OA and DJD

Question 1

Prevalence of OA is ↑↑↑ due to what 2 factors?

Answer 1

Obesity & Aging populations

Question 2

OA is the leading cause of what?

Answer 2

Pain and disability in LE in older patients

Question 3

RF for OA

Answer 3

1. Age >55
2. F
3. Obesity
4. Occupation: repetitive motion or physical labor
5. Mutations: in proteins involved in bone/articular cartilage structure
6. Joint loading
7. Injury- trauma
8. Malalignment

Question 4

What is OA?

Answer 4

Disabling joint disease characterized by a noninflammatory degeneration of the joint complex (articular cartilage, subchondral bone, and synovium) that occurs with old age or from overuse.

Question 5

Pathophysiology of OA

Answer 5

Combination of MANY stressors:

1. Aging
2. Loss of hyaline articular cartilage (type 2 collagen and proteoglycans - aggrecan)
3. ↑↑↑ thickness and sclerosis of subchondral bone plate
4. Outgrowth of osteophytes at the joint margin
5. Joint injury
6. Degeneration of ECM

Synovial inflammation with hypertrophy and effusion

Inflammatory cytokines (IL-1B and TNF-a) => destroy tissue

Weakness of muscles that bridge the joint.

Question 6

Characteristics of OA

Answer 6

1. Altered function of chondrocytes
2. Thinning/loss of cartilage
3. Thickening/ sclerosis and cyst formation in subchondral bone
4. Remodeling of bone
5. Marginal spurs: ostephytes
6. Mild reactive synovitis

Question 7

What joints does OA usually affect?

Answer 7

Weight bearing joints and joints you use frequently:

1. Hips
2. Knees
3. Spine (Cervical and lumbar)
4. Hands (DIP, PIP, 1st CMC –thumb base)

Question 8

Describe the pain experienced with OA

Answer 8

1. Affects 1 or a few joints at a time
2. Insideous onset of intermittant symptoms that become more persistant and severe over time.
3. Pain is worse with activity, ↓↓↓ with restm MC in hands, hips and knees
4. Brief morning stiffness: lasts about 30 minutes

Question 9

PE findings of OA

Answer 9

1. Crepitus, ↓↓↓ ROM, effusion (hands are cool, not hot)
2. Bone swelling: Heberdens (DIPS) and Bouchard nodes (PIPS)
3. Hip involved=> groin pain
4. Knees involved => pain when walking or climbing stairs
5. Spondylosis in OA of spine => spinal stenosis.
6. Joint instability

Question 10

Labs and joint fluid in OA patient

Answer 10

1. ↑ ESR with synovitis
2. Joint fluid: straw-clear colored with good viscosity; WBC < 2000/uL
   
   1. Look for crystals or infection

Question 11

Imaging of OA

Answer 11

1. Asymmetric joints - joint narrowing
2. Joint mice (loose bone fragments)
3. Subchondral sclerosis (thickening) and cysts
4. Ostephytes and marginal lipping

Question 12

What is Erosive/inflammatory OA; seen most often in whom?

Answer 12

• Affects DIP and PIP joints; causing more pain than typical hand OA
• More common in women

Question 13

What is commonly seen on XR in pt with Erosive OA and how can it be differentiated from RA?

Answer 13

Central erosions (vs. marginal erosions in RA) w/ “seagull” appearance in joints of fingers

Question 14

In secondary OA, what joints are affected?

Answer 14

Secondary OA can occur in joints not typically affected in primary OA

Question 15

Which endocrine abnormality can cause secondary OA; which joints most often affected?

Answer 15

- Hyperparathyroidism => affects wrist and MCP

Question 16

Which underlying GI disease can cause secondary OA; which joints most often affected?

Answer 16

Hemochromatosis: 2nd/3rd MCP joints and wrist

Question 17

OA

1. Primary joints affected
2. Heberden nodes
3. Joint characteristics
4. Stiffness
5. Lab findings

Answer 17

1. DIP and CMC (carpometacarpal)
2. Often present
3. Hard, bony, cold
4. Brief 30 minute morning stiffness: worse after effort
5. Lab findings
   
   1. (-) Rheumatoid factor
   2. (-) Anti- CCP AB
   3. NL ESR and CRP

Question 18

RA

1. Primary joints affected
2. Heberden nodes
3. Joint characteristics
4. Stiffness
5. Lab findings

Answer 18

1. MCP and PIP
2. Non
3. Soft, warm and tender
4. Stiffnes is worse after resting (morning)
5. Labs
   
   1. (+) Rheumatoid factor
   2. (+) anti-CCP AB
   3. ↑↑↑ ESR and CRP

Question 19

OA DDx

Answer 19

1. Pseudogout (calcium pyrophosphate deposition) in the hands/knees
   
   1. X-rays show cartilage calcification (chondrocalcinosis)
2. Gout can coexist with OA, particularly in DIP joint
3. Psoriatic arthritis can involve DIP;
   1. Causes morning stiffness, joint swelling dactylitis and history of psoriasis
4. Charcot Joint
5. RA
6. Osteonecrosis

Question 20

What is seen with Diffuse Idiopathic Skeletal Hyperostosis (DISH); what are the criteria?

Answer 20

- Non-inflammatory condition where you get calcification and ossification of spinal ligaments (anterior longitudinal ligament) and enthesis (where tendon/lig. attach to bone) => back pain.

- SI joints NOT involved* (T-spine is more often involved)

- Ossifications of at least 4 contiguous vertebral levels, usually on the R side of spine

Question 21

DISH is MC in who?

Answer 21

Males

Question 22

Cure for OA

Answer 22

NO CURE: nothing can prevent, delay or remit the progression of OA

- Nonpharmacologic ++++ pharmacologic treat for pain and disability

Question 23

What are the non-pharmacologic treatment for OA?

Answer 23

1. Education on OA and joint protection
2. WL
3. Proper footwear + cane + bracing
4. Isometric - aerobic exercise + strength training

Question 24

Pharmacologic treatment for OA

Answer 24

1. Oral agents:
   
   1. NSAIDS
   2. Duloxetine (Cymbalta)
   3. Tramadol (Ultram)
   4. Acetominophen COX2 inhibitors (watch side effect)
2. Topical capsaicin cream on hands and knees
3. Topical NSAIDS
4. Glucocorticoid /hyaluronic acid intra-articular injections into knee or hip.

Question 25

Surgery for OA

Answer 25

1. Total joint replacement: can get infection and hardware loosening