• OA is the most common joint disease worldwide ^[1][5].
• Radiographic OA of the knee is present in ~30–40% of adults over 65; symptomatic knee OA affects ~10–15% of adults > 60 years.
• OA is the leading cause of disability in the elderly globally, contributing enormously to healthcare costs and loss of productivity.

• Increasingly common with old age; age of onset > 40 years ^[5].
• Females are more commonly affected than males — particularly after menopause (suggesting a hormonal protective role of oestrogen on cartilage and bone). The sex difference is most pronounced for hand and knee OA ^[5].
• In Hong Kong, with a rapidly ageing population (median age ~46 years, among the highest globally), OA is a major public health burden. Knee OA is extremely common in elderly patients presenting to Orthopaedics and Geriatrics clinics.

• Articular cartilage is avascular, aneural, and alymphatic — it receives nutrition solely by diffusion from synovial fluid (and to a lesser extent, from subchondral bone).
• Chondrocytes (the only cells in cartilage) have very low metabolic activity and low proliferative capacity.
• The extracellular matrix (ECM) is the functional unit: type II collagen fibres provide tensile strength; proteoglycans (especially aggrecan, bound to hyaluronic acid) attract water via osmotic pressure → this water content provides compressive resistance ("like a water balloon").
• Because of avascularity and low cellularity, cartilage has extremely limited intrinsic repair capacity. This is the fundamental reason why OA is progressive and, once established, largely irreversible.

This is a very commonly asked question. Since cartilage has no nerves, cartilage loss itself is painless. The sources of pain in OA are:

As noted in the senior notes ^[9]:

• Role of OA: usually present prior to CPPD disease; ?due to proteoglycan loss → ↓inhibition of mineralisation + interference of growth factor; cell damage → ↑release of cellular ATP
• CPPD crystal deposition (chondrocalcinosis) is very commonly seen in osteoarthritic joints, particularly the knee. The OA process may predispose to calcium crystal deposition, and conversely, CPPD crystals may amplify OA-related cartilage destruction.

Classification of OA progression: WOMAC (Western Ontario and McMaster Universities Arthritis Index) ^[2]

The WOMAC index is a patient-reported outcome measure used to assess OA severity, comprising 3 subscales:

1. Pain (5 items)
2. Stiffness (2 items)
3. Physical function (17 items)

Higher scores = worse symptoms. Used in clinical trials and to monitor treatment response.

Weight-bearing joints, e.g. hip, knee, spine; UL joints spared, except 1st CMC joint and IPJ ^[2]

Degenerative arthritis vs inflammatory arthritis ^[2]:

An important differential in elderly patients with back/leg pain:

Neurogenic claudication: Prolapsed IVD or OA spine → spinal stenosis → compression on spinal arteries → lumbosacral root ischaemia ^[11]

• OA of the lumbar facet joints and disc degeneration can lead to spinal stenosis, causing neurogenic claudication.
• Key distinction from vascular claudication: neurogenic claudication has a variable claudication distance, is relieved by flexion of the spine ("park bench to park bench"), and may be associated with paraesthesia, numbness, and weakness ^[11].

• Haemophilic arthropathy: occurs in up to 50% in severe haemophilia; target joint → synovial hypertrophy, cartilage destruction, secondary OA ^[12]
• Recurrent haemarthrosis → iron deposition in synovium → chronic synovitis → cartilage damage → secondary OA.

Work-related diseases: OA knees (e.g., with occupational factors like prolonged kneeling/squatting) ^[13]

OA is one of the "geriatric giants" in terms of contributing to immobility, falls, and loss of independence. In elderly patients:

• Pain management must balance efficacy vs side effects (e.g., NSAID-related GI bleeding, renal impairment).
• Functional assessment and falls risk are critical.
• Consider polypharmacy interactions (STOPP/START criteria ^[14]).

This is the single most important differential for OA, especially in the hands, because both can present as chronic polyarthritis. However, they are fundamentally different diseases.

Features distinguishing OA from RA: ^[5][1]

Why this distinction matters from first principles:

• RA is an autoimmune synovitis — the primary pathology is a proliferative pannus (inflamed synovial tissue) that invades and destroys cartilage and bone from the outside in. Hence: erosions, juxta-articular osteopenia (from inflammatory cytokine-driven osteoclast activation), soft and boggy swelling, and prolonged morning stiffness (active inflammation takes time to "warm up").
• OA is a biomechanical/degenerative process — the primary pathology is cartilage loss from the inside out. The body's repair response produces osteophytes and subchondral sclerosis (new bone formation). Hence: hard bony swelling, preserved bone density, no erosions, and brief morning stiffness (no significant active inflammation to "warm up").

RA spares DIP ^[16]. This is a critical differentiating point. If DIP joints are swollen and nodular → think OA (Heberden's nodes) or psoriatic arthritis, NOT RA.

Psoriatic arthritis targets DIP of hands which can mimic OA; presents as dactylitis with characteristic nail changes ^[5]

• PsA can present as asymmetric oligoarthritis or symmetric polyarthritis involving DIP joints → can look like OA.
• Key distinguishing features: nail changes (pitting, onycholysis, subungual hyperkeratosis), dactylitis ("sausage digits"), psoriatic skin plaques, enthesitis.
• Why it mimics OA: Both affect DIP. But PsA has active inflammation (warmth, redness, soft tissue swelling), whereas OA DIP nodes are hard and bony.
• X-ray: PsA shows "pencil-in-cup" erosive changes and periostitis; OA shows LOSS pattern without erosions.

Gout and pseudogout can become chronic and assume a polyarticular distribution ^[5] Diagnosis of gout and pseudogout is established by finding urate or calcium pyrophosphate crystals respectively in synovial fluid ^[5]

Why gout/pseudogout enter the DDx of OA:

• Chronic tophaceous gout can produce chronic polyarthritis with joint destruction mimicking OA.
• CPPD disease and OA frequently coexist — chondrocalcinosis is commonly found in OA joints ^[17]. CPPD can present as chronic pyrophosphate arthropathy with an OA-like picture, but with superimposed acute inflammatory flares.
• An acutely inflamed knee in an elderly patient could be either a flare of OA (secondary synovitis), pseudogout, or gout — and you cannot reliably distinguish these clinically. Arthrocentesis with crystal analysis is definitive.

OA of a single joint can present with acutely painful synovitis mimicking septic arthritis ^[3][5]

OA of a single joint can present as acutely painful synovitis mimicking septic arthritis; diagnosis is established by culturing pathogen from synovial fluid or blood ^[5]

• Septic arthritis is a rheumatological emergency ^[15] — bacterial infection can destroy joint cartilage within days.
• Why it enters the OA DDx: An elderly patient with pre-existing OA of the knee who develops sudden worsening of pain, swelling, and warmth could have either an OA inflammatory flare or septic arthritis superimposed on the OA joint. Pre-existing joint disease (including OA) is itself a risk factor for septic arthritis ^[3][15].
• Key differentiating features: high fever, very hot/erythematous joint, refusal to move joint, systemic toxicity, markedly elevated WCC/CRP.
• Rule: Hot, swollen tender joint = septic arthritis until proven otherwise, even without fever, elevated WBC, or elevated ESR/CRP ^[15]. Always aspirate if in doubt.

Spondyloarthritis: Younger age, Insidious onset, Mono or polyarthritis, Any joint could be involved, Psoriasis, IBD, STD/dysentery, uveitis, Back pain, Family history ^[1]

• SpA (including ankylosing spondylitis, psoriatic arthritis, reactive arthritis, IBD-associated arthritis) classically presents as asymmetric oligoarthritis in young men < 45 years ^[3].
• Why it enters the OA DDx: Peripheral SpA can affect weight-bearing joints (knee, ankle) — overlapping with OA. Spinal OA vs ankylosing spondylitis can be confusing in patients with back pain and stiffness.
• Key differentiating features: Age < 45, inflammatory back pain (worse at rest, better with activity — opposite of mechanical OA back pain), sacroiliitis, enthesitis, dactylitis, extra-articular features (uveitis, psoriasis, IBD), HLA-B27 positivity.

• Particularly important in the hip DDx. AVN of the femoral head can mimic hip OA.
• Risk factors: corticosteroid use, alcohol, SLE, sickle cell disease, trauma (neck of femur fracture).
• Why it mimics OA: Both present with groin pain worse on weight-bearing, limited ROM, and limp. AVN can lead to secondary OA if left untreated (collapse of femoral head → incongruent joint surface → cartilage damage).
• Key differentiating features: Younger age, risk factor history, early MRI showing bone marrow oedema and necrosis (X-ray may be normal early). Pain may be disproportionate to X-ray changes.

These are not intra-articular but are important to exclude before diagnosing OA:

Meniscal tears may present after the development of secondary osteoarthritis of the joint ^[18]

Clinical features of OA — history: Insidious onset, DIP joints or weight-bearing joints, Older age ^[1]

The practical diagnostic approach boils down to:

1. Who: Age > 40–50, risk factors present (obesity, prior trauma, occupation)
2. What: Mechanical joint pain (worse with activity, better with rest), morning stiffness < 30 minutes
3. Where: Characteristic joint distribution (knee, hip, DIP, PIP, 1st CMC, spine)
4. What you find: Bony enlargement, crepitus, limited ROM, no systemic features, no warmth
5. What the X-ray shows: Joint space narrowing, subchondral sclerosis, marginal osteophytes, subchondral cysts ^[1][7]
6. What is absent: Normal inflammatory markers, negative serology (RF, anti-CCP, ANA), no erosions on X-ray

These are NOT routine for OA diagnosis but are used in specific clinical scenarios.

Arthrocentesis is not required for routine OA diagnosis but is essential when the clinical picture raises concern for septic arthritis, crystal arthritis, or an acute flare in known OA.

OA of a single joint can present with acutely painful synovitis mimicking other d/dx ^[3]

When OA occurs in an atypical patient (young, unusual joint distribution, bilateral severe disease), investigate for secondary causes:

• What: Explain the nature of OA (degenerative, not "curable" but manageable), the importance of staying active, weight management, and when to seek help.
• Why it works: Empowered patients adhere better to exercise and weight loss programmes, have better pain coping strategies, and require fewer healthcare visits.
• How: Structured self-management programmes (e.g., Arthritis Self-Management Programme), patient information leaflets, group classes.

• Obesity is the strongest modifiable risk factor for OA ^[5][8]. Every 1 kg lost reduces the load on the knee by ~4 kg during walking.
• A 10% body weight reduction in obese patients with knee OA leads to clinically significant improvement in pain and function.
• Mechanism: Reduces both (a) mechanical joint loading and (b) systemic adipokine-driven inflammation (leptin, TNF-α, IL-6).
• Target: BMI < 25 kg/m² ideally, but even modest loss (5–10%) is beneficial.

• The single most important non-pharmacological intervention — strong evidence for pain reduction and functional improvement in knee and hip OA.
• Types of exercise:

• Joint protection advice, activity modification, ergonomic workplace assessment.
• Provision of assistive devices (jar openers, built-up handles, raised toilet seats, bath rails).
• Especially important for hand OA and for elderly patients at risk of falls.

• Heat (warm packs, paraffin wax baths for hands): Improves blood flow, relaxes muscles, reduces stiffness. Best used before exercise.
• Cold (ice packs): Reduces inflammation and pain during acute flares. Best used after activity or during inflammatory episodes.

Geriatrics AOS case: Mr. Wong on ibuprofen 400 mg TDS — recommended to discontinue ibuprofen and recommend paracetamol for pain ^[25]

The decision to operate depends on:

1. Symptom severity: Pain at rest, night pain, inability to walk meaningful distances
2. Functional impairment: Cannot perform ADLs (walking, stairs, rising from chair, dressing)
3. Failed conservative treatment: Adequate trial of non-pharmacological + pharmacological measures
4. Patient factors: Age, comorbidities, fitness for anaesthesia, expectations, motivation for rehab
5. Radiographic severity: Supports but does not determine surgical indication (recall radiograph-symptom discordance)

Options: Arthroplasty for big joints, Arthrodesis for small joints, Realignment surgery (osteotomy), Arthroscopic debridement ^[2]

• Why it works: In medial compartment knee OA with varus alignment, the mechanical axis passes medial to the knee centre → the medial compartment bears disproportionate load → accelerated cartilage wear. A high tibial osteotomy (HTO) corrects the alignment to slight valgus → shifts the mechanical axis laterally → redistributes load to the healthier lateral compartment.
• Who benefits: Young (< 60y) ^[2] with single-compartment disease and preserved cartilage in other compartments. Good ligament integrity required. This is a joint-preserving procedure — it buys time (typically 5–10 years) before eventual arthroplasty.
• Think of it as "buying time" for a young active patient who would otherwise outlive a prosthesis (which lasts 15–20 years and revision surgery is more complex).

Geriatric AOS case: Discontinue ibuprofen and chlorpheniramine, recommend paracetamol for pain ^[25]

• Avoid long-term NSAIDs in elderly: ↑ GI bleeding, renal impairment, heart failure exacerbation, drug interactions.
• Avoid long-term opioids: Falls, confusion, constipation, dependence ^[23].
• Avoid anticholinergics (e.g., chlorpheniramine for sleep in OA patients): ↑ confusion, falls, urinary retention ^[25].
• Paracetamol remains safest option; topical NSAIDs preferred over oral.
• IA steroid injections are useful in elderly patients who cannot tolerate systemic analgesics.
• Falls prevention: Address as part of OA management — pain, stiffness, muscle weakness, and medication side effects all increase falls risk.

Frailty-guided clinical management: Preserve physiologic reserve, Prevent avoidable stressors, Consider trade-off between diseases and treatment burden ^[26]

• What happens: Ongoing cartilage loss → bone-on-bone contact → asymmetric joint loading → progressive malalignment and deformity.
• Knee: Genu varum (medial compartment) or genu valgum (lateral compartment) → further accelerates cartilage loss in a vicious cycle (malalignment → ↑ load on already damaged compartment → ↑ cartilage loss → ↑ malalignment).
• Hip: Fixed flexion, adduction, and external rotation deformity → functional leg length discrepancy → compensatory lumbar hyperlordosis → secondary back pain.
• Hand: Heberden's and Bouchard's nodes → cosmetic concerns; 1st CMC OA → squaring of thumb base → loss of pinch grip.

Late Complications of hip: Secondary OA — Pain due to joint incongruency and chondral damage; Stiffness due to ankylosis and short tissue contracture (flexion and adduction contracture); Deformity: angulation, coxa vara, shortening; Instability, dislocation; Leg length discrepancy ^[27]

• As cartilage is lost and ligaments become lax (from chronic stretching over deformed joint surfaces), the joint can become unstable.
• This manifests as "giving way" — particularly at the knee — increasing the risk of falls.
• In advanced hip OA, subluxation or even dislocation can occur (though this is uncommon in primary OA; more common in secondary OA from dysplasia or AVN).

• Osteochondral fragments (pieces of cartilage and bone) can detach and float within the joint — these are loose bodies.
• Clinical significance: Loose bodies can cause true locking (sudden inability to extend the joint — the loose body jams in the joint mechanism like a stone in a hinge), catching, and episodic sharp pain.
• This is one of the few scenarios where arthroscopic intervention is justified in OA — to remove the offending loose body ^[28].

• Cartilage degradation products (collagen fragments, basic calcium phosphate crystals, proteoglycan fragments) are released into the synovial fluid → activate synovial macrophages → release of IL-1β, TNF-α → secondary synovitis.
• Presents as acute worsening of pain, swelling (effusion), warmth in a joint with known OA.
• Clinically important because it mimics crystal arthritis and septic arthritis — must aspirate if in doubt to exclude infection.
• The presence of synovitis also contributes to ongoing pain and cartilage damage (cytokines stimulate MMP production by chondrocytes → vicious cycle).

OA with calcium pyrophosphate deposition (CPPD): May be present in as many as 30–60% of unselected OA patients ^[5]

• CPPD crystals deposit preferentially in degenerative cartilage — OA predisposes to crystal formation through proteoglycan loss (proteoglycans normally inhibit mineralisation) and release of cellular ATP (chondrocyte damage → ↑ extracellular ATP → pyrophosphate production → CPPD crystal nucleation).
• OA with CPPD is not any more rapidly progressive than OA alone but some may develop rapidly progressive destructive arthropathy ^[5].
• Presence of CPPD may modify OA symptoms especially with longer early morning stiffness and more signs of synovitis ^[5].
• Clinical implication: If an OA patient has unexpectedly prominent inflammatory features (more swelling, longer morning stiffness, more warmth than typical OA), consider coexisting CPPD disease. Chondrocalcinosis on X-ray supports this. Joint aspiration showing weakly positive birefringent rhomboid crystals confirms it.

• An uncommon but important complication where cartilage and bone are destroyed much faster than typical OA — over months rather than years.
• Associated with CPPD deposition, basic calcium phosphate (BCP) crystal deposition, or atrophic OA.
• Milwaukee shoulder syndrome: Rapidly destructive shoulder OA associated with BCP crystal deposition → massive rotator cuff tear + cartilage destruction + large effusion containing BCP crystals.
• X-ray shows rapid joint space loss, bone destruction, and sometimes a relatively "quiet" clinical picture (less pain than expected for the degree of destruction — because the cartilage is destroyed so quickly that nociceptive mechanisms cannot keep up).

• Spinal OA (spondylosis): Osteophytes and disc degeneration in the cervical or lumbar spine can narrow the spinal canal (spinal stenosis) or intervertebral foramina (foraminal stenosis) → compression of spinal cord (myelopathy) or nerve roots (radiculopathy).
  • Cervical spondylotic myelopathy: Osteophytes + disc bulge + ligamentum flavum hypertrophy → spinal cord compression → progressive upper motor neuron signs in limbs (spasticity, hyperreflexia, clonus), gait disturbance, hand clumsiness, bladder dysfunction.
  • Lumbar spinal stenosis: OA of facet joints + disc degeneration → central canal narrowing → neurogenic claudication (bilateral LL pain/numbness/weakness on walking, relieved by flexion — "park bench to park bench").
  • Nerve root compression: Foraminal osteophytes → radiculopathy (dermatomal pain, sensory loss, motor weakness, reflex changes).

• A synovial fluid-filled cyst in the popliteal fossa, arising from the semimembranosus-gastrocnemius bursa.
• Why it occurs in OA: Increased synovial fluid production from secondary synovitis → fluid is pushed into the bursa through a one-way valve mechanism (fluid enters but cannot easily return to the joint).
• Clinical significance:
  • Usually asymptomatic or causes a sensation of fullness behind the knee.
  • Can rupture → synovial fluid dissects into the calf → acute calf pain, swelling, and erythema → mimics deep vein thrombosis (DVT) (pseudothrombophlebitis syndrome). Must do Doppler ultrasound to differentiate.
  • Can compress popliteal vein → true DVT secondary to venous stasis.

• Pain → reduced activity → disuse atrophy (particularly quadriceps in knee OA and gluteus medius in hip OA).
• Additionally, arthrogenic muscle inhibition — reflex inhibition of quadriceps firing due to intra-articular pathology (effusion, pain) → preferential VMO wasting.
• Quadriceps weakness is both a consequence of knee OA and a risk factor for OA progression (loss of dynamic stabilisation → increased cartilage loading → more cartilage damage).
• Hip abductor weakness → positive Trendelenburg sign → Trendelenburg gait (waddling) → increased energy expenditure, ↑ falls risk.

• Progressive pain and stiffness → reduced walking distance → reduced ADLs (cannot climb stairs, dress, bathe independently) → loss of independence.
• In elderly patients, this can precipitate institutionalisation (nursing home placement).
• OA is the leading cause of disability in the elderly worldwide — even more impactful than cardiovascular disease in terms of quality-adjusted life years lost.

AOS Geriatrics: A 79-year-old male with hypertension, osteoarthritis, and mild cognitive impairment — two falls in 2 months ^[29]

• OA contributes to falls through multiple mechanisms:
  • Pain → antalgic gait → altered balance
  • Muscle weakness → quadriceps/hip abductor weakness → impaired postural control
  • Joint stiffness and deformity → reduced ROM → difficulty navigating obstacles
  • Proprioceptive deficits → damaged joint capsule and ligaments contain mechanoreceptors; OA impairs proprioception → poor joint position sense
  • Medication side effects → NSAIDs (dizziness), opioids (sedation, falls), anticholinergics (confusion)
• Falls → fractures (especially neck of femur, distal radius, vertebral compression fractures in osteoporotic patients) → further immobility → spiralling decline.

• Chronic pain + functional limitation → depression, anxiety, social isolation, poor self-esteem.
• Depression itself amplifies pain perception (via central sensitisation and impaired descending pain inhibition) → creates a pain-depression cycle.
• Sleep disturbance from night pain → fatigue → worsening mood and function.
• Quality of life is significantly impaired — comparable to or worse than many other chronic diseases.

• Reduced physical activity due to OA pain → cardiovascular deconditioning → increased risk of ischaemic heart disease, metabolic syndrome, type 2 diabetes.
• OA patients have higher rates of cardiovascular events than age-matched controls, partly due to shared risk factors (obesity, sedentary lifestyle) and partly due to NSAID use (↑ CVS risk).

• OA causes pain → reduced activity → weight gain → increased joint loading + increased adipokine-driven inflammation → worsening OA → more pain → further reduced activity. A self-perpetuating cycle.
• Breaking this cycle (through weight loss and exercise) is one of the most important management goals.

Carefully review indications of NSAID → does it really have to be used? I.e. osteoarthritis with no active inflammation, no point to use ^[24]

STOPP: NSAID with concurrent corticosteroids — increased risk of peptic ulcer disease ^[23]

Opioids offer only limited benefit for chronic OA pain and function; potentially serious adverse effects including drug abuse and addiction; Elderly patients are at particular risk — sedation and dizziness which predispose to falls and fractures ^[28]

Pre-operative use of opioids independently predicted opioid requirement post-surgery, associated with prolonged hospital stay, greater risks of in-hospital complications, and early revision surgery ^[28]

Specific complications of total replacement: ^[2]

Arthroscopy potential complications: Adverse outcomes — DVT (0.4%), PE (0.1%), death (0.03%); increases rate of progression of osteoarthritis; shortens time to joint replacement ^[28]