Osteoarthiritis

Question 1

Define Osteoarthritis

Answer 1

Natural wear and tear of joints over time. NOT an inflammatory condition.
Progressive loss of articular cartilage and remodeling of underlying bone, due to genetic factors, overuse and injury.

Question 2

Pathophysiology of OA.

Answer 2

OA = Imbalance between degradation of cartilage and chondrocytes repairing it – leads to structural issues in articular cartilage.

1. When cartilage is broken down – chondrocytes and synovial tissue increases release of inflammatory cytokines (e.g TNF- α and IL-1) – these cytokines trigger an inflammatory cascade (i.e the release of more cytokines).
2. Together all these cytokines increase MMP activity and decrease the production of inhibitors of these MMP / degradative enzymes.
3. The chondrocytes respond to the degradation by increasing rate of matrix synthesis and by releasing anti-inflammatory cytokines. BUT the degradative activity ultimately outweighs this.
4. Breakdown and loss of the cartilage (chrondropenia) reveals the underlying subchondral bone undergoes sclerosis (hardening/ thickening) – if cartilage wears down completely the bone will rub on bone.
   o Overtime:
    Joint space is lost progressively over time
    Formation of osteophytes – small abn formation of bone (bony lumps)
    Subchondral bone cyst – fluid filled sac that born on bones that make up joint (knee and hip).

Question 3

Risk factors for OA.

Answer 3

can be primary or secondary

obesity

advanced age

manual labour job/ sporting activity

female

FHx

Question 4

What joints does OA typically affect?

Answer 4

Commonly affects: hips, knee, sacro-iliac joint, DIP in hands, wrist, cervical spine and CMC joint of thumb.

Question 5

Symptoms of OA

Answer 5

• Usually unilateral
• Joint pain and stiffening – insidious onset, chronic and gradually worsening.
• Pain is worse with activity and relieved by rest.
• Morning stiffness lasts < 20 min
• Pain is worsens throughout the day, but stiffness improves.
• Prolonged OA – deformities and reduced range of movements.

Question 6

How does OA differ from inflammatory conditions?

Answer 6

In OA the ain gets worse w/movement/ exercise and stiffness is not prolonged (morning stiffness < 20 mins)

Contrast – inflammatory arthropathies – the pain improves with movement and morning stiffness is > 30mins.

Question 7

What are the signs of OA on examination?

Answer 7

• Bouchard nodes (swelling of PIPJs)
• Heberden nodes (swelling of DIPJs) in the hands
• Fixed flexion deformity – when unable to fully straighten, bend or move limb.
• Varus malalignment in the knees – aka bowlegged – knee deviate out.
  o Happens when tibia turns inwards instead of aligning w/ femur.
• Movement of joint is reduced and painful/ weak grip.
• Crepitus (crunchy sound/ feeling).
• Swelling over joint – won’t be hot/swollen.
• Squaring at the base of the thumb (saddle joint) – lot of use in everyday – therefore likely to wear out.

Question 8

How is OA diagnosed?

Answer 8

• Diagnose OA WITHOUT any investigations if Ptx is >45yrs, pain after activity AND has no morning stiffness or stiffness lasting < 30 mins.

other cases:
- bloods to rule out inflammation and infection
- Xray to see changes and rule out fracture

Question 9

What are the radiological features/changes are seen in OA?

Answer 9

 L – Loss of joint space
 O – Osteophytes
 S – Subchondral sclerosis (increased density of the bone along the joint line) – white line on bone
 S – Subchondral cysts (fluid-filled holes in the bone, aka geodes)

Question 10

How is OA managed?

Answer 10

• conservative Mx = weight loss, exercise, physio, walking aids, ice packs etc.
• medical - analgesia:
  1. Oral paracetamol and topical NSAIDs or topical capsaicin.
  2. Add oral NSAIDs and consider PPI to protect stomach. NSAIDs better used intermittently rather than continuously.
  3. Consider opiates e.g codeine and morphine - Use w/ caution

intra-articular injection is severe cases

• surgical - arthroplasty, osteotomy and arthrodesis.