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.

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.

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]

What the normal-vs-OA diagram shows: cartilage breakdown, osteophytes, synovial hypertrophy, meniscal damage, subchondral sclerosis, and muscle atrophy side by side — not “cartilage only.” ^[1]

Key points from the lecture slides:

• Cartilage health depends on repeated cyclical loading (Hunter, Annals of Internal Medicine 2007) ^[1]
• Muscle exercise prevents atrophy — the quadriceps is the key muscle for knee OA ^[1]
• This is why exercise is therapeutic, not harmful

The lecture slide contrasts a normal knee with an osteoarthritic knee side by side ^[1]:

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).

The lecture (Nature Reviews Rheumatology, Roos & Arden) illustrates two converging pathways leading to symptomatic OA ^[1]:

• Systemic factors: age, gender, obesity, inactivity, genetics
• Mechanical factors: obesity, joint morphology & alignment, joint loading, muscle weakness, injury

Both pathways converge on susceptibility of joints to damage and failure of repair, which is then amplified by a downstream cascade: comorbidities → pain processing → depression → anxiety → pain sensitisation → symptomatic OA. ^[1]

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.

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]

1. Pain — activity-related, worse after use, improves with rest; if patellofemoral → worse on stairs
2. Swelling — intermittent (effusion) or persistent (capsule thickening/osteophytes)
3. Stiffness — typically < 30 minutes after immobility (vs > 30 min in inflammatory arthritis)
4. Mechanical disorders — locking, giving way, clicking
5. Limp
6. Deformity

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.

Essential Features of Acute Knee Injuries (from lecture slide) ^[1]:

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

Differential Diagnosis of Knee Pain by Anatomic Site ^[1]:

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

The gait cycle consists of a stance phase (heel strike → loading response → mid-stance → terminal stance → pre-swing) and a swing phase (toe-off → mid-swing → terminal swing), with periods of double support at transitions ^[1].

• 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]

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.

Examination tip: Assess passive hip internal rotation — normal ROM is 40°. Restriction or pain on internal rotation is a sensitive sign of hip pathology. ^[1]

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]

1. Weight-bearing AP — assesses medial and lateral tibiofemoral compartments
2. Lateral — assesses flexion contracture, posterior osteophytes
3. Skyline (sunrise/Merchant) — assesses patellofemoral compartment

The hallmarks of knee osteoarthritis (radiographic features): ^[1]

What the weight-bearing XR pair shows: AP + lateral with severe joint-space loss, marginal osteophytes, and subchondral sclerosis — order films standing or you undercall the disease. ^[1]

1. Joint space narrowing (JSN)
2. Subchondral sclerosis
3. Marginal osteophytes
4. Subchondral cysts

A helpful mnemonic: LOSS (used in Maksim Surgery Notes ^[4]):

• Loss of joint space
• Osteophytes
• Subchondral sclerosis
• Subchondral cysts

Kellgren and Lawrence system for grading severity of knee OA: ^[1]

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]

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]

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:

1. Cartilage nutrition — cartilage is avascular; nutrients reach chondrocytes by diffusion through synovial fluid, driven by cyclic loading and unloading during movement
2. Quadriceps and hamstring strengthening — the quadriceps and hamstrings are the focus of training ^[1]; the quadriceps acts as a shock absorber for the knee; weakness → increased impact loading → faster cartilage degeneration
3. Weight management — exercise helps with caloric expenditure
4. Pain modulation — exercise activates endogenous opioid and serotonin pathways
5. 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]

Collaborators: Dept O&T QMH, Nursing Dept MMRC, Physiotherapy Dept MMRC, Occupational Therapy Dept MMRC ^[1]

COME Care Pathway ^[1]:

COME Programme Quantitative Outcomes (n = 55; Kan, Chan et al., HKMJ 2019) ^[1]:

†p < 0.05; ‡p < 0.01 (consecutive significant improvements over each assessment time point). ^[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.

• 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