Question 26

What joints are commonly affected by OA?

Answer 26

One or more joints. Usually weight bearing joints like knees, hips, lower cervical or lumbar vertebrae. Also interphalangeal joints, the thumb and big toe joints.

Question 27

When do people with OA experience with pain?

Answer 27

Occurs at rest and in the morning or after periods of inactivity. Goes away with movement as joints become lubricated.

Question 28

What are some signs that this person is experiencing advanced OA?

Answer 28

Large joint from deformity, decreased joint motion, muscle atrophy due to disuse, and difficulty walking and risk of falling when the knee joint becomes unstable

Question 29

How do we diagnose OA?

Answer 29

No lab marker for OA. Rule out RA, gout and SLE. ESR, CRP and CBC should all be normal. Mostly dx through history, stiffness and physical findings.

Question 30

What are some physical findings of someone with OA?

Answer 30

Muscle atrophy, crepitus, joint enlargement and deformity, limited ROM/joint instability

Question 31

What would an Xray show if someone had OA?

Answer 31

Joint space narrowing, subchondral sclerosis, subchondral cysts, and bone spurs/osteophytes

Question 32

What other ways could OA be dx’d?

Answer 32

Arthroscopy, u/s, MRI, bone scans. Synovial fluid analysis would show inflammation, and markers for cartilage breakdown but this isn’t really used clinically. Would not have Rheumatoid factor.

Question 33

Treatment goals?

Answer 33

Strengthen joint through exercise. Minimize joint stress (lose weight, assistive devices). Reduce pain and inflammation (nsaids, steroids, tylenol). Improve joint function (viscosupplementation, dietary supplements), cartilage restoration or joint surgery.

Question 34

How can we restore cartilage?

Answer 34

Microfracture procedure, autologous chondrocyte implantation, osteochondral autograft/allograft transplantation.