GC228 Knee Osteoarthritis: Part A
Knee osteoarthritis is a degenerative joint disease characterized by progressive loss of articular cartilage, subchondral bone changes, and osteophyte formation, leading to pain, stiffness, and impaired mobility.
Knee Osteoarthritis – Part A
Big Idea: Knee osteoarthritis (KOA) is not just "wear and tear" of cartilage — it is a whole joint and whole person disease with systemic consequences including increased cardiovascular mortality. Management follows a treatment pyramid where the core first-line therapy for ALL patients is education, exercise, and weight control, with pharmacological and surgical options reserved for escalation. This lecture by Professor Lewis PK Chan (GC 228, Part A) walks through epidemiology → pathophysiology → clinical assessment → investigations → non-pharmacological management, setting up Part B's coverage of pharmacological and surgical options.
Learning Objectives (from slide 2) [1]:
- Epidemiology & clinical importance of KOA
- Pathophysiology & risk factors for developing KOA
- Clinical presentation & workup of KOA
- Non-pharmacological & pharmacological treatment options
- Surgical interventions for managing KOA
- Case studies
How it fits into exams: KOA is a bread-and-butter orthopaedic topic tested in MCQs (radiographic features, treatment evidence), SAQs (clinical assessment, management pyramid), and OSCE stations (knee examination, gait assessment, X-ray interpretation). The 2025 Fourth Summative MCQ Q48 directly tests which KOA treatments are evidence-supported [13].
1. Introduction & Epidemiology
KOA is a major cause of adult disability. The Global Burden of Disease (GBD) study estimates almost 1 billion individuals will be affected by 2050 (Lancet Rheumatol 2023). [1]
Why this matters: OA is not a trivial condition of aging. It is a leading contributor to years lived with disability (YLD) globally, and with population aging, demand for KOA services will surge.
By 2050, 40% of the Hong Kong population will be aged 65 or above — ranking fifth in the world (WHO forecast; Office of the Government Economist, HKSAR, 2023). [1]
This demographic shift means KOA prevalence in HK will rise dramatically, making knowledge of non-surgical management critical for every doctor, not just orthopaedic surgeons.
High Yield – OA Can Kill You
OA is associated with increased risk of: [1]
- Cardiovascular/respiratory disorders
- Psychological disorders
- Sleep disturbance
- Increased mortality
A 15-year Japanese longitudinal study (Kasai et al., 601 subjects, mean age 67.8, FU 2000–2014) showed:
- Knee OA hazard ratio for mortality: 1.97 (same as DM!)
- Osteoporosis HR: 1.61
- DM HR: 1.97
- HT HR: 1.39
- Common cause of death: cardiovascular disease
The lecture's emphatic point: "OA Can KILL you!!" — this reframes OA from a nuisance to a serious systemic disease.
Why does OA increase mortality? The mechanism is largely through inactivity. Knee pain → reduced mobility → physical deconditioning → metabolic syndrome worsening → increased cardiovascular risk. Additionally, chronic pain drives psychological distress and sleep disturbance, which independently raise CV mortality risk.
2. Pathophysiology: Not Just "Wear and Tear"
The "wear and tear" mindset results in INACTIVITY — this is harmful because it leads patients to avoid exercise, accelerating disease progression. [1]
This is a critical teaching point. If you tell a patient "your knee is worn out," they will stop moving. Inactivity causes:
- Muscle atrophy (especially quadriceps)
- Cartilage degeneration (cartilage is avascular and depends on repeated cyclical loading for nutrient diffusion)
- Weight gain → increased joint load → more pain → more inactivity (vicious cycle)
OA is a whole joint disease — it involves cartilage, subchondral bone, synovium, ligaments, menisci, periarticular muscles, and capsule. [1]
Key points from the lecture slides:
OA is a whole person disease [1] — it affects physical function, mental health, social participation, and overall quality of life. This framing underpins the need for multidisciplinary management (not just pills and surgery).
81% of knee OA patients are highly unsatisfied with current treatment (Peoplemetrics Patient Segmentation Research, 2007). Today's treatment paradigm is trapping patients in a vicious cycle of OA knee pain. [1]
The traditional patient journey (HA statistics, April 2023–March 2024) shows patients cycling through pain → NSAIDs → more pain → repeat visits → eventual surgery, without adequate investment in the first-line core treatments. This is the problem that programmes like BOA (Better Management of Osteoarthritis, Sweden 2004) and COME (Hong Kong) aim to solve.
Risk factors for knee OA: [1]
- Obesity — strongest modifiable risk factor; OA is more common at extremes of body weight; places excess load on weight-bearing joints
- Injury — previous knee injury (ACL tear, meniscal tear, intra-articular fracture) → post-traumatic OA
- Occupation — repetitive kneeling/squatting (farmers, tilers, miners)
- Other — age, female sex, genetics, joint malalignment
| Risk Factor | Mechanism | Clinical Relevance |
|---|---|---|
| Obesity | Increased mechanical load + systemic inflammation (adipokines) | Weight loss of even 5–10% significantly reduces symptoms |
| Previous injury | Disrupted articular cartilage, altered biomechanics, instability | Always ask about trauma history — post-traumatic OA can present in younger patients |
| Occupation | Repetitive microtrauma | "Farmer's hip," kneeling occupations |
| Age | Cumulative cartilage damage, reduced regenerative capacity | Most common in > 50y |
| Female sex | Hormonal factors, joint laxity | More common after menopause |
| Malalignment | Varus → medial compartment overload; valgus → lateral overload | Predisposes to asymmetric OA |
The Shaquille O'Neal Example
The lecture uses NBA superstar Shaquille O'Neal as an example: OA for over a decade, extreme body weight, toll on weight-bearing joints (knees, hips), THA done in 2023. This illustrates that OA affects both extremes of body weight (obesity and elite athletes with high joint loading). [1]
4. Clinical Assessment of Knee Osteoarthritis
M/70, IHD/AF on apixaban, history of gastritis, complains of knee pain — how do you assess? [1]
This case is important for exam purposes because:
- Apixaban = anticoagulation → relevant for surgical planning (perioperative management)
- History of gastritis = caution with NSAIDs (even COX-2 selective) → management implications
- Comorbidities affect treatment choice at every level
Chief complaints in knee OA: [1]
- Pain — activity-related, worse after use, improves with rest; if patellofemoral → worse on stairs
- Swelling — intermittent (effusion) or persistent (capsule thickening/osteophytes)
- Stiffness — typically < 30 minutes after immobility (vs > 30 min in inflammatory arthritis)
- Mechanical disorders — locking, giving way, clicking
- Limp
- Deformity
| Feature | OA (Degenerative) | Inflammatory Arthritis (e.g. RA) |
|---|---|---|
| Morning stiffness | < 30 min | > 30 min (often > 1 hour) |
| Pain pattern | Worse with activity, better with rest | Better with gentle activity, worse with rest |
| Swelling | Bony + occasional effusion | Soft, boggy synovial thickening |
| Systemic features | Usually absent | Fatigue, malaise, fever possible |
| Joint distribution | Weight-bearing: knee, hip, spine; hands (DIP, PIP, 1st CMC) | Small joints: MCP, PIP, wrist (RA spares DIP) |
Location of pain helps identify the compartment involved: [1]
- Medial → medial compartment OA (most common)
- Lateral → lateral compartment OA
- Anterior → patellofemoral OA (worse on stairs, squatting)
- Posterior → Baker's cyst, posterior structures
- Diffuse → tricompartmental disease
Always ask about trauma history — knee pain after injury suggests post-traumatic OA or internal derangement (meniscal/ligamentous injury). [1]
In younger patients (< 50y) with knee OA, secondary causes must be actively sought: previous ACL injury, meniscectomy, intra-articular fracture.
Infective causes must be excluded — septic arthritis is a surgical emergency. [1]
Other differentials for knee pain include:
- Crystal arthropathy (gout, pseudogout — especially in elderly patients with KOA)
- Referred pain from the hip (see below)
- Inflammatory arthritis (RA, SpA)
- Meniscal pathology, ligament injury
- Osteonecrosis
5. Physical Examination
5.1 The Orthopaedic Exam Framework
Look → Feel → Move [1]
This is the universal orthopaedic examination framework. For knee OA:
- Standing: assess alignment — varus (bow-leg) or valgus (knock-knee) deformity [1]
- Knee deformity on standing — varus is the most common deformity in KOA (medial compartment disease) [1]
- Muscle wasting — especially quadriceps (compare both sides)
- Scars from previous surgery
- Skin changes, swelling
- Walking aids
- Warmth (suggests active inflammation or infection)
- Effusion (patellar tap, bulge test)
- Tenderness along joint lines
- Bony enlargement (osteophytes)
- Crepitus on movement
Key movement assessment in knee OA: [1]
FFD vs Extension Lag – Key Exam Discriminator
This distinction is commonly tested:
- Fixed flexion deformity = structural block to extension (both active AND passive limited) — caused by osteophytes, capsular contracture, or posterior meniscal fragment
- Extension lag = full passive extension is possible but active extension is deficient — caused by quadriceps weakness (e.g. muscle atrophy, post-operative, vastus medialis dysfunction)
If the examiner asks "what is the difference between FFD and extension lag?" — the key discriminator is whether passive extension is preserved.
Gait examination is essential — the lecture shows a video of a 77-year-old female with antalgic gait. [1]
Key gait features in KOA:
- Antalgic gait — shortened stance phase on the painful side
- Lateral thrust/varus thrust — worsening of varus alignment while the limb is bearing weight, with return to less varus as weight is transferred off the limb [1]
Varus Thrust – High Yield Definition
Varus thrust = dynamic worsening of varus malalignment during weight-bearing, which reduces as weight is unloaded. It indicates lateral ligamentous laxity and is a sign of medial compartment overloading — a poor prognostic sign associated with faster disease progression. [1]
Pain can be referred to the knee from other sites, most notably the ipsilateral hip. Every patient with knee pain should have a careful examination of the hip. [1]
Why? The obturator nerve (L2–L4) innervates both the hip joint capsule and the medial knee area. Hip pathology (OA, AVN, fracture, slipped capital femoral epiphysis in adolescents) can present solely as knee pain. Missing a hip fracture in an elderly patient presenting with "knee pain" is a classic clinical and exam error.
6. Investigations / Workup of Knee OA
Weight-bearing X-rays are essential — non-weight-bearing films underestimate joint space narrowing. [1]
The lecture directly contrasts non-weight-bearing XR vs weight-bearing XR side by side to demonstrate this point [1]. This is reinforced by Apley's textbook which states: "An anteroposterior x-ray must be obtained with the patient standing and bearing weight; only in this way can small degrees of articular cartilage thinning be revealed." [3]
Standard XR Knee Views
Standard views: [1]
- Weight-bearing AP — assesses medial and lateral tibiofemoral compartments
- Lateral — assesses flexion contracture, posterior osteophytes
- Skyline (sunrise/Merchant) — assesses patellofemoral compartment
The hallmarks of knee osteoarthritis (radiographic features): [1]
- Joint space narrowing (JSN)
- Subchondral sclerosis
- Marginal osteophytes
- Subchondral cysts
A helpful mnemonic: LOSS (used in Maksim Surgery Notes [4]):
- Loss of joint space
- Osteophytes
- Subchondral sclerosis
- Subchondral cysts
| Feature | Mechanism / Explanation |
|---|---|
| Joint space narrowing | Articular cartilage is radiolucent; as cartilage is lost, the "joint space" on X-ray narrows. Earliest and most important sign. Asymmetric (usually medial > lateral in KOA) |
| Subchondral sclerosis | Increased bone density beneath the damaged cartilage due to remodeling under increased stress. Appears as a whiter/denser line on XR |
| Marginal osteophytes | New bone formation at joint margins — the body's attempt to redistribute load by increasing the articular surface area. Hallmark of OA |
| Subchondral cysts | Focal areas of bone resorption due to microfractures allowing synovial fluid intrusion, or necrosis of subchondral trabeculae |
OA vs RA on X-ray – Key Discriminator
| Feature | Osteoarthritis | Rheumatoid Arthritis |
|---|---|---|
| Joint space | Asymmetric narrowing | Uniform/symmetrical narrowing |
| Bone density | Preserved (or sclerotic) | Juxta-articular osteopenia |
| Osteophytes | Present | Absent |
| Erosions | Absent | Marginal erosions present |
| Distribution | Weight-bearing joints, DIP/PIP hands | MCP, PIP, wrist (spares DIP) |
Kellgren and Lawrence system for grading severity of knee OA: [1]
| Grade | Description |
|---|---|
| 0 | No features of OA |
| 1 | Doubtful — minute osteophytes of doubtful significance |
| 2 | Minimal — definite osteophytes, unimpaired joint space |
| 3 | Moderate — moderate diminution of joint space |
| 4 | Severe — joint space greatly reduced with subchondral sclerosis, large osteophytes, altered bone contour |
Clinical significance: KL grade correlates with disease severity but does NOT always correlate with symptoms. Some patients with KL 4 have minimal pain, while others with KL 2 may have significant functional impairment. Treatment should be guided by symptoms and function, not just radiographic grade.
The lecture does not emphasize blood tests because KOA is primarily a clinical + radiological diagnosis. However, in the context of the case (M/70 with IHD, AF, gastritis):
- Bloods may be needed to exclude inflammatory arthritis (ESR, CRP, RF, anti-CCP — all normal in primary OA)
- Joint aspiration if effusion present — OA synovial fluid is clear, viscous, low cell count (< 2,000 WBC/mL) vs inflammatory (cloudy, high cell count) or septic (purulent, > 50,000) [6]
7. Non-Pharmacological Management of Knee OA
The OA Treatment Pyramid (Roos & Juhl, Osteoarthritis and Cartilage 2012): [1]
Surgery ← FEW patients
Pharmacological Rx, ← SOME patients
Aids, Passive Tx
Education, Exercise & ← ALL patients
Weight Control (CORE)First line treatment for ALL patients: Education, Exercise, and Weight Control [1] First + second line: add pharmacological pain relief, aids and passive treatments (given by a therapist) for SOME patients [1] First + second + third line: add surgery for FEW patients [1]
The Pyramid – Core Exam Point
Education, exercise, and weight control are the CORE first-line treatment for ALL KOA patients, regardless of severity. They must be tried before escalating to pharmacological or surgical options. This is the most commonly tested management principle. [1]
Passive modalities in physiotherapy DON'T work in the long run. [1] Evidence-based PT = Active Exercise [1]
This is a critical lecture point. Many patients (and some clinicians) think physiotherapy means heat packs, TENS, ultrasound, etc. The lecture explicitly states these passive modalities have no long-term benefit. The evidence supports active exercise.
Exercise needs to have sufficient intensity, frequency & duration (Juhl et al., Arthritis & Rheumatology 2014 — systematic review and meta-analysis, 48 trials): [1]
- Focus on: improving aerobic capacity, quadriceps muscle strength, or lower extremity performance
- Dose: supervised, 2–3 times weekly for 6 weeks minimum
- To enhance compliance: behavioral change model, individual goal setting
Why exercise works in KOA:
- Cartilage nutrition — cartilage is avascular; nutrients reach chondrocytes by diffusion through synovial fluid, driven by cyclic loading and unloading during movement
- Quadriceps strengthening — the quadriceps acts as a shock absorber for the knee; weakness → increased impact loading → faster cartilage degeneration
- Weight management — exercise helps with caloric expenditure
- Pain modulation — exercise activates endogenous opioid and serotonin pathways
- Psychological benefit — reduces depression, improves self-efficacy
COME = Comprehensive Osteoarthritis ManagEment (MMRC, Queen Mary Hospital) [1]
The COME programme is a local HKU/HA initiative demonstrating the lecture's principles in practice:
Team members: [1]
- O&T Surgeon
- Nurse
- Physiotherapist
- Occupational Therapist
- Prosthetist & Orthotist (P&O)
- Dietician
- Psychologist
- Pharmacist
Programme structure: [1]
| Stage | Content |
|---|---|
| Assessment | OA knee patient referred to MMRC — individual visit |
| Education (3 occasions) | Occasion 1: What is OA? Risk factors, Symptoms, Treatment. Occasion 2: Exercise, Physical activity in daily living, Coping, Management. Occasion 3: OA communicator, To live with OA |
| Minimal intervention | — |
| PT | Supervised group exercise (6 weeks) |
| OT | ADL management and training |
| FU I | 3 months — individual visit with PT |
| FU II | 1 year — telephone follow-up |
Collaborators: Dept O&T QMH, Nursing Dept MMRC, Physiotherapy Dept MMRC, Occupational Therapy Dept MMRC [1]
Successful case: F/64, minimal knee pain (VAS 1-2), walks unaided > 1 hour, exercises every day, does NOT want TKA. [1]
This case illustrates that with proper non-surgical management, even patients who might otherwise progress to surgery can achieve excellent functional outcomes and avoid arthroplasty.
| Intervention | Evidence Level | Details |
|---|---|---|
| Patient education | Strong | Understanding OA as whole-joint disease; dispelling "wear and tear" myth; self-management strategies |
| Exercise therapy | Strong (meta-analyses) | Quadriceps strengthening, aerobic fitness, supervised 2-3×/week for ≥6 weeks |
| Weight loss | Strong | Even 5-10% weight loss improves symptoms; reduces mechanical load and systemic inflammation |
| Walking aids | Moderate | Stick in contralateral hand reduces ipsilateral knee load by ~20% |
| Knee braces/orthotics | Moderate | Unloader braces for unicompartmental OA; lateral wedge insoles (debated) |
| Passive PT (heat, TENS, US) | Weak/no long-term benefit | May provide short-term symptom relief but NOT a substitute for active exercise |
BOA = Better Management of Osteoarthritis (Sweden, 2004) [1]
The lecture references BOA as the inspiration for the COME programme. BOA demonstrated that structured first-line non-surgical care reduces the need for joint replacement and improves patient outcomes. The Hong Kong adaptation (HKJM 2019, HKJM 2024) confirmed similar benefits in the local population. [1]
9. Integration with Related Material
- OA is differentiated from RA by: non-inflammatory pattern, < 30 min morning stiffness, DIP involvement, osteophytes on XR, preserved bone density
- RA spares DIP; OA commonly affects DIP (Heberden's nodes)
- Hip and knee OA are the two major indications for joint replacement — the most common reconstructive procedures in orthopaedics
- Must differentiate OA flare from crystal arthropathy (gout/pseudogout) and septic arthritis — joint aspiration is key
- OA with CPPD (calcium pyrophosphate deposition) can present with acute flares mimicking gout [5]
- Same radiographic features (LOSS) and treatment principles apply to all OA joints
- Hand OA: Heberden's nodes (DIP), Bouchard's nodes (PIP), 1st CMC squaring
Past Paper Questions
Stem: "A 68-year-old lady suffered from left knee mechanical pain for 3 years. X-ray of the left knee showed reduced joint space in the medial compartment with marginal osteophyte formation. Which of the following is an effective and evidence-supported treatment of knee osteoarthritis?"
A. Arthroscopic debridement B. Glucosamine C. Knee replacement D. Paracetamol
Correct Answer: C. Knee replacement
Rationale: This question tests which treatments have robust evidence.
- Arthroscopic debridement — RCTs (Moseley 2002, Kirkley 2008) showed NO benefit over sham surgery for OA knee; NOT evidence-supported
- Glucosamine — meta-analyses show NO clinically significant benefit over placebo; NOT recommended by most guidelines
- Knee replacement — strong evidence for pain relief and functional improvement in patients with severe KOA who have failed non-operative management
- Paracetamol — recent large meta-analyses (Machado 2015) show paracetamol has minimal/clinically insignificant effect on OA pain; updated guidelines (OARSI 2019) have moved away from recommending it
Trap: Many students pick D (paracetamol) because it is traditionally taught as first-line analgesic. However, the evidence no longer supports paracetamol as an effective treatment for KOA. The 2025 paper reflects this updated evidence.
Stem: "A 50-year-old business man presented to the Accident and Emergency Department with severe low back pain... X-ray showed osteopenia and wedge fracture of the 3rd lumbar vertebra. Further questioning revealed that he had been receiving frequent injections for osteoarthritis of his knee for over 1 year. Which of the following is the MOST LIKELY cause of his osteoporosis?"
A. Hyperparathyroidism B. Hypogonadism C. Hypothyroidism D. Iatrogenic due to exogenous steroid
Correct Answer: D. Iatrogenic due to exogenous steroid
Rationale: "Frequent injections for osteoarthritis of his knee" = repeated intra-articular corticosteroid injections. Chronic exogenous steroid → suppressed bone formation (osteoblast inhibition) → osteoporosis → pathological vertebral fracture. This is a classic complication of repeated steroid injections for KOA.
Stem: "Which of the following is NOT associated with anterior uveitis?"
A. Juvenile idiopathic arthritis B. Osteoarthritis C. Psoriatic arthritis D. Behcet disease
Correct Answer: B. Osteoarthritis
Rationale: Anterior uveitis is associated with inflammatory conditions (JIA, PsA, Behcet's, AS). OA is a non-inflammatory/degenerative disease and is NOT associated with uveitis. This tests the fundamental distinction between degenerative and inflammatory joint disease.
Stem: "A 50-year-old lady complains of deformities of her fingers in the distal-interphalangeal joints and the proximal-interphalangeal joints. There are Heberden's nodes in the distal-interphalangeal joints."
Diagnosis options include: Collateral ligament rupture / Gonococcal arthritis / Gouty arthritis / Joint subluxation/dislocation / Osteoarthritis / Rheumatoid arthritis / Scleroderma / Septic arthritis
Correct Answer: E. Osteoarthritis
Rationale: Heberden's nodes = bony enlargement at DIP joints = pathognomonic for OA. RA spares DIP. Bouchard's nodes at PIP also suggest OA.
Stem: "A 52-year-old man presents with epigastric pain for 3 months... He takes ibuprofen daily for knee osteoarthritis. Labs: Hb 10.8 g/dL (baseline 14), MCV 82 fL..."
A. Directly offer upper endoscopy B. Faecal occult blood test C. Trial of PPI D. Urea breath test
Correct Answer: A. Directly offer upper endoscopy
Rationale: Alarm features present: age > 50, weight loss (4 kg), anaemia, daily NSAID use. These are red flags for upper GI malignancy → direct endoscopy, not empirical PPI trial. This case links KOA management (daily NSAID use) to GI complications — relevant to the lecture case stem (M/70 with gastritis on apixaban).
Exam Intelligence
| Trap | Correct Approach |
|---|---|
| Ordering non-weight-bearing XR for suspected KOA | Always specify weight-bearing AP — non-WB films miss early JSN |
| Confusing FFD with extension lag | FFD = both active + passive limited; Extension lag = passive full, active limited (quadriceps problem) |
| Saying "paracetamol is first-line analgesic" for KOA | Updated evidence: paracetamol is minimally effective for OA pain; exercise is first-line |
| Treating OA as just "cartilage wear" | OA = whole joint + whole person disease |
| Prescribing NSAIDs without considering comorbidities | Always check for GI risk (gastritis, PUD), CV risk (IHD, AF), renal function, anticoagulation |
| Recommending passive PT (TENS, heat) as main therapy | Passive PT has no long-term benefit; active exercise is the evidence-based approach |
| Missing hip pathology in a patient with "knee pain" | Always examine the ipsilateral hip — obturator nerve refers pain to knee |
| Thinking arthroscopic debridement works for OA | Multiple RCTs show no benefit — this is NOT an evidence-supported treatment |
| If asked about... | Key differentiator |
|---|---|
| OA vs RA on XR | Osteophytes + sclerosis + preserved bone density = OA; Erosions + osteopenia = RA |
| OA morning stiffness vs RA | OA < 30 min; RA > 30 min (often > 1 hr) |
| KL Grade 2 vs Grade 3 | Grade 2 = definite osteophytes but unimpaired joint space; Grade 3 = moderate JSN |
| Varus thrust vs static varus | Varus thrust is dynamic (worsens with weight-bearing, improves off-loading); static varus is present at rest |
High Yield Summary
- KOA is a serious disease — HR for mortality 1.97 (equal to DM!), mainly via cardiovascular death from inactivity
- OA is a whole joint and whole person disease, NOT just "wear and tear" of cartilage
- Risk factors: obesity (strongest modifiable), injury, occupation, age, female sex, malalignment
- Clinical assessment: Pain (activity-related, < 30 min morning stiffness), swelling, stiffness, mechanical symptoms, deformity; ALWAYS examine the hip
- Look-Feel-Move: FFD (both active + passive limited) ≠ extension lag (passive full, active limited)
- Varus thrust: dynamic worsening of varus during weight-bearing — poor prognostic sign
- Imaging: ALWAYS request weight-bearing AP, lateral, and skyline views
- Radiographic features (LOSS): Loss of joint space, Osteophytes, Subchondral sclerosis, Subchondral cysts
- Kellgren-Lawrence grading: 0 (normal) → 4 (severe) — but symptoms don't always correlate with grade
- Treatment pyramid: Core first-line for ALL = Education + Exercise + Weight Control; Pharmacological for SOME; Surgery for FEW
- Exercise must be active (not passive PT), supervised, 2-3×/week for ≥6 weeks, focusing on quadriceps strength and aerobic capacity
- Multidisciplinary care (COME programme): surgeon, nurse, PT, OT, dietician, psychologist, pharmacist, P&O
- Paracetamol has minimal efficacy for OA pain (updated evidence); glucosamine and arthroscopic debridement are NOT evidence-supported
Active Recall - Knee OA Part A
[1] Lecture slides: GC 228. Knee Osteoarthritis_Part A.pdf (all pages) [2] Lecture slides: GC 228. Knee Osteoarthritis_Part B.pdf (p1, p28 — objectives review) [3] Lecture slides: LL exam Clinical Skill Practice Session 2023.pdf (pp67–78 — Apley's knee OA section) [4] Senior notes: Maksim Surgery Notes.pdf (p270 — Osteoarthritis section) [5] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (pp1663, 1671 — OA section) [6] Senior notes: Ryan Ho Rheumatology.pdf (pp4, 43 — joint examination and OA) [7] Lecture slides: GC 074. Multiple joint pain.pdf (p2 — OA vs RA approach) [8] Lecture slides: CFB (OT04) Reconstruction.pdf (p33 — hip and knee OA) [9] Lecture slides: GC 075. Pain red joint.pdf [10] Lecture slides: Upper Limb Painful Conditions_Dr. Margaret Woon Man FOK_4. Osteoarthritis.pdf [11] Senior notes: Ryan Ho Fundamentals.pdf (pp125, 406, 409 — rheumatological examination, monoarthritis approach) [12] Senior notes: Block A - Multiple joint pain_ Rheumatoid arthritis and the concept of inflammatory arthritis.pdf (p1 — OA vs RA) [13] Past papers: 2025 Fourth Summative MCQ.pdf (Q48, Q85) [14] Past papers: 2024 Fourth Summative MCQ.pdf (Q31) [15] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q12) [16] Past papers: 2018 Fourth Summative MCQ.pdf (Q22)
GC227 Cervical Spine Pathology
Cervical spine pathology encompasses a range of disorders affecting the cervical vertebrae, intervertebral discs, spinal cord, and surrounding structures, including degenerative disc disease, herniation, stenosis, myelopathy, fractures, and inflammatory conditions that can result in neck pain, radiculopathy, or neurological deficits.
GC228 Knee Osteoarthritis: Part B
Knee osteoarthritis is a degenerative joint disease involving progressive cartilage loss, subchondral bone changes, and inflammation of the knee, with Part B focusing on its clinical management, rehabilitation, and surgical treatment options.