Knee Osteoarthritis
Degenerative joint disease of the knee characterized by progressive articular cartilage loss, subchondral bone remodeling, osteophyte formation, and chronic pain with functional impairment.
Osteoarthritis (OA) — let's break down the name: "osteo" = bone, "arthro" = joint, "itis" = inflammation. Though traditionally thought of as a purely "wear-and-tear" degenerative disease, we now understand it as a whole-joint disease involving cartilage, subchondral bone, synovium, ligaments, capsule, and periarticular muscles [1].
OA is a whole person disease — it is not simply cartilage wearing out. It encompasses susceptibility of joints to damage, failure of repair mechanisms, and the downstream symptomatic and structural consequences [1].
Knee osteoarthritis (KOA) specifically refers to the progressive, heterogeneous condition characterised by the degradation of articular cartilage, subchondral bone remodelling, osteophyte formation, and synovial inflammation affecting one or more of the three compartments of the knee joint (medial tibiofemoral, lateral tibiofemoral, patellofemoral) [1][2].
Key Concept
KOA is not just "cartilage loss." It is a disease of the entire joint organ — including subchondral bone sclerosis, synovitis, meniscal degeneration, ligament laxity, and periarticular muscle weakness. Think of it as "joint failure," analogous to heart failure being failure of the whole cardiac system, not just the myocardium.
2. Epidemiology
- The Global Burden of Disease (GBD) study estimates almost 1 billion individuals will have OA by the year 2050 [1].
- KOA is a major cause of adult disability worldwide [1].
- OA is the most common form of arthritis globally and the single most common cause of disability in older adults.
- Prevalence increases steeply with age: approximately 10% of men and 13% of women aged ≥ 60 have symptomatic KOA.
- The knee is the most commonly affected large joint.
- By 2050, the World Health Organization forecasts that 40% of the population in Hong Kong will be aged 65 or above, ranking fifth in the world [1].
- This demographic shift means KOA will become an enormous healthcare burden in Hong Kong — more elderly people = more OA = more joint replacements, more disability, more healthcare costs.
- Secondary OA of the hip is more common in Chinese populations (often related to developmental dysplasia of the hip and AVN), but primary OA of the knee is the predominant large-joint OA in Hong Kong [2][3].
OA is a serious disease — it is associated with [1]:
- Increased risk of cardiovascular and respiratory disorders (because pain and stiffness → reduced physical activity → metabolic syndrome → CV risk)
- Increased risks of psychological disorders (chronic pain → depression, anxiety)
- Increased risks of sleep disturbance (nocturnal pain, difficulty repositioning)
- Increased risk of mortality (likely mediated through reduced mobility, comorbidities, and polypharmacy)
Why Does OA Increase Mortality?
This surprises many students. The mechanism is indirect: chronic pain → immobility → obesity/metabolic syndrome → cardiovascular disease. Additionally, NSAIDs used chronically for OA carry their own cardiovascular and GI risks. OA patients also have higher rates of depression, which independently increases mortality.
3. Risk Factors
| Risk Factor | Explanation |
|---|---|
| Age | Aging is the strongest risk factor. Cartilage loses water content, proteoglycan concentration decreases, and repair capacity diminishes with age. But note: aging ≠ OA (see biochemical differences below) |
| Female sex | Women have higher prevalence, especially post-menopause — oestrogen has chondroprotective effects; its loss accelerates cartilage degradation. Women also have different knee biomechanics (wider pelvis → increased Q angle → more lateral patellofemoral stress) |
| Genetics / Heredity | Heredity is a recognised primary cause [1]. Polymorphisms in genes encoding collagen type II, aggrecan, and GDF5 contribute to susceptibility |
| Risk Factor | Explanation |
|---|---|
| Obesity | Osteoarthritis is more common in people at the extremes of body weight and often takes a toll on weight-bearing joints like the knees, hip [1]. Mechanism is twofold: (1) Mechanical — increased joint loading (every 1 kg of body weight = ~4 kg of force across the knee during walking); (2) Metabolic — adipokines (leptin, adiponectin) and systemic low-grade inflammation from adipose tissue directly damage cartilage, which explains why obese patients also get OA in non-weight-bearing joints like hands |
| Injury / Previous trauma | Acute trauma is a major secondary cause [1][2]. ACL tears, meniscal injuries, tibial plateau fractures, and patellar fractures → altered joint biomechanics and direct cartilage damage → post-traumatic OA. A young person with OA knee — always ask about previous trauma and chronic joint instability [2] |
| Occupation | Repetitive knee loading — farmers, miners, carpet layers, construction workers. Prolonged kneeling and squatting are particularly damaging |
| Mechanical stress | Mechanical stress is listed as a primary cause [1]. Malalignment (varus/valgus), joint dysplasia, leg length discrepancy all concentrate force on specific compartments |
| Muscle weakness | Quadriceps weakness is both a risk factor and a consequence. The quadriceps act as "shock absorbers" for the knee; weakness → increased impact loading on cartilage |
| Low bone density | Paradoxically listed as a risk factor — the relationship is complex. Higher bone density may actually predispose to OA through stiffer subchondral bone that transmits more stress to cartilage |
- Defective load (force): Obesity, occupational overuse
- Defective load (area): Joint dysplasia (e.g., developmental dysplasia of the hip)
- Defective cartilage — damage: Trauma, haemophilia (recurrent haemarthroses destroy cartilage)
- Defective cartilage — disease: Inflammatory arthritis (RA), metabolic (gout, pseudogout/CPPD), infection
- Unsupported cartilage: Avascular necrosis (AVN — subchondral bone dies → overlying cartilage collapses)
- Surgery (e.g., previous meniscectomy removes the "shock absorber" → increased point-loading on cartilage → accelerated OA) [1]
- Congenital abnormalities [1]
- Rheumatoid arthritis or other inflammatory conditions [1]
- Diabetes or other hormone disorders [1] (diabetes → advanced glycation end-products in cartilage → stiffening and increased susceptibility to damage; also associated with metabolic syndrome)
- Infective causes → post-septic arthritis OA [1]
Primary vs Secondary OA
A common exam trap: Primary (idiopathic) OA — elderly patient ( > 70y), no identifiable cause beyond aging. Secondary OA — younger patient ( < 50y), there IS a cause (trauma, inflammatory, metabolic, congenital). If a 35-year-old presents with KOA, you MUST look for a secondary cause.
4. Anatomy and Function of the Knee Joint
Understanding the anatomy is essential to understanding why OA affects the knee the way it does.
The knee joint is the largest and most complex synovial joint in the body. It comprises three compartments:
- Medial tibiofemoral compartment — between the medial femoral condyle and medial tibial plateau
- Lateral tibiofemoral compartment — between the lateral femoral condyle and lateral tibial plateau
- Patellofemoral compartment — between the patella and femoral trochlear groove
Three compartments: medial, lateral, patellofemoral [2].
Why is the medial compartment most commonly affected?
- Genu varum (bow-legged alignment) in normal individuals → medial compartment most commonly affected [2].
- The mechanical axis of the lower limb normally passes slightly medial to the knee centre. In most people, there is a slight physiological varus, meaning 60–70% of the load is borne by the medial compartment. Over time, this preferential loading accelerates medial compartment wear.
- Hyaline cartilage covers the articular surfaces (femoral condyles, tibial plateaus, posterior surface of patella).
- Composed of: water (65–80%), type II collagen (15–22%), proteoglycans (aggrecan) (4–7%), and chondrocytes ( < 5% of volume).
- Chondrocytes are the only cells in cartilage — they produce and maintain the extracellular matrix (ECM). They are avascular, anueral, and alymphatic, receiving nutrition solely by diffusion from synovial fluid.
- Proteoglycans (especially aggrecan) attract water via osmotic pressure, giving cartilage its compressive resistance — like a sponge that resists being squeezed.
- Type II collagen provides tensile strength — the "rebar" in the concrete.
- Cartilage is avascular and anueral — this is why: (1) it has very limited healing capacity, and (2) early cartilage damage is painless (the pain in OA comes from subchondral bone, synovium, capsule, and periarticular structures, NOT from the cartilage itself).
- Fibrocartilaginous C-shaped (medial) and O-shaped (lateral) structures sitting on the tibial plateaus.
- Functions: load distribution, shock absorption, joint stability, lubrication, proprioception.
- Loss of meniscus (e.g., after meniscectomy) → reduced contact area → increased point-loading → accelerated OA. This is why meniscal-preserving surgery is preferred over total meniscectomy.
- ACL and PCL (cruciate ligaments) — provide anteroposterior stability.
- MCL and LCL (collateral ligaments) — provide mediolateral stability.
- Chronic instability from ligament deficiency → abnormal joint kinematics → accelerated OA.
- The synovial membrane lines the inner surface of the joint capsule (but NOT the articular cartilage surface).
- Produces synovial fluid — a dialysate of plasma enriched with hyaluronic acid (HA).
- HA provides viscosity and lubrication. In OA, HA concentration and molecular weight decrease → thinner, less protective fluid.
- The layer of bone just beneath the articular cartilage.
- Acts as a "shock absorber" — distributes load from cartilage to cancellous bone.
- In OA, subchondral bone undergoes sclerosis (thickening) and cyst formation — both visible on X-ray.
- Standing scanogram of bilateral lower limbs is used to assess alignment [2].
- Tibiofemoral angle (TFA): the angle between the anatomical axes of the femur and tibia. Normal is ~5–7° of valgus.
- Mechanical axis of the lower limb: a line from the centre of the femoral head to the centre of the ankle. Normally passes through or just medial to the centre of the knee.
- If it passes through the medial side → varus malalignment → medial compartment overloaded.
- If it passes through the lateral side → valgus malalignment → lateral compartment overloaded [2].
5. Pathophysiology
OA is fundamentally a failure of the joint as an organ. The disease process involves all joint tissues simultaneously, though cartilage degradation is the hallmark.
Biochemical changes of articular cartilage in aging and osteoarthritis [4]:
| Parameter | Aging | Osteoarthritis |
|---|---|---|
| Water content | Decrease | Increase (early — oedema of cartilage as proteoglycan matrix breaks down and can't retain water in an organised manner) |
| Collagen | Relatively unchanged | Becomes disorderly; decrease in severe OA |
| Proteoglycan concentration | Decrease | Decrease |
| Proteoglycan synthesis | Decrease | Increase (attempted repair — chondrocytes try to compensate but produce inferior quality proteoglycans) |
| Proteoglycan degradation | Decrease | Markedly increase (this is the key — degradation far outstrips synthesis) |
| Chondroitin sulphate concentration | Decrease | Increase (shift in GAG composition — more chondroitin sulphate, less keratan sulphate, reflecting immature/reparative cartilage) |
Aging ≠ OA
This table is high yield. The key distinction: in aging, everything slows down (synthesis AND degradation both decrease). In OA, there is a net catabolic state — degradation markedly increases and outpaces the attempted increase in synthesis. OA is an active, metabolically driven process, NOT just passive wear.
5.3 Molecular Biology of KOA
Biology of OA Knee — the molecular cascade [5]:
This is a complex interplay between mechanical stress, inflammation, and failed repair:
- Increased loading, cytokines, growth factors, Wnts act on chondrocytes [5].
- Mechanical overload → chondrocyte stress → release of damage-associated molecular patterns (DAMPs).
- Stressed chondrocytes upregulate ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) and MMPs (matrix metalloproteinases) [5].
- ADAMTS-4 and ADAMTS-5 — "aggrecanases" — cleave aggrecan (the main proteoglycan).
- MMP-13 — "collagenase-3" — cleaves type II collagen.
- These enzymes break down the structural framework of cartilage.
- Simultaneously, inhibition of Collagen II, Proteoglycan, and TIMP (tissue inhibitors of metalloproteinases) occurs [5] — so not only is destruction increased, but the brakes on destruction are released AND new matrix production is suppressed.
- Cartilage antigens (fragments of degraded cartilage) are released into the synovial fluid [5].
- These are taken up by synoviocytes → triggering synovial inflammation (synovitis) [5].
- Inflammatory cytokines and growth factors (e.g., IL-1, IL-6, Wnts) are released by activated synoviocytes [5].
- This creates a vicious cycle: cartilage breakdown → synovitis → more cytokines → more cartilage breakdown.
- Macrophages (M0) are polarised:
- T helper cells (Th0) differentiate into:
- The balance is tipped toward pro-inflammatory (Th1/Th17 and M1) in OA.
- Release of cytokines and degenerative enzymes into the synovial fluid [5] — amplifies the destruction throughout the joint space.
- Subchondral bone sclerosis — thickening of subchondral bone in response to increased mechanical stress (attempted reinforcement) [5].
- Osteophyte formation — bony spurs at joint margins, driven by TGFβ and mechanical stress. These are the body's attempt to increase the joint surface area and redistribute load — a failed repair mechanism [5].
- Fibrosis of the joint capsule and synovium occurs, mediated by TGFβ [5] → contributes to stiffness and reduced ROM.
Natural history of OA: structural changes before symptoms [5]:
Molecular changes → Pre-radiographic structural changes (MRI/biomarkers) →
Radiographic changes (X-ray) → Symptoms → End-stage disease (joint failure/death) →
Joint replacementDefining Disease State of Osteoarthritis [5]:
| Stage | Detection Method | What's Happening |
|---|---|---|
| Initiation of disease process | MRI/Biomarkers | Changes in the composition of bone, cartilage, other soft tissues |
| Pre-radiographic | MRI/US | Structural changes in bone, cartilage, other soft tissues |
| Clinically detectable OA (Radiographic) | X-ray | Structural changes in bone (i.e., joint failure) + Symptoms |
| End-stage disease | Clinical | Joint death → Joint replacement |
More effective to prevent disease progression by intervention at early stages [5].
Clinical Pearl
This natural history is crucial: by the time you see joint space narrowing on X-ray, significant disease is already established. X-rays are relatively insensitive for early OA. MRI can detect early cartilage changes, bone marrow oedema, and synovitis before any radiographic change appears. This is why there's a push toward earlier detection and intervention.
6. Classification
| Type | Details |
|---|---|
| Primary (Idiopathic) | Aging, mechanical stress, heredity [1]. No identifiable underlying cause beyond risk factors. More common in elderly > 70y. |
| Secondary | Identifiable cause — obesity, acute trauma, surgery, congenital abnormalities, RA or other inflammatory conditions, diabetes or other hormone disorders, infective causes [1]. More common in young < 50y. |
Three compartments: medial, lateral, patellofemoral [2]:
- Medial compartment — most common (due to physiological varus and medial load concentration)
- Patellofemoral compartment — common, especially in women; presents with anterior knee pain worse going downstairs
- Lateral compartment — least common in isolation; when present, think of valgus malalignment
- Tricompartmental — all three compartments involved; end-stage disease
Kellgren-Lawrence (KL) classification for OA knee [2]:
| Grade | Description |
|---|---|
| Grade 0 | No joint space narrowing (JSN) |
| Grade 1 | Possible osteophytes, doubtful JSN |
| Grade 2 | Definite osteophytes |
| Grade 3 | Definite JSN |
| Grade 4 | Bone-on-bone deformity |
KL Grading — High Yield
Grade 2 is the radiographic threshold for "definite OA." Grade 4 is bone-on-bone — this is end-stage and typically the point where joint replacement is considered. Remember: radiographic severity does not always correlate with symptom severity — some patients with KL grade 4 have minimal pain, and some with KL grade 2 are severely symptomatic.
WOMAC (Western Ontario and McMaster Universities Arthritis Index) — used to classify OA progression and assess treatment response [2]. It's a patient-reported outcome measure assessing:
- Pain (5 questions)
- Stiffness (2 questions)
- Physical function (17 questions)
Higher scores = worse disease. Used in clinical trials and clinical practice to track disease impact and treatment efficacy.
7. Clinical Features
7.1 Symptoms
Knee pain is the cardinal symptom [2].
- Character: Deep, aching, poorly localised.
- Aggravating factors: Aggravated by exertion, relieved by rest [2]. Weight-bearing activities (walking, standing, climbing stairs) worsen pain. This is because mechanical loading on denuded/thinning cartilage transmits force to the innervated subchondral bone beneath.
- Worse on going downstairs — this specifically implicates the patellofemoral joint [2]. Why? Going downstairs requires eccentric quadriceps contraction, which compresses the patella against the femoral trochlea with forces up to 3–4× body weight. If the patellofemoral cartilage is damaged, this produces significant pain.
- Night pain / rest pain: In advanced OA, pain may occur at rest and disturb sleep — this is a red flag for severe disease (or consider alternative diagnoses like tumour, infection, or inflammatory arthritis).
- Mechanism of pain in OA: Cartilage itself is anueral — it cannot generate pain signals. Pain arises from:
- Subchondral bone: Microfractures, increased intraosseous pressure, bone marrow oedema
- Synovium: Synovitis with inflammatory mediators stimulating nociceptors
- Joint capsule: Stretching from effusion, fibrosis
- Periarticular structures: Ligament strain, muscle spasm, bursitis
- Osteophytes: Periosteal irritation at attachment sites
Morning stiffness < 30 minutes after immobility [2].
- This is an important differentiator from inflammatory arthritis where morning stiffness is typically > 60 minutes (RA) or > 30 minutes (inflammatory).
- Mechanism: During rest, synovial fluid redistributes away from the cartilage surfaces, and the thickened, fibrotic capsule "sets." With movement, fluid returns and the capsule stretches — stiffness resolves quickly.
- Also called "gelling" — the joint "gels" after a period of inactivity (sitting in a cinema, sleeping overnight) and loosens up with a few minutes of movement.
- Intermittent: Due to effusion — overproduction of synovial fluid in response to synovitis or mechanical irritation. Comes and goes with activity levels.
- Continuous: Due to capsular thickening and osteophyte formation — a permanent structural change.
- Progressive deformity develops as cartilage loss becomes asymmetric:
- Genu varum (bow-legged): Medial compartment OA — most common
- Genu valgum (knock-kneed): Lateral compartment OA — less common
- Deformity worsens the biomechanical malalignment → accelerates further cartilage loss in that compartment (vicious cycle).
- Instability [2] — patients report the knee "giving way."
- Mechanism: Ligament laxity (from chronic stretching by effusion and deformity), quadriceps weakness, and proprioceptive loss from degenerate menisci and ligaments.
- Locking of joints [2] — the knee suddenly becomes unable to fully extend.
- Mechanism: Loose bodies (fragments of cartilage or osteophytes) become trapped in the joint, or a degenerate meniscal tear flips into the joint space and mechanically blocks movement.
- True locking (mechanical block) must be distinguished from "pseudolocking" (inability to extend due to pain and muscle spasm).
- Difficulty with activities of daily living (ADLs) — walking, climbing stairs, rising from a chair, putting on shoes/socks.
- Progressively reduced walking distance.
7.2 Signs
- Antalgic gait: Shortened stance phase on the affected side — the patient spends less time weight-bearing on the painful leg.
- In advanced bilateral disease, a slow, shuffling, wide-based gait.
- Trendelenburg gait if hip OA coexists.
- Genu varum (most common in KOA) — inspect from the front with patient standing.
- Genu valgum — less common, lateral compartment disease.
- Joint deformities, e.g., genu varum [2].
- Effusion: Detected by patellar tap test (moderate-large effusion) or bulge/sweep test (small effusion).
- Bony enlargement: Hard, non-tender swelling from osteophytes — palpable along the joint margins. Distinguish from soft-tissue swelling of inflammatory arthritis.
- Bony enlargement at affected joints [2].
- Reduced ROM with crepitations [2].
- Crepitus: Palpable and/or audible grinding sensation during passive knee movement. Caused by roughened, irregular articular surfaces rubbing against each other and by osteophytes.
- Flexion deformity: There are two types [2]:
- Extension lag — the patient cannot actively fully extend the knee, but passive full extension is achievable. This is due to quadriceps weakness (the muscle can't generate enough force to achieve the last few degrees of extension).
- Fixed flexion contracture — the knee cannot be passively fully extended. This is due to structural changes — capsular fibrosis, osteophyte impingement, hamstring contracture.
Extension Lag vs Fixed Flexion Contracture
Students commonly confuse these. Extension lag = correctable passively (muscle problem). Fixed flexion contracture = NOT correctable passively (structural/mechanical problem). Always check BOTH active and passive extension.
- Joint line tenderness — palpable along the medial or lateral joint line (depending on compartment involved).
- Periarticular tenderness — pes anserinus bursitis, iliotibial band syndrome often coexist.
- Quadriceps wasting (especially vastus medialis obliquus — VMO) is common.
- Mechanism: Pain → reflex inhibition of the quadriceps (arthrogenic muscle inhibition) → disuse atrophy. This creates a vicious cycle: weaker quads → less shock absorption → more joint loading → more pain → more inhibition.
- The joint may be slightly warm in the presence of active synovitis, but NOT as hot as in septic arthritis or crystal arthropathy.
8. Radiological Features
Radiological features (LOSS) [2]:
| Feature | Explanation |
|---|---|
| Loss of joint space | Earliest radiographic sign. Due to loss of articular cartilage (cartilage is radiolucent — you see the "space" between bones narrowing as cartilage thins). Asymmetric narrowing is characteristic of OA (cf. symmetric in RA). |
| Osteophytes | Bony spurs at joint margins. Represent attempted repair — new bone formation at the periosteum, driven by TGFβ and mechanical stress. The body is trying to increase the surface area to distribute load. |
| Subchondral sclerosis | Increased density (whiteness) of subchondral bone. Represents bone remodelling — increased osteoblastic activity in response to increased mechanical stress. Like callus formation in bone healing, but maladaptive. |
| Subchondral cysts | Radiolucent areas in subchondral bone. Formed by: (1) intrusion of synovial fluid through microfractures in the damaged subchondral plate, or (2) focal osteonecrosis. Surrounded by sclerotic bone. |
Views [2]:
| View | What it Shows |
|---|---|
| Weight-bearing AP | Medial vs lateral compartment joint space. MUST be weight-bearing — non-weight-bearing AP can underestimate joint space narrowing because the cartilage surfaces aren't compressed |
| Lateral | Anteromedial vs posteromedial changes, posterior osteophytes, patella position (patella alta/baja), tibial slope |
| Skyline (merchant view) | Patellofemoral joint space — assess patellofemoral compartment OA, patellar tilt/subluxation |
| Valgus/Varus stress views | Assess medial/lateral joint space under stress — useful for evaluating ligament integrity and correctable deformity |
| Standing scanogram of bilateral lower limbs | Alignment — tibiofemoral angle (TFA): valgus vs varus; mechanical axis of lower limb: pass through medial or lateral side |
| Schuss view (30° flexion PA) | More sensitive for early OA — the posterior femoral condyles bear most load at 30° flexion, so this view reveals posterior cartilage loss that may be missed on full-extension AP |
Weight-Bearing X-rays Are Essential
A non-weight-bearing X-ray can miss significant joint space narrowing. Always request weight-bearing views for suspected KOA. If a patient has a "normal" knee X-ray but was done non-weight-bearing, it doesn't rule out OA.
This comparison is extremely high-yield for exams [2]:
| Feature | Degenerative (OA) | Inflammatory (e.g., RA) |
|---|---|---|
| Joint involvement | Weight-bearing joints: knee, hip, L-spine, C-spine. Small hand joints: 1st CMC joint, IPJ | Any joint (typically MCP, PIP, wrist in RA) |
| Bone density | Preserved (bone is being remodelled, not resorbed) | Juxta-articular osteopenia (RA) — inflammatory mediators activate osteoclasts near the joint |
| Periarticular bony erosion | No | Yes (RA) — pannus erodes bone |
| Reactive bony changes | Yes (osteophytes, subchondral sclerosis — attempted repair) | No (RA) — destruction without repair |
| Morning stiffness | < 30 minutes | > 60 minutes (RA) |
| Effusion quality | Non-inflammatory (WBC < 2000/mm³) | Inflammatory (WBC 2,000–50,000/mm³) |
| Hand involvement | DIP (Heberden's nodes), PIP (Bouchard's nodes), 1st CMC | MCP, PIP, wrist (spares DIP) |
While the focus is KOA, hand OA features are often tested in comparison:
- Heberden's nodes — bony enlargement at DIP joints (osteophytes)
- Bouchard's nodes — bony enlargement at PIP joints
- 1st CMC joint (base of thumb) — grind test positive (axial compression + rotation reproduces pain)
- UL joints generally spared except 1st CMC and IPJ [2]
High Yield Summary
Definition: KOA = whole-joint disease (not just cartilage) involving cartilage degradation, subchondral bone remodelling, osteophyte formation, and synovitis in the three knee compartments.
Epidemiology: ~1 billion affected globally by 2050. In Hong Kong, 40% population > 65 by 2050. KOA increases mortality via CV disease, depression, immobility.
Risk Factors: Age, female sex, obesity (mechanical + metabolic), previous trauma, occupation, malalignment, muscle weakness, genetics. Secondary causes in young patients — always look for a cause.
Pathophysiology: Catabolic > anabolic. ADAMTS + MMPs degrade cartilage matrix → cartilage fragments trigger synovitis → IL-1, IL-6, TNF → more MMP release → vicious cycle. Subchondral bone sclerosis and osteophytes are failed repair attempts.
Aging vs OA (High Yield Table): In aging, both synthesis and degradation decrease. In OA, degradation markedly increases while synthesis increases insufficiently → net cartilage loss.
Clinical Features: Pain (worse with activity, better with rest; going downstairs = patellofemoral), stiffness ( < 30 min), swelling, deformity (genu varum most common), crepitus, reduced ROM. Extension lag (muscle) vs fixed flexion contracture (structural).
Radiology — LOSS: Loss of joint space (earliest), Osteophytes, Subchondral sclerosis, Subchondral cysts. Always weight-bearing AP + skyline. KL grading: Grade 2 = definite OA, Grade 4 = bone-on-bone.
Key Distinction: OA = preserved bone density, osteophytes, no erosions. RA = osteopenia, erosions, no osteophytes.
Active Recall - Knee Osteoarthritis (Definition to Clinical Features)
[1] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf [2] Senior notes: maxim.md (sections 7.4 OA knee, 9.1 Osteoarthritis) [3] Senior notes: maxim.md (section 6.3 OA hip) [4] Lecture slides: GC 230. Knee Sport Injuries_Part 1.pdf (p19 — biochemical changes table) [5] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p12–13 — biology of OA, natural history)
Differential Diagnosis of Knee Osteoarthritis
When a patient walks into your clinic with a painful, stiff knee, your job is not to jump straight to "OA knee." Your job is to systematically consider what else could be causing this presentation, then use the history, examination, and investigations to narrow down. Think of it this way: "knee pain" is the symptom — OA is only one of many possible diagnoses.
The differential diagnosis of KOA is best approached by considering:
- Anatomical location of the pain (anterior, medial, lateral, posterior)
- Acuity (acute injury vs chronic/insidious)
- Category of pathology (degenerative, inflammatory, crystal, infective, traumatic, referred, neoplastic)
1. Approach by Anatomical Location
Differential Diagnosis of Knee Pain by Anatomic Site [1]:
This is a classic framework and is very high-yield. The knee is a large, complex joint, and different structures live in different compartments. The location of pain gives you a strong clue.
| Condition | Why it mimics KOA / Key Distinguishing Features |
|---|---|
| Patellofemoral pain syndrome (chondromalacia patellae) | Anterior knee pain worse on stairs, squatting, prolonged sitting ("theatre sign"). Common in young women. Differs from OA: younger age, no radiographic OA features, patellar grind test positive. "Chondromalacia" = "chondro" (cartilage) + "malacia" (softening) — softening of the patellar cartilage, a precursor to patellofemoral OA |
| Patellar subluxation or dislocation | History of the patella "popping out," usually laterally. Positive apprehension test on lateral patellar translation. Risk factors: young obese female, patella alta, wide Q angle, genu valgum, shallow trochlear groove [6] |
| Quadriceps tendonitis | Pain above the patella, worse with resisted knee extension. Point tenderness at the superior pole of patella |
| Patellar tendonitis ("Jumper's knee") | Jumper's knee (patellar tendonitis) [1] — pain at the inferior pole of the patella, common in athletes who jump (basketball, volleyball). Point tenderness at patellar tendon origin |
| Tibial apophysitis (Osgood-Schlatter disease) | Osgood-Schlatter lesion [1] — adolescents (10–15 years), pain and swelling at the tibial tuberosity. Traction apophysitis from repetitive quadriceps pull on the growth plate. Self-limiting |
| Housemaid's knee (prepatellar bursitis) | Housemaids Knee [1] — swelling and tenderness directly over the patella (not within the joint). Caused by repetitive kneeling. The bursa is superficial to the patella — fluctuant swelling that doesn't communicate with the joint space |
| Arthritis | Arthritis is listed as an anterior cause [1] — this includes patellofemoral OA specifically |
| Condition | Key Features |
|---|---|
| Medial collateral ligament (MCL) sprain | History of valgus force injury. Tenderness along the MCL (medial joint line to medial femoral epicondyle). Valgus stress test positive [6] |
| Medial meniscal tear | Medial meniscus tear [1] — history of twisting injury while flexed and weight-bearing [6]. Delayed swelling (6–12 hours), joint line tenderness, McMurray test positive, locking in flexion [7]. Degenerative meniscal tears are common in older patients and coexist with OA |
| Pes anserine bursitis | Pes anserine bursitis [1] — pain and tenderness over the anteromedial tibia, ~5 cm below the joint line. "Pes anserinus" = "goose's foot" (the conjoint tendons of Sartorius, Gracilis, semiTendinosus — "Say Grace before Tea" [6]). Common in obese women with KOA — the two conditions often coexist, so don't attribute all medial knee pain to OA without palpating below the joint line |
| Medial plica syndrome | Medial plica syndrome [1] — a plica is a synovial fold (embryological remnant). When thickened/inflamed, it catches over the medial femoral condyle causing snapping and pain. More common in young patients |
| Condition | Key Features |
|---|---|
| Lateral collateral ligament (LCL) sprain | LCL injury [1] — less common than MCL. History of varus force. Tenderness at fibular head/lateral femoral condyle. Varus stress test positive |
| Lateral meniscal tear | Lateral meniscus tear [1] — similar to medial but lateral joint line tenderness |
| Iliotibial band (ITB) syndrome | ITB syndrome [1] — most common cause of lateral knee pain in runners [6]. The ITB is the shared aponeurosis of tensor fasciae latae and gluteus maximus, inserting on Gerdy's tubercle [6]. Repetitive flexion-extension → friction of ITB against the lateral femoral condyle → inflammation. Pain at 30° flexion (Noble's test, Renne test). Risk factors: runners, cyclists, genu varum, hip abductor weakness [6] |
| Condition | Key Features |
|---|---|
| Popliteal cyst (Baker's cyst) | Baker's cyst [1][8] — a popliteal synovial cyst arising from the gastrocnemius-semimembranosus bursa. Usually secondary to underlying joint pathology (OA, meniscal tear, RA) — the joint produces excess fluid which herniates posteriorly through a one-way valve mechanism. Presents with posterior knee pain, stiffness, and a palpable mass behind the knee [8]. Can rupture and mimic DVT (pseudothrombophlebitis syndrome) |
| Posterior cruciate ligament (PCL) injury | PCL injury [1] — mechanism: dashboard injury (direct blow to proximal tibia with knee flexed), hyperextension. Posterior drawer test positive. Less common than ACL |
Baker's Cyst — Don't Forget the Underlying Cause
A Baker's cyst is almost always secondary. In a middle-aged/elderly patient, the underlying cause is usually OA or a degenerative meniscal tear. In a younger patient, think RA or inflammatory arthritis. Always investigate the joint — don't just treat the cyst.
2. Approach by Category of Pathology
This is the more systematic approach for exams — thinking through the broad categories of "what causes a painful, stiff knee?"
- Osteoarthritis (our index condition)
- Degenerative meniscal tear — degenerated meniscus, including degenerative meniscus tears, are very common incidental findings on MRI in patients suffering from osteoarthritis of the knee [7]. This is crucial: in patients with established KOA, an MRI will often show meniscal tears that are incidental and not the primary pain generator. Caution should be exercised against the treatment of "incidental" meniscus lesions found on MRI in patients who have no symptoms of locking [7]. If the patient has no mechanical symptoms (locking, catching), the degenerative meniscal tear is likely a bystander, not the culprit.
- Chondromalacia patellae — softening and fibrillation of patellar cartilage, a precursor/early form of patellofemoral OA.
| Condition | Key Distinguishing Features from OA |
|---|---|
| Rheumatoid Arthritis (RA) | Symmetrical polyarthritis, morning stiffness > 60 min, soft tissue swelling (not bony), RF/anti-CCP positive, radiographs show juxta-articular osteopenia and erosions (NOT osteophytes). Valgus deformity (rheumatoid arthritis) vs varus deformity (osteoarthritis) [1] |
| Psoriatic Arthritis (PsA) | Look for psoriatic skin lesions/nail changes. Can be oligoarticular or polyarticular. DIP involvement (unlike RA). "Pencil-in-cup" deformity on X-ray |
| Ankylosing Spondylitis (AS) | Young male, HLA-B27 positive, predominantly axial but can involve peripheral joints including the knee. SI joint fusion on imaging |
| Reactive Arthritis | Acute monoarthritis/oligoarthritis following GU or GI infection. "Can't see, can't pee, can't climb a tree" (conjunctivitis, urethritis, arthritis) |
Exam pearl: The classic deformity distinction: varus = OA, valgus = RA [1]. This is because OA predominantly destroys the medial compartment (varus), while RA destroys diffusely but lateral structures and ligaments are often more severely involved → valgus.
| Condition | Key Features |
|---|---|
| Gout | Acute, excruciatingly painful monoarthritis. Knee is the second most common large joint affected (after 1st MTP). Red, hot, swollen joint. Raised serum urate. Negatively birefringent needle-shaped monosodium urate crystals on joint aspiration. Tophi in chronic disease |
| Pseudogout (CPPD) | Calcium pyrophosphate dihydrate deposition disease. Older patients, knee is the most commonly affected joint. Chondrocalcinosis on X-ray (calcification of meniscal cartilage — a linear calcification within the joint space that OA does NOT produce). Weakly positive birefringent rhomboid crystals on aspiration |
CPPD vs OA — A Common Trap
CPPD and OA frequently coexist in the elderly knee. If you see chondrocalcinosis (calcification of the meniscus/cartilage) on X-ray, consider CPPD. An acute flare of pseudogout can occur on top of chronic OA and be misdiagnosed as "OA flare" — always aspirate if an acutely hot, swollen joint in an OA patient doesn't fit the usual pattern.
| Condition | Key Features |
|---|---|
| Septic arthritis | Acute hot, red, swollen, extremely painful joint with fever and markedly restricted ROM. Single most important condition to exclude in any acute monoarthritis — medical emergency because cartilage destruction occurs within hours. Risk factors: elderly, immunosuppressed, diabetes, RA, recent joint injection/surgery, skin infection. Joint aspiration: turbid fluid, WBC > 50,000/mm³ (often > 100,000), positive Gram stain/culture. Infective causes can lead to secondary OA [1] |
| Tuberculosis (TB) | Chronic monoarthritis, especially in endemic areas (Hong Kong). Insidious onset, doughy synovial thickening. X-ray: Phemister triad (juxta-articular osteoporosis, peripheral erosions, gradual joint space narrowing). Synovial biopsy with caseating granulomas |
| Condition | Key Features |
|---|---|
| ACL tear | Importance of trauma history [1] — sudden deceleration/pivoting, audible "pop," immediate haemarthrosis (swelling within hours), instability ("give way"). Lachman test, anterior drawer test, pivot shift test positive [6] |
| Meniscal tear (traumatic) | Symptoms: mechanical pain, swelling (delayed onset), locking, giving way [7]. Signs: joint line tenderness, effusion, reduced ROM, provocative signs (McMurray test, Apley grinding test) [7]. Traumatic tears are associated with acute injury, degenerative tears with aging/OA |
| Collateral ligament injuries | MCL: valgus stress mechanism; LCL: varus stress mechanism [6] |
| Fractures | Patellar fracture (inability to extend knee, palpable defect [6]), tibial plateau fracture (high-energy trauma, lipohaemarthrosis, lateral plateau most common [6]), distal femoral fracture. Always get X-rays in acute trauma |
| Osteochondritis dissecans | Osteochondritis dissecans [1] — subchondral bone undergoes avascular necrosis, and a fragment of cartilage + bone may separate and become a loose body. Young patients (adolescents/young adults), medial femoral condyle most common. Mechanical symptoms (locking, catching) if loose body present |
Meniscus tear — "Traumatic" vs "Degenerative" [7]: Traumatic tears occur at the time of injury in younger patients. Degenerative tears develop over 1–2 months post-minor injury or insidiously with aging, and may lead to secondary OA. Degenerative tears in the context of OA are often incidental on MRI.
| Condition | Key Features |
|---|---|
| Pes anserine bursitis | Medial knee pain BELOW the joint line (distinguish from medial compartment OA which is AT the joint line). Common in obese women with coexisting OA [6] |
| Prepatellar bursitis | Anterior swelling OVER the patella, not within the joint. Occupational (kneeling) |
| ITB syndrome | Lateral knee pain at 30° flexion, runners/cyclists [6] |
| Quadriceps/patellar tendon rupture | Acute inability to extend knee, palpable gap in tendon. Different from OA (acute event, not chronic) |
| Source | Mechanism |
|---|---|
| Hip pathology | Hip pain radiating to knee [3] — the obturator nerve (L2–L4) innervates both the hip joint and the medial knee. Hip OA, AVN, or hip fracture can present as isolated knee pain, especially in the elderly. Always examine the hip in a patient with knee pain! This is a classic exam trap |
| Lumbar spine | L3/L4 radiculopathy can refer pain to the anterior/medial knee. Sciatica [8] — L5-S1 radiculopathy from herniated disc can cause posterior leg pain that patients localise to "behind the knee." Sharp/burning, dermatomal distribution, positive straight leg raise |
| Vascular | Popliteal artery aneurysm (pulsatile mass behind knee), chronic compartment syndrome (exercise-induced pain in young athletes) [8] |
The Hip-Knee Trap
A patient presents with "knee pain" but the knee examination is completely normal. Always examine the hip. OA hip commonly refers pain to the anterior/medial knee via the obturator nerve. This is tested in virtually every orthopaedic OSCE.
- Primary bone tumours (osteosarcoma — around the knee is the most common site; typically adolescents/young adults; night pain, progressive swelling)
- Metastases (less common at the knee compared to spine/pelvis/proximal femur, but possible)
- Pigmented villonodular synovitis (PVNS) — benign but locally aggressive proliferative disorder of the synovium. Recurrent haemarthroses, boggy synovial thickening, "rusty" joint fluid. MRI shows characteristic blooming artefact from haemosiderin.
Importance of Trauma History [1]:
| Clue | Points toward |
|---|---|
| Insidious onset, age > 50, worse with activity, better with rest, stiffness < 30 min | OA |
| Acute onset after trauma, "pop" sound, immediate swelling | ACL tear |
| Twisting injury, delayed swelling (6–12h), locking | Meniscal tear [7] |
| Acute hot red joint, fever, unable to move | Septic arthritis |
| Morning stiffness > 60 min, symmetrical, small joint involvement | RA |
| Acute excruciating monoarthritis, red/hot, raised urate | Gout |
| Chondrocalcinosis on X-ray, acute flare in elderly | CPPD/pseudogout |
| Night pain, progressive, adolescent, bony mass | Tumour |
| Normal knee exam, limited hip ROM | Referred from hip |
| Dermatomal pain, positive SLR, back pain | Referred from lumbar spine |
Knee pain after injury — the lecture specifically emphasises checking for joint swelling characteristics [1]:
- Immediate swelling (haemarthrosis, within 2 hours): ACL tear (highly vascular ligament), fracture, patellar dislocation
- Delayed swelling (6–12 hours): Meniscal tear (meniscus is avascular in inner zones, so bleeding is minimal; effusion is reactive)
- No acute swelling, gradual: OA, overuse injuries
Locking is an important presenting complaint that can be confused with OA stiffness [7]:
| Feature | Acute Locking | Intermittent Locking |
|---|---|---|
| Pathology | Displaced bucket-handle tear of meniscus | Displaceable meniscus tear or loose body (usually bony in nature) |
| Preceding injury | Usually yes | Yes or no (loose body: usually no) |
| Locking position | Inability to fully extend the knee passively | Can be in any position of knee flexion |
| Duration | Persistent | Transient |
| Cause of pain | Tethering of capsule by the meniscus fragment that remains attached to the capsule | Meniscus: tethering of capsule; Loose body: increase in pressure at the subchondral bone resulting from impingement of the LB within the joint |
This is important because OA patients may describe "stiffness" or "difficulty straightening the knee" — but this is usually a fixed flexion contracture or extension lag, NOT true mechanical locking. True locking (sudden inability to extend, with a clear onset event) suggests a meniscal tear or loose body.
| Condition | Age | Onset | Morning Stiffness | Swelling | X-ray | Key Test |
|---|---|---|---|---|---|---|
| OA | > 50 | Insidious | < 30 min | Bony +/- effusion | LOSS features | Clinical + X-ray |
| RA | Any (30–50) | Insidious | > 60 min | Soft tissue, symmetrical | Erosions, osteopenia | RF, anti-CCP, US |
| Gout | > 40 (M), post-menopause (F) | Acute | N/A | Red, hot, tense | Soft tissue swelling, tophi | Aspirate: MSU crystals |
| CPPD | > 60 | Acute/chronic | Variable | Warm effusion | Chondrocalcinosis | Aspirate: CPP crystals |
| Septic arthritis | Any | Acute | N/A | Red, hot, very tense | Soft tissue swelling, late: destruction | Aspirate: WBC > 50k, culture |
| Meniscal tear | Any | Acute/chronic | No | Delayed (traumatic) | Often normal | McMurray, MRI |
| ACL tear | Young/active | Acute (trauma) | No | Immediate (haemarthrosis) | Segond fracture | Lachman, MRI |
| Referred from hip | > 50 | Insidious | Variable | None at knee | Normal knee | Hip ROM limited |
High Yield Summary
Anatomical approach to DDx of knee pain: Anterior (patellofemoral syndrome, patellar tendonitis, Osgood-Schlatter, prepatellar bursitis), Medial (MCL sprain, medial meniscal tear, pes anserine bursitis, medial plica), Lateral (LCL sprain, lateral meniscal tear, ITB syndrome), Posterior (Baker's cyst, PCL injury).
Category approach: Degenerative (OA, degenerative meniscal tear), Inflammatory (RA, PsA, AS), Crystal (gout, CPPD), Infective (septic arthritis — EMERGENCY, TB), Traumatic (ACL/meniscal/ligament tears, fractures), Periarticular (bursitis, tendonitis), Referred (hip OA, lumbar radiculopathy), Neoplastic (osteosarcoma, PVNS).
Critical distinctions: (1) Varus deformity = OA, Valgus = RA. (2) Stiffness < 30 min = OA, > 60 min = RA. (3) LOSS features on X-ray = OA; erosions + osteopenia = RA; chondrocalcinosis = CPPD. (4) Always examine the hip when knee exam is normal — referred pain via obturator nerve. (5) Degenerative meniscal tears on MRI in OA patients are often incidental — don't operate unless mechanical symptoms (locking). (6) Acute hot joint = septic arthritis until proven otherwise — aspirate.
Swelling timing post-injury: Immediate = haemarthrosis (ACL, fracture); Delayed 6–12h = meniscal tear; Chronic = OA.
Active Recall - Differential Diagnosis of Knee OA
References
[1] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf (p16–p22, p32–p33) [2] Senior notes: maxim.md (section 9.1 Osteoarthritis) [3] Senior notes: maxim.md (section 6.3 OA hip) [6] Senior notes: maxim.md (sections 7.2 Soft tissue injuries, 7.3 Bone and joint injuries — ACL tear, MCL/LCL, meniscal tear, ITB syndrome, patella dislocation, tibial plateau fracture) [7] Lecture slides: GC 230. Knee Sport Injuries_Part 3.pdf (p16, p18, p27) [8] Senior notes: felixlai.md (Baker's cyst, sciatica, chronic compartment syndrome)
Diagnostic Criteria, Algorithm, and Investigations for Knee Osteoarthritis
1. Diagnostic Criteria
There is no single "gold standard" laboratory test for OA — the diagnosis is fundamentally clinical + radiographic. Unlike RA (which has formal ACR/EULAR classification criteria with serological markers), OA diagnosis relies on the constellation of history, examination, and imaging findings. Let's go through the two most widely used criteria sets.
1.1 ACR Clinical Classification Criteria for OA of the Knee (1986/1991)
The American College of Rheumatology developed these criteria specifically for classifying KOA. They exist in three formats — clinical alone, clinical + radiographic, and clinical + laboratory. The clinical + radiographic version is the most commonly used and the most relevant for exams.
Knee pain PLUS at least 1 of the following 3:
- Age > 50 years
- Morning stiffness < 30 minutes
- Crepitus on active motion
PLUS osteophytes on X-ray
The logic here is intuitive: you need knee pain (the symptom), features consistent with a degenerative rather than inflammatory process (age, brief stiffness, crepitus), and radiographic confirmation of OA (osteophytes).
Knee pain PLUS at least 3 of the following 6:
- Age > 50 years
- Morning stiffness < 30 minutes
- Crepitus on active motion
- Bony tenderness
- Bony enlargement
- No palpable warmth
The clinical-only criteria are less specific (more false positives) because you're not using imaging. They are useful in primary care settings where X-rays may not be immediately available. Note the inclusion of "no palpable warmth" — this helps exclude inflammatory or septic arthritis.
Knee pain PLUS at least 5 of the following 9:
- Age > 50 years
- Morning stiffness < 30 minutes
- Crepitus on active motion
- Bony tenderness
- Bony enlargement
- No palpable warmth
- ESR < 40 mm/hr
- RF negative
- Synovial fluid signs of OA (clear, viscous, WBC < 2,000/mm³)
The laboratory criteria incorporate blood tests and synovial fluid analysis primarily to exclude inflammatory and infective arthritis, not to positively diagnose OA. OA is a diagnosis where labs are used to rule out mimics, not to confirm the condition.
Key Exam Point
OA is a clinical + radiographic diagnosis. There is no blood test that "confirms" OA. Labs (ESR, CRP, RF, anti-CCP, urate) are done to exclude inflammatory, crystal, and infective arthritis. If a question asks "What investigation confirms KOA?" — the answer is weight-bearing X-ray showing osteophytes + joint space narrowing in the right clinical context.
The European League Against Rheumatism provides a more practical, clinically oriented approach:
Three symptoms + three signs are considered highly predictive of KOA:
Symptoms:
- Persistent knee pain
- Limited morning stiffness ( ≤ 30 minutes)
- Reduced function
Signs:
- Crepitus
- Restricted movement
- Bony enlargement
If all six are present in a patient > 40 years old, the diagnosis of KOA can be made with high confidence without imaging. However, in practice, imaging is almost always obtained to confirm the diagnosis, assess severity, plan treatment, and exclude other pathology.
The UK National Institute for Health and Care Excellence states that OA can be diagnosed clinically without investigations if:
- Patient is ≥ 45 years old
- Has activity-related joint pain
- Has either no morning stiffness, or morning stiffness ≤ 30 minutes
This reflects the reality that KOA is so common in the appropriate demographic that imaging adds little diagnostic value for typical presentations. Imaging is reserved for atypical features, young patients, or when surgical planning is needed.
The approach to a patient with suspected KOA follows a logical sequence: History → Examination → Investigations (if needed) → Grading → Treatment planning.
3. Investigation Modalities
3.1 Plain Radiography (X-ray) — The Cornerstone
Workup of Knee Osteoarthritis [1] — X-ray is the first-line and most important imaging modality.
Radiographic views for KOA [2]:
| View | Technique | What it Shows | Why it Matters |
|---|---|---|---|
| Weight-bearing AP | Standing, full extension, beam directed at joint line | Medial vs lateral compartment joint space narrowing | Must be weight-bearing — non-weight-bearing films underestimate JSN because the cartilage surfaces aren't compressed. This is the single most important view |
| Lateral | Supine or standing, knee in 20–30° flexion | Anteromedial vs posteromedial osteophytes, posterior osteophytes, patella position (alta/baja), joint effusion (suprapatellar pouch fullness), tibial slope | Reveals pathology missed on AP — especially posterior osteophytes that can cause impingement in flexion |
| Skyline (Merchant) view | Knee flexed 30–45°, beam tangential to patella | Patellofemoral joint space, patellar tilt, subluxation, trochlear dysplasia | Essential for assessing the patellofemoral compartment — anterior knee pain with normal AP/lateral films should prompt a skyline view |
| Valgus stress view | AP with manual valgus stress applied | Assess medial joint space under stress (opens medial compartment) | Tests MCL integrity and whether varus deformity is correctable (useful for surgical planning — unicompartmental vs total knee replacement) |
| Varus stress view | AP with manual varus stress applied | Assess lateral joint space under stress | Tests LCL integrity and lateral compartment cartilage |
| Standing scanogram of bilateral lower limbs | Full-length standing film from hip to ankle | Alignment: Tibiofemoral angle (TFA) — valgus vs varus; Mechanical axis of lower limb — pass through medial or lateral side | Critical for surgical planning — determines degree of malalignment and guides osteotomy vs arthroplasty decisions. The mechanical axis line runs from the centre of the femoral head to the centre of the ankle — if it falls medial to the knee centre, there is varus malalignment [2] |
| Schuss view (30° flexion PA) | Standing, knee flexed 30°, PA projection | Posterior femoral condyle cartilage, posterior joint space | More sensitive for early OA [2] — the posterior femoral condyles bear the most load in flexion, so early cartilage loss here is visible on this view but missed on the standard AP in full extension |
Why Weight-Bearing?
This cannot be over-emphasised: a non-weight-bearing knee X-ray can be falsely reassuring. Under load, the thinned cartilage compresses and the true joint space narrowing becomes apparent. If you order a supine AP knee X-ray and it looks "normal," you may miss significant OA. Always specify "weight-bearing" on the request form.
The hallmarks of knee osteoarthritis [1]:
| Feature | Radiographic Appearance | Pathophysiological Basis |
|---|---|---|
| Joint space narrowing | Reduced distance between femoral condyle and tibial plateau on weight-bearing AP | Loss of articular cartilage (cartilage is radiolucent — as it thins, the "gap" narrows). Earliest radiographic change [2]. Typically asymmetric (medial > lateral in varus OA) |
| Subchondral sclerosis | Increased whiteness/density of bone immediately beneath the joint surface | Increased osteoblastic activity in subchondral bone responding to increased mechanical stress transmission (the "shock absorber" cartilage is gone, so bone takes the hit and remodels/thickens) |
| Marginal osteophytes | Bony spurs at the joint margins | New bone formation at the periosteum, driven by TGFβ and mechanical stress. The body attempts to increase surface area to redistribute load — a failed repair mechanism. Found at margins of femoral condyles, tibial plateaus, and patella |
| Subchondral cysts | Well-defined radiolucent areas within subchondral bone, often surrounded by a sclerotic rim | Two theories: (1) Synovial fluid intrusion — high intra-articular pressure forces fluid through microfractures in the damaged subchondral plate; (2) Focal osteonecrosis from localised ischaemia under repeated mechanical stress |
Kellgren-Lawrence OA Classification Scale [1][2]:
| Grade | JSN | Osteophytes | Description |
|---|---|---|---|
| Grade 0 | No radiographic features of OA | None | Normal |
| Grade 1 | Doubtful | Possible | Doubtful OA |
| Grade 2 | Possible | Definite | Mild — Radiographic threshold for "definite OA" |
| Grade 3 | Definite | Multiple | Moderate — clear structural damage |
| Grade 4 | Marked | Large | Severe — bone-on-bone, end-stage |
KL Grade 2 is the minimum grade for a radiographic diagnosis of OA. Below this, the diagnosis is "possible" but not definite. KL Grade 4 (bone-on-bone) typically warrants discussion of joint replacement if symptoms are concordant.
Radiographic-Symptom Discordance
A critical concept: radiographic severity does NOT always correlate with symptom severity. Up to 40% of patients with KL Grade 3–4 changes may report minimal symptoms, while some patients with only KL Grade 2 may be severely disabled. Treatment decisions must be based on the clinical picture (pain, function, quality of life), not the X-ray alone. You treat the patient, not the X-ray.
3.2 Advanced Imaging
MRI is the most sensitive imaging modality for detecting early OA and assessing the whole joint organ [5]:
| What MRI Shows | Clinical Relevance |
|---|---|
| Changes in the composition of bone, cartilage, other soft tissues [5] | Detects disease at the molecular/pre-radiographic stage — before X-ray changes appear |
| Cartilage defects | Focal or diffuse cartilage thinning, fissuring, full-thickness loss — graded by modified Outerbridge classification |
| Bone marrow oedema (BME) / bone marrow lesions | Increased signal on fluid-sensitive sequences (STIR/T2 fat-sat) in subchondral bone. Strongly associated with pain in OA (one of the best MRI predictors of who has symptomatic OA). Represents microtrabecular damage, fibrosis, and osteonecrosis |
| Meniscal pathology | Degenerative meniscus tears are very common incidental findings on MRI in patients with KOA [7]. Meniscal extrusion, horizontal tears, complex tears. Caution: not all MRI-detected meniscal tears are symptomatic — caution should be exercised against the treatment of "incidental" meniscus lesions found on MRI in patients who have no symptoms of locking [7] |
| Synovitis/effusion | Gadolinium-enhanced MRI can show synovial thickening and hyperaemia — evidence of active inflammation. Effusion volume and signal characteristics |
| Ligament integrity | ACL and PCL integrity — relevant for surgical planning (unicompartmental arthroplasty requires functionally intact ACL [2]) |
| Osteophytes | MRI detects osteophytes earlier and more comprehensively than X-ray |
| Structural changes in bone, cartilage, other soft tissues [5] | MRI/Ultrasound can detect structural changes at the pre-radiographic stage |
When to order MRI in KOA:
- Suspected early OA with normal/equivocal X-rays
- Mechanical symptoms (locking, catching) — to assess for meniscal tears or loose bodies
- Pre-operative planning — assessing ligament integrity, cartilage status in each compartment
- Young patient with suspected secondary OA — to identify the underlying cause (AVN, osteochondral defect)
- Atypical features — to exclude other pathology (tumour, PVNS, stress fracture)
Natural History of OA: Structural Changes before Symptoms — more effective to prevent disease progression by intervention at early stages [5]. This underpins the rationale for MRI: detecting disease earlier allows earlier intervention.
| Disease Stage | Detection | Key Feature |
|---|---|---|
| Molecular | MRI/Biomarkers | Changes in composition of bone, cartilage, other soft tissues |
| Pre-Radiographic | MRI/US | Structural changes in bone, cartilage, other soft tissues |
| Radiographic | X-ray | Structural changes in bone (joint failure) + symptoms |
| End-stage | Clinical | Joint death → Joint replacement |
- Non-invasive, no radiation, real-time dynamic assessment, bedside availability.
- Can detect: effusion, synovitis (power Doppler shows hyperaemia), Baker's cyst, popliteal pathology, superficial osteophytes, periarticular soft tissue pathology (bursitis, tendinopathy).
- MRI/US can detect structural changes in bone, cartilage, other soft tissues at the pre-radiographic stage [5].
- Limitations: Operator-dependent, cannot assess deep structures (cruciate ligaments, deep cartilage) as well as MRI.
- Useful for: Guiding joint aspiration/injection, assessing periarticular soft tissue causes of knee pain (pes anserine bursitis, ITB syndrome), and when MRI is contraindicated.
- Not routinely used for KOA diagnosis.
- Useful for: Complex fractures involving the tibial plateau (pre-operative planning), suspected loose bodies (CT arthrography), assessing bony anatomy when MRI is contraindicated.
- CT arthrography (CT with intra-articular contrast) can provide excellent cartilage assessment as an alternative to MRI.
3.3 Laboratory Investigations
OA is a clinical-radiographic diagnosis — laboratory tests are used to exclude other diagnoses, not to confirm OA.
| Test | Expected in OA | Purpose |
|---|---|---|
| ESR | Normal or mildly elevated ( < 40 mm/hr) | Exclude inflammatory arthritis (ESR > 40 in RA, PMR) |
| CRP | Normal or mildly elevated | Exclude active inflammation/infection. Note: mild CRP elevation can occur in OA with significant synovitis, but > 50 mg/L should raise concern for infection |
| Rheumatoid Factor (RF) | Negative | Exclude RA. Note: RF is not specific — can be positive in 5–10% of healthy elderly, and in other conditions (Sjögren's, HCV). Anti-CCP is more specific |
| Anti-CCP antibodies | Negative | More specific than RF for RA (specificity > 95%) |
| Serum urate | Normal | Exclude gout. Caveat: urate may be normal during an acute gout flare (urate is consumed in crystal formation); a normal level does NOT exclude gout |
| FBC | Normal | Exclude infection (leucocytosis), anaemia of chronic disease (RA) |
| Calcium, phosphate, ALP | Normal | Exclude metabolic bone disease, hyperparathyroidism, Paget's |
| HLA-B27 | Not routinely tested | Only if spondyloarthropathy suspected (young patient, inflammatory back pain, enthesitis) |
In a typical elderly patient with classic KOA on weight-bearing X-rays, no blood tests are strictly necessary. Blood tests are indicated when: (1) the presentation is atypical, (2) the patient is young, (3) there is suspicion of an inflammatory or crystal arthropathy, or (4) pre-operative screening before surgery.
Joint aspiration is not routinely required for straightforward KOA but is essential when:
- Acute monoarthritis (to exclude septic arthritis or crystal arthropathy)
- Significant effusion causing pain (therapeutic aspiration)
- Diagnostic uncertainty
| Parameter | OA | Inflammatory Arthritis | Septic Arthritis | Crystal Arthropathy |
|---|---|---|---|---|
| Appearance | Clear, straw-coloured, viscous | Turbid, yellow | Turbid/purulent, thin | Turbid, yellow-white |
| Viscosity | High (normal HA) | Low | Very low | Low |
| WBC count | < 2,000/mm³ | 2,000–50,000/mm³ | > 50,000/mm³ (often > 100,000) | 2,000–100,000/mm³ |
| % Neutrophils | < 25% | > 50% | > 75% | > 50% |
| Culture | Negative | Negative | Positive (75%) | Negative |
| Crystals | None | None | None | MSU (gout): negatively birefringent, needle-shaped. CPP (pseudogout): weakly +ve birefringent, rhomboid |
| Mucin clot | Good (firm, ropy) | Poor (friable) | Poor | Poor |
The string test (stretching the fluid between fingers) gives a quick bedside assessment of viscosity. OA fluid forms a long string ( > 5 cm) because hyaluronic acid is preserved. Inflammatory/infected fluid breaks immediately because enzymes degrade HA.
Septic Arthritis — Don't Miss It
In any patient presenting with an acute hot, red, swollen knee — even one with known OA — you must aspirate the joint before assuming it's an "OA flare." Septic arthritis destroys cartilage within hours and can be fatal. The presence of pre-existing OA does NOT protect against septic arthritis — in fact, damaged joints are MORE susceptible to infection.
MRI/Biomarkers can detect changes in the composition of bone, cartilage, other soft tissues at the molecular stage of disease [5]. Research biomarkers include:
| Category | Examples | What They Measure |
|---|---|---|
| Cartilage degradation | CTX-II (C-terminal crosslinked telopeptide of type II collagen), COMP (cartilage oligomeric matrix protein) | Collagen and matrix breakdown products |
| Bone remodelling | CTX-I, NTX-I, osteocalcin | Subchondral bone turnover |
| Synovial inflammation | HA (hyaluronic acid), YKL-40 | Synovitis activity |
These are not yet used in clinical practice but are being studied in clinical trials for early detection, prognostication, and monitoring treatment response. The concept is important: more effective to prevent disease progression by intervention at early stages [5].
| Clinical Scenario | Investigations Needed |
|---|---|
| Typical presentation (age > 50, mechanical pain, crepitus, bony enlargement) | Weight-bearing AP + lateral X-rays. Skyline view if anterior knee pain. Blood tests usually NOT needed |
| Atypical features (young age, hot/red joint, fever, morning stiffness > 60 min, rapid progression, night pain) | X-rays + bloods (ESR, CRP, RF, anti-CCP, urate, FBC) + joint aspiration (cell count, crystals, culture) |
| Mechanical symptoms (locking, catching, giving way) in addition to OA features | X-rays + MRI (to assess for meniscal tears, loose bodies, ligament integrity) |
| Pre-operative planning (considering surgery) | Weight-bearing AP + lateral + skyline + standing scanogram (alignment) + stress views (ligament integrity). Bloods for pre-op workup. Consider MRI if unicompartmental arthroplasty contemplated (need to confirm intact ACL, full-thickness lateral cartilage) [2] |
| Suspected secondary OA in young patient | X-rays + bloods (as above) + MRI (to identify underlying cause — AVN, osteochondral defect, inflammatory arthritis). Consider aspiration |
| Finding | Interpretation | Clinical Implication |
|---|---|---|
| Medial JSN on weight-bearing AP | Medial compartment OA | May be candidate for medial UKA or HTO if young |
| Lateral JSN on weight-bearing AP | Lateral compartment OA (less common) | Consider valgus malalignment. Less suitable for standard HTO |
| PFJ narrowing on skyline | Patellofemoral OA | Explains anterior knee pain, especially on stairs. PFJ replacement rarely done in isolation |
| Bone-on-bone (KL Grade 4) | End-stage OA | Strong indication for TKR if symptomatic |
| Varus mechanical axis on scanogram | Medial overloading | Guides osteotomy planning (HTO corrects varus to slight valgus) |
| Intact ACL on MRI | Functional ACL | Required for unicompartmental knee arthroplasty (Oxford criteria: functionally intact ACL) [2] |
| Bone marrow oedema on MRI | Active subchondral stress/inflammation | Strongly correlates with symptomatic OA — may explain pain in patients with minimal radiographic changes |
| Chondrocalcinosis on X-ray | CPPD (pseudogout) | Consider crystal arthropathy as coexisting or alternative diagnosis |
| Normal X-ray + knee pain | Early OA, or not OA at all | Order Schuss view (more sensitive for early OA [2]). Examine the hip. Consider MRI. Consider periarticular causes |
High Yield Summary
Diagnostic criteria: ACR clinical + radiographic criteria = knee pain + age > 50 / stiffness < 30 min / crepitus + osteophytes on X-ray. NICE 2022: age ≥ 45, activity-related pain, no/brief stiffness → diagnose clinically without imaging.
First-line imaging: Weight-bearing AP and lateral X-rays. Always weight-bearing! Add skyline for PFJ, Schuss view for early OA, standing scanogram for alignment (surgical planning).
LOSS features: Joint space narrowing (earliest), Osteophytes, Subchondral sclerosis, Subchondral cysts. Grade with Kellgren-Lawrence (KL 2 = definite OA, KL 4 = bone-on-bone).
MRI role: Early detection (pre-radiographic stage), assessing meniscal/ligament integrity, pre-operative planning (UKA needs intact ACL). Beware incidental degenerative meniscal tears — don't operate unless mechanical symptoms.
Labs: Not needed for typical KOA. Done to EXCLUDE mimics: ESR/CRP (inflammation), RF/anti-CCP (RA), urate (gout), joint aspirate (infection/crystals). OA synovial fluid: clear, viscous, WBC < 2,000/mm³.
Key principle: Treat the patient, not the X-ray — radiographic severity does not always correlate with symptoms.
Active Recall - Diagnosis and Investigations for Knee OA
References
[1] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf (p2, p13, p22, p28, p32, p33) [2] Senior notes: maxim.md (sections 7.4 OA knee, 9.1 Osteoarthritis) [5] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p13) [7] Lecture slides: GC 230. Knee Sport Injuries_Part 3.pdf (p27)
Management of Knee Osteoarthritis
The management of KOA follows a stepwise, evidence-based pyramid approach. This is a core concept from the lectures and is the single most important framework for managing KOA:
The OA Treatment Pyramid [1]:
| Level | Who Gets It | What It Includes |
|---|---|---|
| First line treatment | All patients | Education, exercise and weight control |
| First + second line treatment | Some patients (inadequate response to first line) | Pharmacological pain relief, aids and passive treatments given by a therapist |
| First + second + third line treatment | Few patients (failed conservative management) | Surgery |
The pyramid is wide at the base (everyone gets non-pharmacological) and narrow at the top (few need surgery). The critical teaching point: the first line management of Knee Osteoarthritis is weight reduction, education and exercise — NOT analgesics, NOT surgery [9].
Patients are NOT unsatisfied: high unmet medical need — 81% of knee OA patients are highly unsatisfied with current treatment [1]. This highlights the need for better comprehensive, multidisciplinary management rather than just handing out painkillers.
Evidence based management — multi-disciplinary chronic disease management [9]:
- Non-surgical Mx in OA (Triad) = Education + Exercise + Weight control [9]
- A paradigm shift urgently needed in aging population in HK [9]
1. Non-Pharmacological Management (First Line — FOR ALL)
The core non-pharmacological Mx of Knee OA [1]:
Core priority treatments for OA include exercise and physical activity, weight-loss, education and support for self-management [9].
Comprehensive Osteoarthritis Education [1]:
- What is OA? Risk factors, symptoms, treatment (Occasion 1) [1]
- Exercise, physical activity in daily living, coping management (Occasion 2) [1]
- OA communicator — to live with OA (Occasion 3) [1]
The purpose of education is to empower the patient. OA is a chronic disease — like diabetes or hypertension, the patient needs to understand and self-manage. Key messages:
- OA is NOT just "inevitable aging" — it is modifiable.
- Exercise does NOT damage the joint further — it protects it (a common patient fear).
- Weight loss has a disproportionate benefit (every 1 kg lost = ~4 kg less force on the knee).
- Self-management reduces reliance on healthcare services and improves outcomes.
COME (Comprehensive Osteoarthritis ManagEment) programme at MMRC [1]:
- Aim: to provide comprehensive non-surgical management care for patient with osteoarthritis [1]
- Collaborators: Department O&T QMH, Nursing Department MMRC, Physiotherapy Department MMRC, Occupational Department MMRC [1]
- Results showed consecutive significant improvements over each assessment time point in: PSEQ score (pain self-efficacy), FACIT score (functional assessment), one-minute chair test repetitions, right and left quadriceps strength, PSFS score (patient-specific functional scale), and weekly time spent for exercise [1]
This is a real HKU/QMH programme — mentioning it shows awareness of local practice.
Strong evidence supports the use of physical therapy as a treatment to improve function and reduce pain for patients with osteoarthritis [10].
- Strength of Recommendation: Strong Evidence [10]
Types of exercise:
- Muscle strengthening [10] — particularly quadriceps strengthening. Why? The quadriceps act as dynamic "shock absorbers" for the knee. When the quads are weak, more force is transmitted directly through the articular cartilage and subchondral bone → more pain and faster progression. Strengthening the quads redistributes load away from the damaged compartment [2].
- Range of motion exercise [10] — maintains joint flexibility, prevents contractures, reduces stiffness.
- Cardiopulmonary function, endurance [10] — aerobic exercise (e.g., bicycle [2], swimming, walking) improves overall fitness, aids weight loss, reduces cardiovascular risk, and improves mood/sleep.
Physiotherapy: quadriceps muscle strengthening to slow disease progression and improve biomechanics [2].
Preoperative physical therapy — limited evidence supports the use of pre-operative physical therapy to improve early function in patients following total hip arthroplasty [10]. The same principle applies to TKR: "prehabilitation" (strengthening before surgery) leads to better post-operative recovery.
Exercise is Medicine
Exercise is the single most effective non-pharmacological intervention for KOA. It has better evidence than paracetamol. The challenge is patient adherence — this is why supervised group exercise programmes (like COME) work better than simply telling patients to "go exercise."
- Weight reduction is part of the non-surgical triad [2][9].
- Lifestyle modifications: weight loss, regular exercise, smoking cessation [2].
- Target: 5–10% body weight reduction produces clinically meaningful improvement in pain and function.
- Mechanism: reduces mechanical load AND reduces systemic inflammation (adipokines, leptin, IL-6 from adipose tissue).
- Even modest weight loss (5 kg) = 20 kg less force on the knee per step = enormous cumulative benefit.
Relief of weight-bearing: weight reduction, walking aids, muscle strengthening [2]:
- Walking stick/cane: Held in the contralateral hand (reduces load on the affected knee by ~25%). Why contralateral? The cane creates a counterbalancing moment arm on the opposite side, reducing the abductor moment needed and thereby reducing joint reaction force.
- P&O to relieve medial compartment pressure (controversial): valgus unloading brace, lateral insole [2]:
- Valgus unloading brace: Applies a valgus (corrective) force to the knee, shifting load from the medial to lateral compartment. Useful in medial compartment OA.
- Lateral wedge insole: Inserted in the shoe, tilts the foot laterally → subtly shifts the mechanical axis → theoretically reduces medial compartment loading. Evidence is mixed — some guidelines no longer recommend it, hence "controversial."
Additional physical or psychological evidence-based adjunctive therapies include [9]:
- Cognitive behavioural therapy (for pain coping and catastrophising)
- Heat therapy
- Walking aids and splints
- Manual therapies
- Transcutaneous electrical nerve stimulation (TENS)
- OT: ADL Mx and training [1]
- Activity modification: avoid prolonged kneeling, squatting, heavy lifting.
- Assistive devices for ADLs: raised toilet seat, grab bars, long-handled shoe horn.
- Home modifications to reduce fall risk.
2. Pharmacological Management (Second Line — SOME)
Pharmacological Mx of Knee Osteoarthritis [9]:
The key principle: pharmacological treatment does NOT modify the disease course — it manages symptoms. Not affect natural history [10]. All drugs are symptomatic relief only.
- Examples: Diclofenac gel, ketoprofen patches.
- Mechanism: Inhibit cyclooxygenase (COX-1 and COX-2) → reduce prostaglandin synthesis → reduce inflammation and pain locally.
- Advantages: Minimal systemic absorption → far fewer GI, renal, and cardiovascular side effects compared to oral NSAIDs. Effective for superficial joints like the knee (good tissue penetration).
- Evidence: OARSI, EULAR, and NICE all recommend topical NSAIDs as first-line pharmacological therapy for KOA, ahead of oral NSAIDs and paracetamol.
- Indications: Mild-moderate KOA pain, especially in patients with GI/CV risk factors.
- Contraindications: Skin sensitivity, open wounds over application site.
NSAIDs have proven benefit [2].
- Mechanism: Inhibit COX enzymes → reduce prostaglandin-mediated inflammation, pain, and effusion in the synovium and periarticular tissues.
- Examples: Ibuprofen, naproxen (non-selective); celecoxib, etoricoxib (COX-2 selective).
- Evidence: Network meta-analysis shows oral NSAIDs are the most effective oral analgesics for KOA — superior to paracetamol [9].
- Prescribing principles:
- Use the lowest effective dose for the shortest duration.
- Always co-prescribe a PPI (proton pump inhibitor) for gastroprotection.
- Consider COX-2 selective agents in patients with high GI risk (but monitor CV risk).
| Side Effect | Mechanism | Management |
|---|---|---|
| GI (peptic ulcer, bleeding) | COX-1 inhibition → reduced gastric prostaglandin → less mucosal protection | Co-prescribe PPI; use COX-2 selective |
| Renal (AKI, fluid retention, HTN) | Prostaglandins maintain renal afferent arteriolar vasodilation; NSAID → afferent vasoconstriction → reduced GFR | Avoid in CKD (eGFR < 30); monitor renal function |
| Cardiovascular (MI, stroke) | COX-2 inhibition → reduced prostacyclin (vasodilator/anti-platelet) → prothrombotic state | Avoid in established CVD; use naproxen (lowest CV risk among non-selective NSAIDs) |
- Contraindications: Active peptic ulcer, severe CKD, heart failure, aspirin-sensitive asthma, pregnancy (3rd trimester), concurrent anticoagulants without PPI cover.
Does paracetamol still have a future in osteoarthritis? [9]:
- Paracetamol is widely used for analgesia in osteoarthritis — largely driven by a lack of effective or tolerated alternative treatments, and their relative safety (cf NSAID) [9].
- Network meta-analysis — paracetamol does not seem to confer any demonstrable effect or benefit in osteoarthritis, at any dose [9].
- Side effects: liver function abnormalities; elderly people with impaired paracetamol clearance [9].
This is a paradigm shift. Traditionally, paracetamol was recommended as first-line oral analgesic. Current evidence (as of 2020s guidelines) shows it is minimally effective for OA pain. It may still have a role as an adjunct or in patients who cannot take NSAIDs, but it should NOT be relied upon as monotherapy.
- Mechanism: Uncertain — thought to involve central COX inhibition and descending serotonergic pathways. Unlike NSAIDs, it has NO peripheral anti-inflammatory effect — which explains its poor efficacy in OA where peripheral inflammation (synovitis) drives much of the pain.
- Maximum dose: 4g/day (but 2g/day in elderly/hepatic impairment).
- For hip OA, Paracetamol (Panadol): first line is still mentioned [10] — the evidence is evolving and some guidelines still list it as a first-line option, particularly for mild symptoms.
Paracetamol in OA — Know the Evidence
Many guidelines are moving away from recommending paracetamol as first-line for KOA. It has minimal benefit over placebo in network meta-analyses. However, some older guidelines and exam questions may still list it as first-line. Know both positions: current evidence says it's poorly effective; traditional teaching says it's "safe first-line." The safest exam answer is: topical NSAIDs are the preferred first pharmacological step.
Very limited role of opioids [9]:
- Opioids offer only limited benefit for chronic OA — pain and function [9].
- Potentially serious adverse effects, including drug abuse and addiction [9].
- Elderly patients are at particular risk of experiencing side effects — sedation and dizziness which predispose to falls and fractures [9].
- Surgery — pre-operative use of opioids independently predicted: opioid requirement post-surgery, associated with a prolonged hospital stay, greater risks of in-hospital complications, and early revision surgery [9].
- Updated guideline for General Practitioners (GPs) in Australia do not recommend opioids as a treatment option [9].
Tramadol: non-narcotic [10]:
Opioids [10]:
The take-home message: opioids should be avoided in KOA management. They don't work well for chronic OA pain, they cause serious harms (especially in the elderly who are the main KOA population), and they worsen surgical outcomes if the patient eventually needs a TKR. If you must use them, tramadol (a weak opioid with serotonin/noradrenaline reuptake inhibition) is preferred, and only as a bridge.
Pain relief: analgesics, intra-articular steroid [2]:
- Mechanism: Potent local anti-inflammatory effect — suppresses synovitis, reduces effusion, inhibits inflammatory cytokines (IL-1, IL-6, TNFα) and MMP activity in the joint.
- Agents: Triamcinolone acetonide, methylprednisolone acetate (depot preparations for prolonged effect).
- Indications: Acute flares of KOA with significant effusion and synovitis; diagnostic/therapeutic aspiration followed by steroid injection; patients who cannot tolerate oral NSAIDs.
- Efficacy: Provides short-term relief (4–8 weeks typically). Does not modify disease progression. May actually accelerate cartilage loss with repeated injections.
- Frequency: Generally no more than 3–4 injections per joint per year. Repeated injections may accelerate cartilage degradation and increase risk of peri-procedural infection.
- Contraindications: Suspected septic arthritis (injecting steroid into an infected joint is catastrophic), uncontrolled diabetes (transient hyperglycaemia), concurrent anticoagulation (relative — increased bleeding risk).
Intra-articular hyaluronic acid / platelet-rich plasma (?evidence) [2]:
- Mechanism: HA is a natural component of synovial fluid. In OA, HA concentration and molecular weight are reduced → decreased viscosity and lubrication. Viscosupplementation aims to restore these properties. May also have anti-inflammatory and chondroprotective effects.
- Evidence: Highly controversial. Some RCTs show modest benefit; many show no superiority over saline injection. AAOS gives a "limited" recommendation. OARSI conditionally recommends it. The placebo effect of intra-articular injection is significant.
- Indications: Patients with mild-moderate KOA who have failed oral therapies and are not yet surgical candidates.
Platelet-rich plasma (?evidence) [2]:
- Mechanism: Autologous blood concentrated in platelets → rich in growth factors (PDGF, TGFβ, VEGF, IGF-1) → theoretically stimulates cartilage repair and reduces inflammation.
- Evidence: Emerging but inconsistent. Some studies show benefit over HA; others show no difference from placebo. Not recommended by most major guidelines as standard of care. Lack of standardised preparation protocols.
- Current status: Experimental/adjunctive. Not routinely funded by public healthcare in Hong Kong.
- These are "nutraceuticals" (dietary supplements), not prescription drugs.
- Mechanism (theoretical): Glucosamine is a building block of glycosaminoglycans in cartilage; chondroitin sulfate is a component of aggrecan. Oral supplementation theoretically provides substrate for cartilage repair.
- Evidence: Large RCTs (GAIT trial) show no significant benefit over placebo for pain reduction. Some subgroup analyses suggest possible benefit in moderate-severe OA, but overall evidence is weak. OARSI recommends "uncertain" appropriateness.
- Mentioned as a common patient question — important to counsel that there is no strong evidence of benefit.
Any New Drug? [5] — The lecture poses this question in the context of the molecular biology of OA (ADAMTS, MMPs, inflammatory cytokines). Currently:
- Disease-modifying OA drugs (DMOADs) remain an unmet need. Unlike RA (which has DMARDs), there is no approved DMOAD for OA.
- Investigational agents targeting:
- Anti-NGF antibodies (e.g., tanezumab) — "NGF" = nerve growth factor; blocking it reduces pain signalling. FDA concerns about rapidly progressive OA/osteonecrosis in some patients.
- Wnt pathway inhibitors — Wnts drive osteophyte formation and subchondral bone remodelling.
- MMP inhibitors — failed in trials due to off-target musculoskeletal toxicity.
- Sprifermin (FGF18) — a recombinant fibroblast growth factor that stimulates chondrocyte proliferation and matrix synthesis. Phase II data showed dose-dependent cartilage thickness increase on MRI, but clinical symptom benefit was marginal.
3. Surgical Management (Third Line — FEW)
Surgical Mx of Knee Osteoarthritis [9]:
Surgery is indicated when:
- Patient factor: age, functional status [2]
- Disease factor: severe impairment to ADL, pain despite conservative treatment [2]
- The key principle: surgery is for patients who have FAILED adequate conservative management (at least 3–6 months of optimised non-pharmacological + pharmacological treatment).
Enhanced recovery after surgery (ERAS) protocol [11]:
Limited role of Knee Arthroscopy in OA Knee [9]:
This is extremely high yield. Multiple landmark RCTs (Moseley 2002, Kirkley 2008) have shown that arthroscopic lavage and debridement for KOA is no better than sham surgery. Arthroscopy does NOT treat OA — it can only address specific mechanical problems (loose bodies, displaced meniscal tears). If you do arthroscopy on an OA knee without a clear mechanical indication, you may actually make things worse by accelerating cartilage loss.
Arthroscopy in OA Knee — Must Know
Arthroscopic debridement/lavage for KOA is NOT recommended. The only indication for arthroscopy in KOA is frequent locking symptoms from a displaced meniscal tear or loose body. Even then, it provides only short-term relief and may accelerate OA progression. This is a common exam topic — students often incorrectly list "arthroscopic debridement" as a treatment for OA.
High tibial osteotomy: if young (M < 70, F < 60) [2]:
- Concept: "Osteotomy" = "osteo" (bone) + "tomy" (cutting). You deliberately cut the tibia and realign it to shift the mechanical axis of the limb.
- Goal: In medial compartment OA with varus malalignment, a medial opening-wedge or lateral closing-wedge HTO corrects the varus to slight valgus → shifts the weight-bearing line from the damaged medial compartment to the healthier lateral compartment.
- Who is it for? Young (< 60y) with preservation of articular cartilage, pre-requisite: single compartment [2].
- Ideal candidate: Active patient, age < 60, medial compartment OA, correctable varus deformity, good lateral and PFJ cartilage, intact ligaments, BMI < 30.
- Advantage: Preserves the native joint — delays or avoids the need for joint replacement. Important in young patients because TKR prostheses have a finite lifespan (15–25 years), and revision TKR is more complex.
- Contraindications: Severe articular damage, ligament laxity, severe varus deformities [2]. Also: lateral compartment OA, inflammatory arthritis, significant PFJ disease, flexion contracture > 15°, flexion < 90°.
Osteotomy: correct deformity and relieve joint pressure [2].
| Feature | Details |
|---|---|
| Indication | Young patient, isolated medial compartment OA, correctable varus, intact lateral cartilage |
| Contraindication | Severe articular damage, ligament laxity, severe varus, multicompartment disease |
| Procedure | Medial opening-wedge or lateral closing-wedge tibial osteotomy |
| Goal | Shift mechanical axis to slight valgus (Fujisawa point: 62% of tibial width from medial edge) |
| Outcome | Delays TKR by 10–15 years if successful |
Unicompartmental knee arthroplasty (UKA): e.g. Oxford implant [2]:
"Uni" = one, "compartmental" = compartment, "arthroplasty" = "arthro" (joint) + "plasty" (moulding/reshaping). You replace only ONE compartment of the knee, preserving the other compartments and cruciate ligaments.
Oxford Partial Knee Replacement Selection Criteria [2]:
- Medial bone-on-bone (end-stage medial compartment OA)
- Functionally intact ACL
- Functionally intact MCL
- Full thickness lateral cartilage
- Acceptable patellofemoral joint
These criteria are essential to memorise. The logic: UKA only replaces the medial compartment, so the rest of the knee must be healthy. If the ACL is deficient → abnormal kinematics → rapid failure of the UKA. If the lateral compartment has cartilage loss → they'll need a TKR, not a UKA. If the PFJ is severely involved → persistent anterior knee pain after UKA.
| Feature | Details |
|---|---|
| Indication | Isolated medial compartment bone-on-bone OA meeting all 5 Oxford criteria |
| Advantages | Smaller incision, preserves bone stock, preserves cruciate ligaments → more natural kinematics, faster recovery, better ROM than TKR |
| Disadvantages | Higher revision rate compared to TKR [2] (~1% per year vs ~0.5% for TKR). Revision to TKR is relatively straightforward |
| Contraindication | ACL deficiency, MCL incompetence, lateral compartment/PFJ disease, inflammatory arthritis, fixed varus > 15°, flexion contracture > 15° |
Total knee replacement (TKR) [2]:
This is the definitive surgical treatment for end-stage KOA. Both tibiofemoral condyles and often the patella are resurfaced with metal and polyethylene components.
TKR is preferred in [2]:
- Posteromedial OA (anteromedial OA may be suitable for UKA, but posteromedial OA is not — the posterior cartilage loss pattern requires total replacement)
- Lateral OA (lateral UKA is technically more difficult and has higher failure rates)
- PFJ OA (significant patellofemoral involvement rules out UKA)
- Significant fixed flexion contracture (≥ 10°) (UKA cannot correct significant fixed deformity)
- Arc of motion ≤ 110° (limited pre-operative ROM suggests more diffuse joint disease)
| Feature | Details |
|---|---|
| Indication | End-stage multicompartment OA, failed conservative management, severe pain/disability. Preferred over UKA when criteria for UKA are not met |
| Procedure | Resurfacing of femoral condyles (metal), tibial plateau (metal baseplate + polyethylene insert), and ± patellar button (polyethylene) |
| Prosthesis types | Cruciate-retaining (CR): preserves PCL → more natural rollback. Posterior-stabilised (PS): PCL sacrificed, replaced by cam-post mechanism → more reliable kinematics when PCL is damaged |
| Fixation | Cemented (most common, immediate fixation) vs uncemented/hybrid (biological fixation, better for younger patients with good bone stock) |
| Expected outcomes | 90–95% survival at 15 years. Functional improvement in 85–90% of patients. Expected ROM: 0–120° |
| Contraindications | Active infection (absolute), severe peripheral vascular disease, neuropathic joint (Charcot), extensor mechanism deficiency, severe medical comorbidities making anaesthesia unsafe |
| HTO | UKA | TKR | |
|---|---|---|---|
| Ideal patient | Young ( < 60), active, medial OA, correctable varus | Any age, isolated medial bone-on-bone, intact ACL/MCL/lateral | Older, multicompartment, failed conservative |
| Preserves native joint? | Yes (completely) | Partially (other compartments preserved) | No (all surfaces replaced) |
| Recovery | 6–12 weeks partial WB | Fastest — early WB, < 6 weeks | 6–12 weeks, intensive rehab |
| Longevity | Delays TKR 10–15 years | ~15–20 year survival | ~15–25 year survival |
| Revision | Conversion to TKR if fails | Straightforward conversion to TKR | Revision TKR (complex) |
| Key contraindication | Severe articular damage, multicompartment | ACL deficient, lateral/PFJ disease | Active infection |
- Arthrodesis for small joints (e.g., MCP) [2] — joint fusion. Eliminates pain by eliminating movement. NOT done for the knee (would eliminate walking ability). Reserved for small joints or salvage situations.
- Arthroscopic debridement e.g., remove osteophytes [2] — as discussed, limited role in KOA. Only for mechanical symptoms.
| Agent | Efficacy in KOA | Key Risks | Role |
|---|---|---|---|
| Topical NSAIDs | Moderate | Local skin irritation, minimal systemic | First-line pharmacological |
| Oral NSAIDs | Proven benefit [2] | GI bleeding, renal impairment, CV events | Second-line; short courses + PPI |
| Paracetamol | Does not confer any demonstrable effect or benefit [9] | Hepatotoxicity in elderly | Adjunctive only; limited role |
| Tramadol | Modest | Nausea, dizziness, seizures, serotonin syndrome | Bridge when NSAIDs contraindicated |
| Opioids | Limited benefit [9] | Abuse, addiction, falls, fractures; worse surgical outcomes [9] | Not recommended |
| IA Corticosteroid | Good short-term | Infection risk, cartilage damage with repeated use, hyperglycaemia | Acute flares, diagnostic |
| IA Hyaluronic acid | ?evidence [2] | Pseudosepsis (local reaction), cost | Uncertain; not standard |
| PRP | ?evidence [2] | Minimal | Experimental |
| Glucosamine | No significant benefit | Minimal | Not recommended |
Multi-disciplinary chronic disease management [9]:
The optimal management of KOA requires coordination between:
- Orthopaedic surgeon — surgical planning, injection therapy
- Physiotherapist — exercise prescription, supervised programmes
- Occupational therapist — ADL adaptation, assistive devices
- Nurse specialist — education, self-management support
- Dietitian — weight management programme
- Pain specialist — for refractory pain
- Psychologist — cognitive behavioural therapy for pain catastrophising, depression
- General practitioner — long-term follow-up, medication management
This mirrors the COME programme model at QMH [1].
High Yield Summary
Treatment pyramid: (1) ALL patients → Education, Exercise, Weight loss (the TRIAD). (2) SOME patients → Pharmacological (topical NSAIDs first, then oral NSAIDs with PPI; paracetamol has limited benefit; opioids NOT recommended; IA steroid for flares). (3) FEW patients → Surgery.
First-line management is NOT analgesics — it is weight reduction, education and exercise.
Paracetamol: Network meta-analysis shows no demonstrable benefit in OA at any dose. Paradigm shift from traditional teaching.
Opioids: Very limited role. Worsen surgical outcomes, cause falls/fractures in elderly, addiction risk. Not recommended by updated guidelines.
Arthroscopy in OA: Limited indication ONLY for frequent locking from meniscal tears/loose bodies. Increases rate of OA progression. Shortens time to joint replacement. NOT for debridement/lavage.
Surgical options: HTO (young, single compartment, correctable deformity), UKA (Oxford criteria: medial bone-on-bone + intact ACL + intact MCL + full lateral cartilage + acceptable PFJ), TKR (multicompartment, FFD ≥ 10°, arc ≤ 110°, failed conservative).
Oxford UKA 5 criteria: (1) Medial bone-on-bone, (2) Functionally intact ACL, (3) Functionally intact MCL, (4) Full thickness lateral cartilage, (5) Acceptable PFJ.
ERAS protocol: MSSA screening + decolonisation, pre-op analgesics, dexamethasone IV, HbA1c < 8, confirmed discharge plan.
Active Recall - Management of Knee OA
References
[1] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf (p2, p11, p34, p35, p36, p42, p43) [2] Senior notes: maxim.md (sections 7.4 OA knee, 9.1 Osteoarthritis) [5] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p12) [9] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p2, p8, p10, p13, p15, p18, p19, p28, p29, p30, p31) [10] Lecture slides: GC 229. Hip Arthritis (1).pdf (p34, p37, p38, p39) [11] Senior notes: maxim.md (section 1.3 Management overview — ERAS)
Complications of Knee Osteoarthritis
Complications of KOA can be divided into two broad categories: (A) complications of the disease itself (what happens if OA progresses untreated or inadequately treated), and (B) complications of treatment (particularly surgical complications, which are heavily tested in exams). Let's go through both systematically.
A. Complications of the Disease Itself
- Mechanism: OA is a progressive disease. Without intervention, the catabolic cycle of cartilage degradation → synovitis → more degradation continues relentlessly. Asymmetric cartilage loss leads to progressive malalignment.
- Genu varum (most common) — progressive medial compartment cartilage loss → the medial joint space collapses → the tibia angulates into varus → this increases medial loading further → vicious cycle of accelerating medial wear.
- Genu valgum — less common, occurs with lateral compartment predominance.
- End-stage disease (joint death) [5] — complete loss of cartilage (bone-on-bone), severe deformity, and essentially a "dead" joint that can only be salvaged by replacement.
- Fixed flexion contracture — progressive capsular fibrosis, posterior osteophyte impingement, and hamstring contracture lead to inability to fully extend the knee. This significantly impairs gait (the knee cannot fully extend during stance phase → shortened stride length → increased energy expenditure → reduced walking distance).
- KOA is the leading cause of mobility disability in older adults.
- Progressive pain and stiffness → reduced walking distance → inability to perform ADLs (climbing stairs, rising from a chair, putting on shoes) → loss of independence → need for assistive devices → eventual wheelchair dependence in severe cases.
- KOA is a major cause of adult disability [1].
- Quadriceps atrophy — the most important muscular consequence.
- Mechanism: Pain → arthrogenic muscle inhibition (a reflex mediated by joint mechanoreceptors that suppresses quadriceps motor neuron activation) → disuse atrophy. This is NOT simply "the patient isn't using their leg" — it is an active neurological inhibition that occurs even if the patient tries to use their quads.
- Weak quadriceps → reduced dynamic knee stabilisation → more abnormal joint loading → more cartilage damage → more pain → more inhibition. A true vicious cycle.
OA is a serious disease [1]:
| Systemic Complication | Mechanism |
|---|---|
| Increased risk of cardiovascular/respiratory disorder [1] | Chronic pain → immobility → reduced physical activity → weight gain → metabolic syndrome (hypertension, dyslipidaemia, insulin resistance) → atherosclerotic cardiovascular disease. Additionally, chronic NSAID use for OA pain carries independent cardiovascular and renal risk |
| Increased risks of psychological disorder [1] | Chronic pain → depression, anxiety, social isolation. Loss of independence and inability to participate in previously enjoyed activities → grief and reduced self-worth. Depression in turn amplifies pain perception (central sensitisation) — another vicious cycle |
| Increased risks of sleep disturbance [1] | Nocturnal pain (especially in advanced OA with rest pain), difficulty repositioning in bed due to stiffness, depression-related insomnia. Poor sleep → fatigue → reduced pain coping → worsening function |
| Increased risk of mortality [1] | Not directly from the joint disease, but mediated through: (1) reduced physical activity → cardiovascular death, (2) depression → suicide/neglect of other health conditions, (3) polypharmacy (NSAIDs, opioids) → GI bleeding, renal failure, falls, (4) immobility → venous thromboembolism. OA patients have a 1.5× increased all-cause mortality compared to age-matched controls without OA |
OA Kills — Indirectly
Students are often surprised that OA increases mortality. The mechanism is entirely indirect — through immobility, metabolic syndrome, depression, and treatment side effects. This is why the emphasis on exercise and weight loss is so important: you're not just treating a sore knee, you're potentially reducing cardiovascular mortality.
- As cartilage thins and joint congruence is lost, the menisci bear disproportionate load → degenerative meniscal tears. These are extremely common in OA (found incidentally on MRI in the majority of patients with KL Grade 3–4).
- Chronic effusion stretches the joint capsule and ligaments → ligamentous laxity → instability → giving way → further abnormal joint loading.
- Cruciate ligament degeneration (especially the ACL) is common in advanced KOA — the ACL becomes attenuated, mucoid, and eventually functionally incompetent.
- Mechanism: Chronic synovitis → excess synovial fluid production → fluid herniates through a weak point in the posterior capsule (usually the gastrocnemius-semimembranosus bursa) → formation of a popliteal cyst.
- Usually asymptomatic but can cause posterior knee pain, stiffness, and a palpable mass.
- Complication of Baker's cyst: Rupture → fluid dissects into the calf → acute calf pain and swelling mimicking deep vein thrombosis (pseudothrombophlebitis syndrome). Always consider ruptured Baker's cyst in the differential of acute calf swelling in an OA patient.
- KOA patients have a significantly increased fall risk due to: quadriceps weakness, proprioceptive loss, pain-induced gait abnormalities, and medication side effects (NSAIDs → dizziness; opioids → sedation).
- Elderly patients are at particular risk of experiencing side effects — sedation and dizziness which predispose to falls and fractures [9] (in the context of opioid use, but the fall risk applies broadly).
- Falls → fractures (hip, distal radius, vertebral) → further immobility → further deconditioning → accelerated disability.
- In longstanding KOA, peripheral nociceptor sensitisation (from chronic synovitis and subchondral bone damage) can lead to central sensitisation — where the central nervous system amplifies pain signals even from normal mechanical stimuli.
- Clinically manifests as: allodynia (pain from normally non-painful stimuli), hyperalgesia (exaggerated pain response), and pain that is disproportionate to the radiographic severity.
- Central sensitisation explains the poor correlation between X-ray severity and symptom severity in some patients, and also explains why some patients continue to have pain even after a technically perfect TKR (10–20% of TKR patients have persistent pain).
B. Complications of Treatment
| Treatment | Complication | Mechanism |
|---|---|---|
| NSAIDs | GI bleeding/peptic ulcer | COX-1 inhibition → reduced gastric mucosal prostaglandins → impaired mucus/bicarbonate barrier |
| Renal impairment | Prostaglandin-mediated afferent arteriolar vasodilation is blocked → reduced GFR, sodium/water retention | |
| Cardiovascular events (MI, stroke) | COX-2 inhibition → reduced endothelial prostacyclin → prothrombotic state | |
| Hypertension | Renal sodium retention + reduced vasodilatory prostaglandins | |
| Paracetamol | Liver function abnormalities [9] | Hepatotoxicity from accumulation of the toxic metabolite NAPQI when glutathione stores are depleted |
| Elderly people with impaired paracetamol clearance [9] | Reduced hepatic metabolism → toxicity at standard doses | |
| Opioids | Drug abuse and addiction [9] | Mu-opioid receptor agonism → dopamine release in nucleus accumbens → reward pathway activation → dependence |
| Sedation and dizziness → falls and fractures [9] | CNS depression, vestibular effects, postural hypotension | |
| Pre-operative opioid use → opioid requirement post-surgery, prolonged hospital stay, greater in-hospital complications, early revision surgery [9] | Opioid tolerance → need higher doses peri-operatively; opioid-induced hyperalgesia; impaired wound healing and immune function | |
| IA corticosteroid | Accelerated cartilage loss (with repeated injections) | Direct chondrotoxicity — steroids suppress chondrocyte matrix synthesis and promote apoptosis |
| Septic arthritis | Introduction of bacteria during injection (rare but devastating — ~1 in 10,000–50,000 injections) | |
| Peri-injection flare | Crystal-induced synovitis from the steroid suspension itself (self-limiting, 24–48 hours) | |
| Skin/fat atrophy, depigmentation at injection site | Local steroid effect on subcutaneous tissue |
Limited role of Knee Arthroscopy in OA Knee [9]:
- Adverse outcomes — DVT (0.4%), PE (0.1%), death (0.03%) [9]
- Increases rate of progression of osteoarthritis [9] — arthroscopic instruments can damage the already thin, friable cartilage surface, and lavage disrupts the synovial fluid environment.
- Shortens time to joint replacement [9]
- Complications of knee arthroscopy: damage to saphenous nerve and vein, peroneal nerve, popliteal vessels [6]
The key teaching point here: arthroscopy for OA is not a benign "keyhole" procedure — it carries real risks and can actually make the disease worse.
No evidence: arthroscopic debridement, arthroscopic chondroplasty (drill holes) [12].
| Complication | Explanation |
|---|---|
| Under-correction / Over-correction | If the mechanical axis is not shifted to the desired point (Fujisawa point), the procedure fails (under-correction) or overloads the opposite compartment (over-correction → lateral compartment OA) |
| Non-union / Delayed union | The osteotomy site may fail to heal, especially in smokers, obese patients, or with inadequate fixation |
| Infection | As with any open surgical procedure |
| Peroneal nerve palsy | The common peroneal nerve wraps around the fibular neck very close to the lateral tibial osteotomy site — at risk during lateral closing-wedge osteotomy |
| Compartment syndrome | Rare but possible — post-operative swelling in the anterior compartment |
| Hardware-related pain | Plates and screws may cause discomfort and require removal |
| Conversion to TKR may be more technically difficult | The altered tibial anatomy can complicate subsequent TKR, though this is generally manageable |
4. Complications of Arthroplasty (UKA and TKR)
These are the most commonly tested complications and are categorised by timing:
| Timing | Complication | Mechanism / Explanation |
|---|---|---|
| Immediate (intraoperative) | Bone fracture | Intraoperative fracture of the femur or tibia during preparation of the bone surfaces or component insertion. Risk factors: osteoporotic bone, excessive force |
| Vascular injury — popliteal artery in TKR | The popliteal artery lies directly behind the posterior capsule of the knee. During posterior capsule release or tibial cut, the artery is at risk, especially in revision surgery or severe fixed flexion contracture. TKR-specific; cf femoral artery in THR [12] | |
| Nerve injury — common peroneal nerve (CPN) in TKR | The CPN wraps around the fibular neck, lateral and superficial. At risk during lateral release, valgus correction, or from post-operative haematoma/swelling. Presents as foot drop (weakness of ankle dorsiflexion and toe extension, sensory loss over dorsum of foot). Cf sciatic nerve in THR [12] | |
| Early (post-operative) | DVT / PE | Venous stasis (immobility during surgery, tourniquet use, post-op bed rest) + endothelial injury (surgical trauma) + hypercoagulability (post-operative inflammation) = Virchow's triad. TKR has one of the highest rates of VTE of any elective surgery. Prophylaxis: LMWH, mechanical (TED stockings, intermittent pneumatic compression), early mobilisation |
| Infection — difficult to detect and treat [12] | Early post-operative infection ( < 4 weeks): acute presentation with wound erythema, swelling, pyrexia, raised CRP. Often haematogenous (Staph. aureus, Staph. epidermidis). Treatment: washout ± liner exchange (DAIR: debridement, antibiotics, implant retention) if within 4 weeks with well-fixed components. Late infection: may require two-stage revision (remove prosthesis → antibiotic spacer → 6 weeks IV antibiotics → re-implantation) | |
| Wound complications | Dehiscence, haematoma, persistent drainage. The anterior knee has relatively poor blood supply → wound healing is slower than many other surgical sites | |
| Stiffness / Arthrofibrosis | Excessive scar tissue formation within the joint. Risk factors: poor pre-operative ROM, inadequate post-operative physiotherapy, infection. May require manipulation under anaesthesia (MUA) if ROM remains < 90° at 6–12 weeks post-op | |
| Late | Leg length discrepancy (LLD) [12] | Must counsel patients beforehand [12]. In TKR, LLD is less common than in THR, but can occur due to component positioning, ligament balancing, or correction of pre-operative flexion contracture (straightening the knee effectively "lengthens" the leg). In THR, LLD is more common due to femoral offset and neck length choices |
| Prosthesis infection (late/chronic) [12] | Can occur months to years after surgery via haematogenous seeding (from dental procedures, UTI, skin infection). Insidious onset: persistent pain, elevated ESR/CRP, loosening on X-ray. Biofilm formation on the prosthesis makes antibiotic penetration poor → often requires prosthesis removal | |
| Patellar instability [12] | Lateral patellar subluxation or dislocation after TKR. Caused by: component malrotation (especially internal rotation of the femoral or tibial component), inadequate lateral release, pre-existing patellar maltracking. Presents as anterior knee pain, catching, giving way | |
| Aseptic loosening | The most common cause of late TKR failure. The prosthesis-cement-bone interface degrades over time due to polyethylene wear debris → macrophage activation → osteolysis (bone resorption around the implant) → loosening. Presents as recurrent pain, radiolucent lines around components on X-ray | |
| Polyethylene wear | The polyethylene insert between the metal femoral and tibial components wears over time. Wear particles trigger osteolysis (see above). Modern highly cross-linked polyethylene has reduced but not eliminated this | |
| Periprosthetic fracture | Fracture of the bone adjacent to the prosthesis, usually from a fall. Risk factors: osteoporosis, female, advanced age. Management depends on fracture location and prosthesis stability — may require ORIF or revision surgery |
UKA: Safer Surgery (Early Perioperative Medical Complications) [9]:
In a study comparing postop complications between UKA and TKA using Medicare data, it was found that the rates of wound complication, myocardial infarction, periprosthetic joint infection, pulmonary embolism, and stiffness were significantly higher among TKA recipients [9].
This makes intuitive sense: UKA is a smaller operation (less bone resection, no tourniquet or shorter tourniquet time, smaller incision, less blood loss, faster surgery) → less physiological insult → fewer perioperative complications. However, UKA has a higher revision rate compared to TKR [2] because progression of OA in the unresurfaced compartments or bearing dislocation may necessitate conversion to TKR.
| Complication | UKA | TKR |
|---|---|---|
| Perioperative medical complications | Lower | Higher |
| Wound complications | Lower | Higher |
| MI, PE | Lower | Higher |
| Periprosthetic infection | Lower | Higher |
| Stiffness | Lower | Higher |
| Revision rate | Higher [2] | Lower |
| Long-term survival | ~85–90% at 15 years | ~90–95% at 15 years |
Post-op [12]:
- Early mobilisation (1 day after operation) — crucial for VTE prevention, maintaining quadriceps function, preventing stiffness.
- Avoid contact sports, extreme ROM [12].
- Survival of replacement (not requiring revision surgery): 15–20 years [12].
The expected lifespan of a modern TKR is 15–25 years. This is why we prefer non-surgical management in younger patients — a 50-year-old who gets a TKR may need a revision at age 65–70, and revision TKR is a much bigger, more complex operation with worse outcomes. This underpins the rationale for HTO (buy time) or UKA (easier to revise to TKR) in younger patients.
High Yield Summary
Disease complications: Progressive deformity (varus most common), fixed flexion contracture, quadriceps wasting (arthrogenic inhibition), loss of function/disability, Baker's cyst (± rupture mimicking DVT), secondary meniscal/ligament degeneration, falls/fractures, central pain sensitisation. Systemic: increased CV/respiratory risk, depression, sleep disturbance, increased mortality — OA is a SERIOUS disease.
Treatment complications:
- NSAIDs: GI bleeding, renal impairment, CV events.
- Paracetamol: liver function abnormalities, especially in elderly.
- Opioids: addiction, sedation/falls, worse surgical outcomes.
- Arthroscopy in OA: DVT/PE/death, accelerates OA progression, shortens time to TKR. No evidence for debridement/chondroplasty.
- TKR specific complications: Immediate (fracture, popliteal artery injury, CPN palsy), Early (DVT/PE, infection — difficult to detect and treat), Late (LLD — must counsel, prosthesis infection, patellar instability, aseptic loosening, periprosthetic fracture).
- UKA is safer perioperatively (lower rates of wound complications, MI, PE, infection, stiffness) but has higher revision rate than TKR.
- Prosthesis survival: 15–20 years.
Active Recall - Complications of Knee OA
References
[1] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf (p5) [2] Senior notes: maxim.md (sections 7.4 OA knee, 9.1 Osteoarthritis) [5] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p13) [6] Senior notes: maxim.md (section 7.2 Soft tissue injuries — complications of knee arthroscopy) [9] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p8, p10, p17, p18, p23, p29) [12] Senior notes: maxim.md (section 9.1 Osteoarthritis — specific complications of total replacement, post-op)
High Yield Summary
Definition: KOA = whole-joint disease (not just cartilage) involving cartilage degradation, subchondral bone remodelling, osteophyte formation, and synovitis in the three knee compartments.
Epidemiology: ~1 billion affected globally by 2050. In Hong Kong, 40% population > 65 by 2050. KOA increases mortality via CV disease, depression, immobility.
Risk Factors: Age, female sex, obesity (mechanical + metabolic), previous trauma, occupation, malalignment, muscle weakness, genetics. Secondary causes in young patients — always look for a cause.
Pathophysiology: Catabolic > anabolic. ADAMTS + MMPs degrade cartilage matrix → cartilage fragments trigger synovitis → IL-1, IL-6, TNF → more MMP release → vicious cycle. Subchondral bone sclerosis and osteophytes are failed repair attempts.
Aging vs OA (High Yield Table): In aging, both synthesis and degradation decrease. In OA, degradation markedly increases while synthesis increases insufficiently → net cartilage loss.
Clinical Features: Pain (worse with activity, better with rest; going downstairs = patellofemoral), stiffness ( < 30 min), swelling, deformity (genu varum most common), crepitus, reduced ROM. Extension lag (muscle) vs fixed flexion contracture (structural).
Radiology — LOSS: Loss of joint space (earliest), Osteophytes, Subchondral sclerosis, Subchondral cysts. Always weight-bearing AP + skyline. KL grading: Grade 2 = definite OA, Grade 4 = bone-on-bone.
Key Distinction: OA = preserved bone density, osteophytes, no erosions. RA = osteopenia, erosions, no osteophytes.
High Yield Summary
Anatomical approach to DDx of knee pain: Anterior (patellofemoral syndrome, patellar tendonitis, Osgood-Schlatter, prepatellar bursitis), Medial (MCL sprain, medial meniscal tear, pes anserine bursitis, medial plica), Lateral (LCL sprain, lateral meniscal tear, ITB syndrome), Posterior (Baker's cyst, PCL injury).
Category approach: Degenerative (OA, degenerative meniscal tear), Inflammatory (RA, PsA, AS), Crystal (gout, CPPD), Infective (septic arthritis — EMERGENCY, TB), Traumatic (ACL/meniscal/ligament tears, fractures), Periarticular (bursitis, tendonitis), Referred (hip OA, lumbar radiculopathy), Neoplastic (osteosarcoma, PVNS).
Critical distinctions: (1) Varus deformity = OA, Valgus = RA. (2) Stiffness < 30 min = OA, > 60 min = RA. (3) LOSS features on X-ray = OA; erosions + osteopenia = RA; chondrocalcinosis = CPPD. (4) Always examine the hip when knee exam is normal — referred pain via obturator nerve. (5) Degenerative meniscal tears on MRI in OA patients are often incidental — don't operate unless mechanical symptoms (locking). (6) Acute hot joint = septic arthritis until proven otherwise — aspirate.
Swelling timing post-injury: Immediate = haemarthrosis (ACL, fracture); Delayed 6–12h = meniscal tear; Chronic = OA.
High Yield Summary
Diagnostic criteria: ACR clinical + radiographic criteria = knee pain + age > 50 / stiffness < 30 min / crepitus + osteophytes on X-ray. NICE 2022: age ≥ 45, activity-related pain, no/brief stiffness → diagnose clinically without imaging.
First-line imaging: Weight-bearing AP and lateral X-rays. Always weight-bearing! Add skyline for PFJ, Schuss view for early OA, standing scanogram for alignment (surgical planning).
LOSS features: Joint space narrowing (earliest), Osteophytes, Subchondral sclerosis, Subchondral cysts. Grade with Kellgren-Lawrence (KL 2 = definite OA, KL 4 = bone-on-bone).
MRI role: Early detection (pre-radiographic stage), assessing meniscal/ligament integrity, pre-operative planning (UKA needs intact ACL). Beware incidental degenerative meniscal tears — don't operate unless mechanical symptoms.
Labs: Not needed for typical KOA. Done to EXCLUDE mimics: ESR/CRP (inflammation), RF/anti-CCP (RA), urate (gout), joint aspirate (infection/crystals). OA synovial fluid: clear, viscous, WBC < 2,000/mm³.
Key principle: Treat the patient, not the X-ray — radiographic severity does not always correlate with symptoms.
High Yield Summary
Treatment pyramid: (1) ALL patients → Education, Exercise, Weight loss (the TRIAD). (2) SOME patients → Pharmacological (topical NSAIDs first, then oral NSAIDs with PPI; paracetamol has limited benefit; opioids NOT recommended; IA steroid for flares). (3) FEW patients → Surgery.
First-line management is NOT analgesics — it is weight reduction, education and exercise.
Paracetamol: Network meta-analysis shows no demonstrable benefit in OA at any dose. Paradigm shift from traditional teaching.
Opioids: Very limited role. Worsen surgical outcomes, cause falls/fractures in elderly, addiction risk. Not recommended by updated guidelines.
Arthroscopy in OA: Limited indication ONLY for frequent locking from meniscal tears/loose bodies. Increases rate of OA progression. Shortens time to joint replacement. NOT for debridement/lavage.
Surgical options: HTO (young, single compartment, correctable deformity), UKA (Oxford criteria: medial bone-on-bone + intact ACL + intact MCL + full lateral cartilage + acceptable PFJ), TKR (multicompartment, FFD ≥ 10°, arc ≤ 110°, failed conservative).
Oxford UKA 5 criteria: (1) Medial bone-on-bone, (2) Functionally intact ACL, (3) Functionally intact MCL, (4) Full thickness lateral cartilage, (5) Acceptable PFJ.
ERAS protocol: MSSA screening + decolonisation, pre-op analgesics, dexamethasone IV, HbA1c < 8, confirmed discharge plan.
High Yield Summary
Disease complications: Progressive deformity (varus most common), fixed flexion contracture, quadriceps wasting (arthrogenic inhibition), loss of function/disability, Baker's cyst (± rupture mimicking DVT), secondary meniscal/ligament degeneration, falls/fractures, central pain sensitisation. Systemic: increased CV/respiratory risk, depression, sleep disturbance, increased mortality — OA is a SERIOUS disease.
Treatment complications:
- NSAIDs: GI bleeding, renal impairment, CV events.
- Paracetamol: liver function abnormalities, especially in elderly.
- Opioids: addiction, sedation/falls, worse surgical outcomes.
- Arthroscopy in OA: DVT/PE/death, accelerates OA progression, shortens time to TKR. No evidence for debridement/chondroplasty.
- TKR specific complications: Immediate (fracture, popliteal artery injury, CPN palsy), Early (DVT/PE, infection — difficult to detect and treat), Late (LLD — must counsel, prosthesis infection, patellar instability, aseptic loosening, periprosthetic fracture).
- UKA is safer perioperatively (lower rates of wound complications, MI, PE, infection, stiffness) but has higher revision rate than TKR.
- Prosthesis survival: 15–20 years.
Infective Tenosynovitis
Infective tenosynovitis is a bacterial infection of the tendon sheath, most commonly affecting the flexor tendons of the hand, characterized by Kanavel's signs including fusiform swelling, flexed posture, tenderness along the sheath, and pain with passive extension.
Necrotizing Fasciitis
Necrotizing fasciitis is a rapidly progressive, life-threatening soft tissue infection characterized by widespread necrosis of the subcutaneous tissue and fascia, often caused by group A Streptococcus or polymicrobial organisms.