Ct-Ms - 2-22 - Osteoarthritis

Front 1

Osteoarthritis presentation

Back 1

Polyarticular, non-inflammatory (better with rest), symmetrical, chronic timing.

Older age, crepitus, no/little inflamm, bony enlargement.

Front 2

Primary vs. secondary OA

Back 2

Primary - more common, poorly understood.

Secondary - preceding inflamm disease, trauma or metabolic factor (e.g. excessive Fe in hemochromatosis)

Front 3

Prevalance of major musculoskeletal issues

Back 3

OA by far most common. Then RA, gout, juvenile idiopathic arthritis.

Then...fibromyalgia, spondylarthritides, systemic lupus erythematosus, systemic sclerosis, Sjogren’s syndrome, polymyalgia rheumatica, giant cell arthritis, back/neck pain

Front 4

Labs of OA

Back 4

ESR<40, Rheum factor is <1:40, noninflammatory synovial fluid (bland appearing)

Front 5

Radiograph of OA

Back 5

Osteophytes, joint space narrowing, subchondral cysts and sclerosis, malalignment.

Front 6

RA is a disease of...

Back 6

synovium

Front 7

Psoriatic arthritis is a disease of...

Back 7

synovium and enthesis

Front 8

Diseases where something gets into the joint that shouldn't be there

Back 8

Acute presentation.

Gout, pseudogout, septic arthritis.

Front 9

OA is a disease of...

Back 9

cartilage

Front 10

Cause of inflamm in OA

Back 10

Debris of bone entering joint space as it is degraded.

Front 11

Chondrocyte changes in OA

Back 11

Hypercellularity and loss of mucopolysacch from matrix resulting in less red dye fixation.

The chondrocytes multiply, cluster, etc.

Front 12

Later changes in OA

Back 12

5. Progressive fibrillation & loss of cartilage

6. Bony changes: osteophyte formation & subchondral sclerosis

7. Modest inflammatory infiltrates in synovium

8. Ligamentous laxity (cart or horse?)

9. Weak periarticular muscles (cart or horse?)

10. “Macro” erosion of cartilage; “bone-on-bone”

Front 13

Early change sin OA

Back 13

1. Small tangential clefts on surface of already altered hyaline cartilage.
2. Deeper vertical cleft has appeared
3. The splitting process of fibrillation
4. Clumping of chondrocytes

Front 14

OA is caused by..

Back 14

both abnormal stresses on normal cartilage and normal stress of abnormal cartilage.

Front 15

Chondrocyte

Back 15

Low metabolic activ, the only cell type in adult cartilage matrix, gives integrity to the cartilage matrix, has little regen capacity.

In OA, they promote matrix degradation (through inflammatory mediators) and down-reg of processes essential for cartilage repair.

Front 16

Main mediators in OA

Back 16

chondrocytes produce IL-1 beta and TNF. And matrix metalloproteinases.

Front 17

CRP with OA

Back 17

goes up slightly.

with RA, it goes up a ton.

It is an inflamm marker.

Front 18

Joints affected by OA

Back 18

shoulder, clavicolo-sternal, hands, hip, knee, big toe.

Front 19

Hand joints inv in OA

Back 19

DIP and PIP. And a tender knob on thumb.

Rarely MIP!

Front 20

Heberden's nodes

Back 20

DIP

Front 21

Bouchard's nodes

Back 21

PIP

Front 22

Radiology of OA

Back 22

Extra bone is present and joint spaces are obliterated

Front 23

Acute Heberden's node

Back 23

Filled with fluid that is tenacious and gooey.

These nodules then transform to be hard and typical of OA

Due to inflammation acutely.

Front 24

Inflammatory/erosive OA

Back 24

A subtype of OA.

It is more inflammatory, it is erosive and without periarticular osteopenia (which is seen in RA)

More aggressive and deforming, responds to prednison.

Presents similarly to psoriatic arthritis.

Front 25

Knees and OA

Back 25

Medial aspect usually --> bow legged knees

If lateral aspect - bows inward.

Front 26

Males or females get OA more?

Back 26

females.

Front 27

Risk factors for OA

Back 27

Inc age, obesity, joint injury, previous deformity, ligamentous laxity.

Genetics play a huge role!

Front 28

Does moderate running put you at risk of OA?

Back 28

no, but violent sports or twisting sports are bad.

Front 29

What single gene has been IDed to account for typical OA?

Back 29

there is no single one.

Front 30

Causes of secondary OA

Back 30

Inflamm joint disease, endocrinopathies, metabolic diseases.

Front 31

If you see OA of the MCPs in a younger person...

Back 31

Suspect hemochromatosis!!!!!

Front 32

Tx of OA

Back 32

Just for the pain and sx.

weight loss, acetaminophen, glucosamine/chondroitin, NSAIDS, COX-2, cortison injections...

Front 33

Should you exercise quads to prevent OA?

Back 33

Yes, unless you have misalignment.

Front 34

Glosamine-sulfate or chondroitin-sulfate?

Back 34

BOTH together with pts with severe OA can benefit.

They help with pain, not progression, of OA.

Front 35

Arthoscopic surgery

Back 35

Cleans out all the crud in the joint space.

Found to be no serious benefit.

Front 36

Hyaluronate injections

Back 36

Modestly helpful.

Front 37

COX-2 vs. NSAIDS

Back 37

COX-2 are much better at stopping cartilage loss.

Front 38

Intraarticular injection of anakinra

Back 38

found not to be all that helpful.

Front 39

Summary

Back 39

OA is the commonest form of arthritis world-wide

Most, but not all, people develop OA somewhere

Age, sex, weight, genetics, & injury are risk factors

OA begins in cartilage & the chondrocyte plays a key role in disease progression

With the exception of wt loss & exercise, nothing has been shown to slow the disease process

To date, medical treatment remains symptomatic, directed at pain relief

Front 40

How many pounds does a women need to lose to reduce CC of OA by 50%

Back 40

10 pounds.

Front 41

Genetics of OA for hands and hips...

Back 41

accounts for 50%

Front 42

Avg life of a prosthetic knee

Back 42

15-20 years.

Front 43

What exercise advice?

Back 43

Aqua therapy is good (gravity and warmth)

shouldn't continue with exercise that gives pain.

quad strength usually good but not with malalignment.

foot wedges with lateral lift helps with lateral knee disease.

Front 44

When to get surgery on knees for OA?

Back 44

when pain is unbearable. women are able to tolerate the pain for longer.

Front 45

OA signs vs. RA

Back 45

OA - PIP, DIP, basilar thumb joint

RA - ULNAR DEVIATION! wrist, MCPs, PIPs. DIP is spared.

Front 46

Which joints can be prosthetically replaced?

Back 46

Good ones - hips and knees
Shoulders - good for pain but not function.
Ankles and MCPs - not that good.