OA definition
- Degenerative disease (with inflammation) of bone & joint cartilage
- Add on to the pre-existing wear and tear
- Impaired repairing process of joints
cases
- Wear and tear
- Not inflammatory initially
- Pain grows with use (more damage)
- Degenerative joint disease
- Progressive and irreversible loss of cartilage
- Most common inflammatory joint disorder
patho of OA
1) Articular cartilage damage
2) Chondrocyte activity (To remove and repair damage)
3) Aberrant chondrocyte – incr breakdown of cartilage
4) Apoptosis of chondrocyte
a. Cartilage loss
b. Subchondral bone release of vasoactive peptides & MMP (more collagen break down)
effect of chondrocyte apoptosis
- production of collagen and the extracellular matrix
5) Formation of fibrillation (cracks) in cartilage & cartilage shards
a. inflammation in joint capsule and synovium
b. effusion and synovial thickening
c. pain (nerve endings in joint)
6) subchondral bones rub against each other
a. smooth (eburnation), brittle
b. decr weight bearing ability
inflammatory – > compensatory response
1) Cartilage degradation (joint space narrow)
2) Bone remodeling (sclerosis, osteocytes)
3) Synovial inflamm
cartilage degradation
a. Articular cartilage damage –> chondrocytes proliferate, phenotypic switch
b. Produce improper mineralised collagen
c. Weaken and degradation of collagen matrix in synovium
Bone remodeling (sclerosis, osteocytes)
- Weakened collagen matrix –> thickening of subchondral bones
i. Sclerosis
ii. Osteophytes, bone spurs - Widen joints to try to stabilise
- Response to abnormal mechanical loads
synovial inflam
a. Weaken and degradation of collagen matrix –> cartilage flakes off (shards)
b. Lymphocytes and macrophages recruited by synovial mem (Remove debris)
c. Proinflamm cytokines produced
d. Synovitis (inflamm)
- Disease progression. More proinflamm cytokines & DAMPs (damage-associated molecular patterns)
features of OA
- Sclerosis (thickening of bone)
- Microfractures
- Osteophytes (compensatory struc to stabilise OA joints)
risk factors
- Genetic predisposition
- Mutation in collagen types II, IX, XI, GDF-5
- Anatomic factors
- Misalignment
○ Bow-legged, knocked knees
- Misalignment
- Joint injuries
- Sports, surgery
- Obesity
- Load on weight-bearing joints
- Metabolic OA
- Aging
- Change in ECM: thin, brittleness, dehydration
- Gender, occupation
- Activities, stress on knee
presentation of OA
- pain
- swelling (joint effusion w/ severity)
- erythematous, warm
- Morning stiffness < 30mins
- Resolves with motion
- Recurs with rest
- Worsens with joint use (late afternoon/ night pain)
- Limited joint movements
- Functional limitation/ instability
- Asymmetrical polyarthritis (weight-bearing joints)
- Hand, knee, hip
- Depend on factors that triggered (trauma)
- Hand, knee, hip
OA pain stage
- Insidious onset (slow progression over yrs)
- Worse with joint use, relieved by rest
○ Going down stairs/ slope
○ Most severe over joint line - Assoc w/: ANX, DEP, sleep disturbances
stage 1: predictable sharp pain with insult (modest effect on function)
stage 2: constant pain, unpredictable stiffness (daily activity affected)
stage 3: constant dull/ ache pain. ep of intense unpredicted pain (severe limit function)
physical exam of OA
- Asymmetric monoarticular or oligoarticular
- Crepitus on motion (air, cartilage shards)
- Reduced range of motion
- Transient joint effusion (incr w/ severity)
- Palpable warmth
- Bone tenderness
- Bone enlargement (fingertips: node)
radiographic exam and lab exam
Radiographic (mostly in ADVANCED STAGE)
- Joint space narrowing
- Marginal osteophytes
- Subchondral bone sclerosis
- Abnormal alignment of joint.
Lab
- ESR < 20mm/h (no inflamm)
dx of OA
- Diagnosed w/ or w/o radiography or lab investigations in presence of typical s&sx (at risk grp)
* Radiographic changes may not be observed until severe (joint space, sclerosis, spurs)
* dx w/o imaging for (>45yo, activity related joint pain, morning stiff <30mins) - additional test for (younger indiv/ atypical s&sx)
* hx of recent trauma, rapid worsen/ deformity, infeciton/ malignancy/ red flags
investigation for differentials dx
- May need joint aspiration (synovial fluid)
- Crystals, WBC
○ Gout? Septic arthritis? - RF, anti-CCP
○ RA - ESR, CRP
○ Inflammatory markers - Imaging
○ Extent of damage
○ Early disease may not be visible (But to have a baseline) - Evaluate tx outcomes
tx plan
1) pain relief (inflammation if any)
2) improve/ preserve range of motion (non-pharm)
3) QOL
pain relief using
1) analgesics (TOP –> PO)
2) slow acting (IA CS)
3) Others - duloxetine, capsaicin
1) pain relief, anti-inflam
- Paracetamol
- Non-selective NSAIDs (diclofenac)
○ Accumulates in joint, longer t1/2 (less GI ADR + better analgesic effects)
○ Topical –> PO - COX2i (celecoxib)
- Corticosteroids
NSAIDS consideration
1) Topical NSAIDs (esp for knee)
a. Diclofenac gel, ketoprofen plaster
b. Considerations: hand (washing), deep joints (hip)
2) Oral (NSAIDs/ coxibs)
a. Considerations: GI, CVS, renal toxicity, AERD,
b. Lowest effective dose, PRN
c. +/- PPI/ change to COXIBS
other analgesics
- paracetamol (ST, mod-severe, NSAID CI)
- tramadol (ST, mod-severe, constipation)
- duloxetine (SNRI, mod-severe, CI/ Fail NSAID)
* 5HT3 (GI, sexual), hypoNa, bleed risk, EPSE - top capsaicin
* agonist for TRPV1 expressed on nociceptive nerve fibers. initial enhance pain –> defunctionalisation and reduce TRPV1)
* TOP site rxn (burn, erythema, pain)
2) sx slow acting drug
Intra-articular hyaluronic acid
* Large glycosaminoglycan (naturally found in synovial fluid)
○ Shock absorber
○ Traumatic energy dissipation
○ Protective coating of cartilage
○ Lubrication
○ Reduce pain & stiffness
* Induce biosynthesis of HA & ECM
IA CS duration & CI
- ST sx relief (4-6wk relief). Mod-severe pain, CI/ fail with NSAIDs
○ No LT benefit w/ regular use - <3 inj/ yr (4mnths)
- CI: periarticular infection/ septic arthritis/ periarticular fracture, joint instability, juxtaarticular osteoporosis
# risk due to effect on osteoblasts & osteoclast
3) suppl
Chondroitin sulphate, glucosamine supplements
- Inadequate or inconsistent evidence
