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SN7 SHORT NOTE 5M

Write a short note on osteoarthritis.

General Medicine · Final Professional

Definition

Osteoarthritis (OA) is a chronic degenerative joint disorder characterised by progressive loss of articular cartilage with accompanying subchondral bone remodelling, osteophyte formation and low-grade synovial inflammation. It is the commonest joint disease and a leading cause of disability in the elderly. It is now understood as a disease of the whole joint as an organ, not simply "wear and tear".

Classification & Risk Factors

  • Primary (idiopathic) — no identifiable cause; related to age, genetics and mechanical factors.
  • Secondary — trauma and previous fracture, meniscal or ligament injury, inflammatory arthritis (RA, gout), septic arthritis, avascular necrosis, congenital and developmental disorders (hip dysplasia, Perthes' disease), metabolic and endocrine disease (haemochromatosis, acromegaly, ochronosis, hyperparathyroidism), and neuropathic joints (Charcot joint in diabetes, syringomyelia, tabes dorsalis).

Risk factors: age (the strongest), female sex, obesity (for knee OA, both mechanical and metabolic), occupational and sporting overuse, joint malalignment, muscle weakness, and family history (notably for nodal hand OA).

Pathology

Chondrocyte-driven imbalance between matrix synthesis and degradation, with matrix metalloproteinase activity exceeding repair. Cartilage fibrillates, fissures and is progressively lost. The exposed subchondral bone becomes sclerotic ("eburnation"), develops subchondral cysts and forms osteophytes at the joint margins. The synovium shows mild secondary inflammation.

Clinical Features

  • Pain of mechanical character — worse with activity and at the end of the day, relieved by rest; in advanced disease pain occurs at rest and at night.
  • Morning stiffness lasting less than 30 minutes, and "gelling" — stiffness after periods of inactivity that eases within minutes of moving.
  • Crepitus on movement; restricted range of movement; joint instability and "giving way"; muscle wasting around the joint.
  • Bony swelling rather than the soft, warm synovial swelling of inflammatory arthritis; joints are cool with little or no erythema.
  • Joints involved: knee, hip, cervical and lumbar spine, first carpometacarpal joint of the thumb, first MTP joint, and the distal interphalangeal joints.
  • Heberden's nodes — bony swellings at the DIP joints; Bouchard's nodes — at the PIP joints. The squaring of the thumb base is characteristic.

OSTEOARTHRITIS versus RHEUMATOID ARTHRITIS

FeatureOsteoarthritisRheumatoid arthritis
AgeOlderAny, typically 30–50
OnsetInsidious, over yearsWeeks to months
Morning stiffness< 30 minutes> 1 hour
Pain patternWorse with use, better with restBetter with use, worse with rest
JointsDIP, first CMC, knee, hip, spineMCP, PIP, wrist — DIP SPARED
SymmetryOften asymmetricalSymmetrical
SwellingBony, hardSoft, warm, boggy synovial
Systemic featuresAbsentFatigue, fever, weight loss, extra-articular disease
ESR/CRPNormalRaised
SerologyNegativeRF and anti-CCP often positive
X-rayOsteophytes, subchondral sclerosis, cysts, asymmetrical joint space lossPeriarticular osteopenia, marginal erosions, symmetrical joint space loss

Investigations

OA is largely a clinical diagnosis; investigations exclude alternatives and assess severity.

  • X-ray — remember "LOSS": Loss of joint space (asymmetrical), Osteophytes, Subchondral sclerosis, Subchondral cysts. Radiographic severity correlates poorly with symptoms.
  • ESR, CRP, RF and anti-CCP are normal or negative — useful to exclude inflammatory arthritis.
  • Joint aspiration if there is an effusion or diagnostic doubt: synovial fluid is non-inflammatory (clear, viscous, white cells under 2000/µL) — and it excludes crystal and septic arthritis.
  • MRI for early cartilage change, meniscal pathology and avascular necrosis where the diagnosis is uncertain.

Management

Non-pharmacological — the foundation, and consistently the most effective:

  • Weight reduction — even modest loss substantially reduces knee pain and progression.
  • Exercise — quadriceps strengthening for knee OA, range-of-movement and aerobic exercise; this is first-line treatment, not an adjunct.
  • Physiotherapy, occupational therapy, walking stick held in the opposite hand, appropriate footwear with shock-absorbing soles, knee braces for malalignment, and home and workplace adaptations.
  • Patient education and self-management; heat and cold application; thermal and topical measures.

Pharmacological:

  • Topical NSAIDs — first-line drug therapy for knee and hand OA, with a far better safety profile than oral agents.
  • Paracetamol — modest benefit; still widely used for mild pain.
  • Oral NSAIDs — effective, but use the lowest dose for the shortest time, with gastroprotection; caution in the elderly and in renal, cardiac and gastrointestinal disease.
  • Intra-articular corticosteroid injection — useful for painful flares with effusion; benefit lasts weeks, and repeated frequent injections are avoided.
  • Duloxetine for chronic pain; topical capsaicin.
  • Opioids are generally avoided in this chronic, non-malignant condition.
  • Glucosamine and chondroitin — evidence of benefit is weak and inconsistent.

Surgical: total joint replacement for the knee or hip where there is severe pain, night pain and functional limitation refractory to conservative treatment — one of the most successful operations in medicine; osteotomy in younger patients with unicompartmental disease; arthroscopic lavage and debridement are not recommended for degenerative knee disease alone.

All questions in Immunology & Rheumatology

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  7. SN6Write a short note on seronegative spondyloarthritis, including ankylosing spondylitis and reactive arthritis.
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