Knee Osteoarthritis

• 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)

Secondary causes ^[1][2]:

• 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]

The knee joint is the largest and most complex synovial joint in the body. It comprises three compartments:

1. Medial tibiofemoral compartment — between the medial femoral condyle and medial tibial plateau
2. Lateral tibiofemoral compartment — between the lateral femoral condyle and lateral tibial plateau
3. 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].

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]:

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 replacement

Defining Disease State of Osteoarthritis ^[5]:

More effective to prevent disease progression by intervention at early stages ^[5].

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]:

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.

Radiological features (LOSS) ^[2]:

Views ^[2]:

• 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.

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.

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.

• 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.

The European League Against Rheumatism provides a more practical, clinically oriented approach:

Three symptoms + three signs are considered highly predictive of KOA:

Symptoms:

1. Persistent knee pain
2. Limited morning stiffness ( ≤ 30 minutes)
3. Reduced function

Signs:

1. Crepitus
2. Restricted movement
3. 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.

MRI/Biomarkers can detect changes in the composition of bone, cartilage, other soft tissues at the molecular stage of disease ^[5]. Research biomarkers include:

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].

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.

• 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.

• 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).

• 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.

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]:

• Combine with paracetamol: synergistic ^[10]
• If contraindication to use NSAIDs ^[10]

Opioids ^[10]:

• CNS depression, addiction ^[10]
• No routine use ^[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.

Limited role of Knee Arthroscopy in OA Knee ^[9]:

• Limited indication ^[9]:
  • Frequent locking symptoms caused by meniscal tears and loose bodies ^[9]
  • Short term relief of locking symptoms ^[9]
• Potential complications ^[9]:
  • Adverse outcomes — DVT (0.4%), PE (0.1%), death (0.03%) ^[9]
  • Increases rate of progression of osteoarthritis ^[9]
  • Shortens time to joint replacement ^[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.

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].

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]:

1. Medial bone-on-bone (end-stage medial compartment OA)
2. Functionally intact ACL
3. Functionally intact MCL
4. Full thickness lateral cartilage
5. 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.

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)

• 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.

• 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]:

• 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).

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].