Osteoarthritis Flashcards
Differential of knee pain
When is urgent referral required
Inflammatory
- RA
- Gout
- Pseudogout (calcium pyrophosphate crystal deposition)
- Spondyloarthritis
Infection
- Septic arthritis
- Osteomyelitis
Degenerative
- Osteoarthritis
Soft tissue rheumatism
- Tendonitis
- Bursitis
Trauma
- Fractures
- Dislocation
- Ligamentous injury
- Patella problems
Tumors
Urgent referral: Red flags for Infection, trauma, malignancy
What lab investigations are needed to differentiate gout VS RA vs septic arthritis vs pseudogout
- Haematologic tests
- Erythrocyte sedimentation rate (ESR)
- C-reactive protein
- Rheumatoid factor
- Anticitrullinated protein antibody (ACPA/anti-CCP)
- Joint aspiration (crystals - gout, WBC - septic)
- X-ray / MRI (imaging to see extent of damage, may not see in early stages, however can be used to evaluate progression/tx outcomes)
What is OA?
Degenerative disease (with synovial inflammation) of bone and joint cartilage
more than just ‘wear and tear’
progressive and irreversible loss of cartilage
Prevalence of OA
Increases with age
- <50y: men > women (could be sports related)
- > 70y: women > men (esp OA in hands)
Risk factors for OA
- Genetic predisposition (e.g., mutation in collagen type in cartilage)
- Anatomic factors (anatomical defects - e.g., bow-legged, valgus alignment, knocked-knee)
- Joint injury (result in inflammation => cytokines have pro-catabolic and reduced anabolic activity, result in cartilage breakdown)
- Obesity (incr load on weight-bearing joints)
- Aging (changes in ECM: thinning, dcr hydration, incr brittleness, chondrocalcinosis)
- Gender
- Occupation
Pathophysiology of OA
Compensatory response
1. Cartilage degradation
- Articular cartilage damage
- Chondrocyte repair (maintain ECM + produce cartilage matrix: type II collagen + proteoglycans)
- Chondrocyte undergo phenotypic switch, produce type I collagen which causes weakening and breakdown of the matrix
- Subchondral bone release vasoactive peptides and matrix metalloproteinases that break down collagen, resulting in cartilage loss and apoptosis of chondrocytes
2. Synovial inflammation
- Weakening and degradation of collagen matrix results in formation of fibrillation in cartilage and cartilage ‘shards’
- These shards cause inflammatory and pathologic changes in the joint capsule and synovium
- Lymphocytes and macrophages recruited by synovial membrane to remove debris, produce pro-inflammatory cytokines, causing synovitis
- Effusion (swelling of the knees)
- Synovial thickening (narrowing of joint space)
3. Bone remodeling and osteophyte formation
- Subchondral bones are exposed and rub against each other
- Sclerosis: thickening of the subchondral bone => narrowing of joint space
- Osteophytes: bone spurs, tiny protrusions of bone => causes widening of joints, intended to stabilize the joint in response to a normal mechanical loads
Clinical Presentation of OA
- Pain
- Swelling (from joint effusion)
- Erythematous and Warm
- Morning stiffness <30min
- Limited joint movement
- Functional limitation/instability
- Asymmetrical polyarthritis (typically weight bearing joints): hand, knee, hip, cervical/spine, finger (DIP, CMC)
Pain in OA arises from:
- Activation of nociceptive nerve endings within the joint by mechanical and chemical irritants
- Distension of synovial capsule from increase joint fluid, microfracture, periosteal irritation, or damage to ligament, synovium or meniscus
OA Pain characteristics:
- Insidious onset => slow progression over years
- Worse with joint use, relieved by rest
Usual presentation:
- Stiff in morning
- Gets better after walking for a bit
- Then worsens again with joint use
- Worse at the end of the day
- Pain is most severe over joint line
- Knees: worse going down stairs rather than going up
- NO nocturnal pain
Pain in OA may be associated with:
- Anxiety
- Depression
- Sleep disturbances
3 progressive stages of OA severity:
Stage 1:
- Predictable sharp pain with mechanical insult, limits high-impact activities and modest effect on function
Stage 2:
- Pain becomes more constant, with unpredictable episodes of stiffness => daily activity start to be affected
Stage 3:
- Constant dull/aching pain punctuated by episodes of often unpredictable intense, exhausting pain => severe limitations in functions
History taking for suspected OA:
- Pain (deep, aching character; occurs on motion)
- Morning stiffness <30min (resolves with motion, recurs with rest)
- Impacts ADL negatively
- Instability of weight-bearing joints
- Symptoms related to weather
Physical exam for suspected OA:
- Asymmetric monoarticular or oligoarticular
- Crepitus on motion
- Reduced range of motion
- Transient joint effusion
- Palpable warmth
- Bone tenderness
- Bone enlargement (e.g., deformities on fingers - Heberden’s/Bouchard’s node; distal)
- Muscle wasting/atrophy
Radiographic findings for suspected OA:
- Joint space narrowing
- Marginal osteophytes
- Subchondral bone sclerosis
- Abnormal alignment of joint
Note: typically only can see in advanced disease; not routinely done
Laboratory findings for suspected OA:
ESR <20mm/h (inflammatory marker)
[Diagnosis of OA]
Clinical diagnosis made without imaging in:
(May be diagnosed without radiography/lab investigations in presence of typical S&S in at-risk age group)
Based on NICE:
- >=45y
- Activity-related joint pain (one or few joints)
- Morning stiffness =<30min or no morning stiffness
RECALL clinical presentation:
- Pain
- Swelling (from joint effusion)
- Erythematous and Warm
- Morning stiffness <30min
- Limited joint movement
- Functional limitation/instability
- Asymmetrical polyarthritis (typically weight bearing joints): hand, knee, hip, cervical/spine
