Osteoarthritis

Osteoarthritis (OA) is the commonest joint disease worldwide and the leading cause of chronic disability in the elderly. It is a non-inflammatory (more correctly, low-grade inflammatory) degenerative disorder of the whole joint as an organ—cartilage, subchondral bone, synovium, ligaments and peri-articular muscle. For NEET PG, the radiological tetrad, Kellgren–Lawrence grading, Heberden vs Bouchard nodes, and the step-up management ladder are repeatedly examined.

Definition & classification

OA is progressive loss of articular (hyaline) cartilage with accompanying subchondral bony reaction and marginal new bone (osteophyte) formation. The old label "degenerative joint disease / osteoarthrosis" reflected the belief that inflammation was absent; we now know low-grade synovitis driven by cartilage breakdown products contributes.

Etiological classification:

Type	Cause	Typical joints
Primary (idiopathic)	Ageing + genetics; no identifiable cause	Knees, hips, DIP/PIP, first CMC, cervical/lumbar spine
Secondary	Pre-existing joint abnormality	Any joint—depends on underlying lesion

Causes of secondary OA (high-yield):

• Trauma – intra-articular fracture, meniscectomy, malunion
• Developmental – DDH, Perthes, SCFE, dysplasia (→ premature hip OA)
• Inflammatory – burnt-out rheumatoid arthritis, septic/tubercular arthritis
• Metabolic – haemochromatosis (MCP joints, hook-like osteophytes), ochronosis/alkaptonuria, gout, acromegaly, Wilson disease
• Avascular necrosis – steroids, alcohol, sickle cell
• Neuropathic (Charcot) – diabetes, syringomyelia, tabes, leprosy
• Crystal – CPPD (chondrocalcinosis)

High-yield: OA is the commonest cause of secondary OA of the hip in young Indians = old DDH / Perthes / SCFE sequelae. In the knee, previous meniscectomy or malunited fracture is the classic secondary cause.

A useful generalised primary OA subset is nodal (Kellgren) generalised OA—middle-aged women with Heberden + Bouchard nodes, first CMC and knee involvement, strongly familial.

Etiology & pathophysiology

OA is driven by an imbalance between catabolic and anabolic activity of chondrocytes. Key risk factors:

Modifiable	Non-modifiable
Obesity (strongest for knee OA)	Age (single biggest risk)
Occupational/repetitive load	Female sex (post-menopause)
Joint injury / instability	Genetics (GDF5, COL2A1)
Muscle weakness (quadriceps)	Malalignment (varus/valgus)

Sequence of events (flow):

Chondrocyte injury → release of matrix metalloproteinases (MMP-13, aggrecanase/ADAMTS) → degradation of type II collagen & aggrecan → cartilage fibrillation & fissuring → loss of cartilage → bone-on-bone → subchondral sclerosis (eburnation) + cyst formation + marginal osteophytes → joint space narrowing & deformity.

Early on, water content of cartilage increases (failed reparative swelling) and proteoglycan content falls—an important contrast to the dehydration seen in normal ageing. IL-1β and TNF-α from synovium amplify MMP release. Loss of the smooth gliding surface leads to eburnation (polished ivory-like subchondral bone), subchondral microfractures forming cysts (geodes), and at joint margins, endochondral ossification produces osteophytes.

High-yield: The earliest histological change in OA is fibrillation of the superficial cartilage with loss of proteoglycan (reduced safranin-O staining). Earliest gross change is surface roughening.

Clinical features

OA is typically monoarticular or oligoarticular, asymmetric, and weight-bearing/large-joint predominant (knee > hip > spine > hands).

Cardinal symptoms:

• Pain – mechanical: worse with activity/weight-bearing, relieved by rest; advanced disease → rest and night pain.
• Stiffness – short-lived morning stiffness < 30 minutes and "gelling" after inactivity. (Contrast RA: > 60 min.)
• Crepitus, joint enlargement (bony), reduced range of motion, deformity (varus knee most common).
• No systemic features (no fever, weight loss, fatigue).

Signs: bony swelling (not boggy/warm synovitis), restricted painful movement, joint-line tenderness, malalignment, effusion (often cool), peri-articular muscle wasting.

Hand OA — the classic eponyms

Feature	Joint	Eponym
Bony swelling at DIP	Distal interphalangeal	Heberden's nodes
Bony swelling at PIP	Proximal interphalangeal	Bouchard's nodes
First carpometacarpal	Thumb base	"Squaring" of the hand / shoulder sign

High-yield mnemonic: Bouchard = Big knuckle = PIP (proximal); Heberden = High up / Distal = DIP. DIP involvement strongly favours OA over RA (RA spares DIP).

Hip vs Knee OA — a favourite comparison

Feature	Hip OA	Knee OA
Pain location	Groin pain (may refer to knee/thigh)	Anteromedial knee, worse on stairs
Earliest movement lost	Internal rotation & extension	Full flexion/extension; flexion deformity late
Deformity	Flexion, adduction, external rotation; limb shortening	Varus (medial compartment) commonest; genu valgum less common
Gait	Antalgic / Trendelenburg	Antalgic; thrust
Special test	C-sign (patient grips hip with C-shaped hand)	Patellofemoral grind, McMurray (if meniscal)

High-yield: Earliest movement lost in hip OA = internal rotation (also first lost in most hip pathology). A hip OA patient classically presents with groin pain referred to the knee—do not miss the hip when a patient complains only of knee pain.

Diagnosis & investigation of choice

OA is largely a clinical + radiological diagnosis. Plain radiograph (weight-bearing for knee/hip) is the investigation of choice.

Radiographic tetrad of OA (must memorise):

1. Joint space narrowing – usually non-uniform / asymmetric (load-bearing compartment); contrast RA where narrowing is uniform/concentric.
2. Subchondral sclerosis (eburnation).
3. Subchondral cysts (geodes / pseudocysts).
4. Osteophytes (marginal new bone) – the most specific radiographic feature.

High-yield mnemonic for X-ray of OA — "LOSS": Loss of joint space, Osteophytes, Subchondral cysts, Subchondral sclerosis.

Kellgren–Lawrence (KL) grading — most asked

Grade	Findings
0	Normal
1	Doubtful joint space narrowing; possible osteophyte lipping
2	Definite osteophyte, possible joint space narrowing
3	Moderate osteophytes, definite joint space narrowing, some sclerosis, possible deformity
4	Large osteophytes, marked joint space narrowing, severe sclerosis, definite deformity

High-yield: KL grading is based primarily on osteophytes and joint space narrowing. Grade 2 = first definite OA (definite osteophyte). Grade 4 = bone deformity.

For the knee, the recommended view is the weight-bearing antero-posterior (Rosenberg / standing PA flexion view) because supine films underestimate joint space narrowing. MRI is not routine—reserved for suspected meniscal/ligament/early cartilage or AVN assessment. Laboratory tests (ESR, CRP, RF, uric acid) are normal in primary OA and are used mainly to exclude inflammatory/crystal arthropathy. Synovial fluid in OA is non-inflammatory: clear, viscous, WBC < 2000/mm³ (group I).

High-yield: Synovial fluid WBC < 2000/mm³ = non-inflammatory (OA, trauma). 2000–50,000 = inflammatory (RA, gout). > 50,000 with low glucose = septic. > 1,00,000 = highly suggestive of sepsis.

Management — the step-up ladder

Treatment is staged from conservative to surgical. The single most effective intervention overall in knee OA is weight reduction + quadriceps strengthening.

Step-up flow: 1. Patient education + weight loss + exercise/physiotherapy + activity modification + walking aids/braces → 2. Topical/oral NSAIDs (first-line drug) ± paracetamol → 3. Intra-articular corticosteroid (flares) / consider hyaluronic acid / PRP → 4. Joint-preserving surgery (osteotomy, arthroscopy for mechanical symptoms) → 5. Arthroplasty (definitive for end-stage).

1. Non-pharmacological (core, first-line)

• Weight reduction – every 1 kg lost markedly reduces knee load; strongest evidence.
• Exercise – quadriceps strengthening for knee, aerobic/low-impact.
• Footwear, lateral wedge insoles, knee braces/unloader braces, walking stick (held in opposite/contralateral hand).
• Thermotherapy, occupational adaptations.

2. Pharmacological

• Topical NSAIDs – preferred first-line drug for knee/hand OA (esp. elderly, fewer GI effects).
• Oral NSAIDs – mainstay for pain; lowest effective dose, shortest duration; add PPI / use COX-2 (e.g. etoricoxib) if GI risk. Paracetamol gives modest benefit and is safer but less effective.
• Duloxetine – useful for chronic/centralised knee OA pain.
• Intra-articular corticosteroid – good for acute flares with effusion; effect lasts only weeks; avoid frequent injections (> 3–4/year) → accelerates cartilage loss.
• Intra-articular hyaluronic acid (viscosupplementation) and PRP (platelet-rich plasma) – may help select knee OA; evidence modest and guideline support conditional.
• Avoid opioids for routine OA. Glucosamine/chondroitin – not recommended (no consistent benefit).

High-yield: First-line drug in OA = NSAID (topical preferred, then oral). Paracetamol is safer but weaker. Walking stick goes in the hand opposite to the affected side.

3. Surgical

• Arthroscopic lavage/debridement – NOT for routine OA; only if true mechanical locking from loose body/meniscal tear.
• High tibial osteotomy (HTO) – young, active patient with isolated medial compartment (varus) knee OA; realigns load to healthy lateral compartment. Femoral osteotomy for valgus.
• Realignment/periacetabular osteotomy – for dysplastic hip in the young.
• Arthrodesis – salvage for single small joints (e.g. first MTP, ankle) in young manual labourers.
• Total joint arthroplasty (TKR / THR) – definitive treatment for end-stage (KL 3–4) symptomatic OA refractory to conservative care; reliably relieves pain and restores function.
• Unicompartmental knee arthroplasty (UKA) – isolated single-compartment disease with intact ligaments.

High-yield: High tibial osteotomy = young patient + unicompartmental varus knee OA + good range of motion. Total knee replacement = elderly + tricompartmental/advanced OA.

Complications

• Progressive deformity – fixed flexion, varus/valgus (knee); fixed flexion-adduction with limb shortening (hip).
• Loss of function & disability, falls in the elderly.
• Muscle wasting (quadriceps), peri-articular soft-tissue contractures.
• Loose bodies → mechanical locking.
• Secondary effusion / Baker's (popliteal) cyst in the knee.
• Subluxation / instability, leg-length discrepancy.
• Post-arthroplasty complications (relevant to the Arthroplasty group): aseptic loosening (commonest long-term cause of revision), periprosthetic infection, dislocation, periprosthetic fracture, DVT/PE, polyethylene wear & osteolysis.

Key differentials

Feature	Osteoarthritis	Rheumatoid arthritis
Joints	DIP, PIP, 1st CMC, knee, hip, spine	MCP, PIP, wrist; spares DIP
Symmetry	Asymmetric	Symmetric
Morning stiffness	< 30 min	> 60 min
Swelling	Bony (hard)	Soft, boggy synovitis, warm
X-ray space	Non-uniform narrowing, osteophytes	Uniform narrowing, erosions, osteopenia, no osteophytes
Labs	Normal ESR/CRP/RF	↑ESR/CRP, RF/anti-CCP positive
Nodes	Heberden / Bouchard	Subcutaneous rheumatoid nodules (extensor)

Other differentials: gout/CPPD (acute, crystal-positive fluid, chondrocalcinosis), septic arthritis (hot joint, fever, very high synovial WBC), avascular necrosis (preserved joint space early, crescent sign), psoriatic arthritis (DIP + nail changes, pencil-in-cup), referred pain (hip OA presenting as knee pain).

High-yield: OA spares the MCP joints; isolated MCP OA should raise suspicion of haemochromatosis (with hook-shaped osteophytes) or CPPD.

Recently asked / exam angle

• Kellgren–Lawrence grading: matching grade ↔ feature (definite osteophyte = grade 2; deformity = grade 4) is a recurrent one-liner.
• Radiographic tetrad / "LOSS" and which feature is most specific (osteophyte).
• Heberden (DIP) vs Bouchard (PIP) node localisation—frequently a single-best-answer image or statement.
• Earliest movement lost in hip OA = internal rotation; hip OA presenting as groin/referred knee pain.
• Step-up management: first-line is non-pharmacological (weight loss/exercise); first-line drug = NSAID; walking stick in opposite hand.
• High tibial osteotomy indication (young, medial compartment varus OA) vs TKR (elderly, advanced).
• Synovial fluid analysis cut-offs (non-inflammatory < 2000).
• Secondary OA causes—haemochromatosis (MCP, hook osteophytes), neuropathic Charcot joint, post-meniscectomy.
• Earliest histological change = superficial fibrillation / proteoglycan loss; early biochemical change = ↑ water content.
• Image-based: standing/weight-bearing knee X-ray showing asymmetric medial joint space loss with osteophytes.

Rapid revision

1. OA = degenerative disease of the whole joint; commonest joint disease; biggest risk factor = age, strongest modifiable for knee = obesity.
2. X-ray tetrad ("LOSS"): Loss of joint space (non-uniform), Osteophytes, Subchondral cysts, Subchondral sclerosis. Osteophyte = most specific.
3. Kellgren–Lawrence: grade 2 = definite osteophyte; grade 4 = marked narrowing + deformity.
4. Heberden = DIP, Bouchard = PIP; OA spares MCP (think haemochromatosis if MCP involved).
5. Morning stiffness < 30 min, mechanical pain worse with use—no systemic features; ESR/CRP/RF normal.
6. Hip OA: groin pain, earliest loss of internal rotation, may refer to knee; deformity = flexion-adduction-external rotation + shortening.
7. Knee OA: medial compartment, varus deformity commonest; weight-bearing X-ray is the right view.
8. Synovial fluid is non-inflammatory (WBC < 2000/mm³), clear and viscous.
9. First-line = weight loss + quadriceps exercise; first-line drug = NSAID (topical preferred); walking stick in opposite hand.
10. Avoid repeated intra-articular steroids, opioids, glucosamine/chondroitin and routine arthroscopic lavage.
11. High tibial osteotomy for young varus medial-compartment knee OA; TKR/THR is definitive for end-stage disease.
12. Commonest long-term cause of arthroplasty revision = aseptic loosening.