Compare OA AND RA FOR MEDICINE MBBS

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Osteoarthritis (OA) vs Rheumatoid Arthritis (RA)

FeatureOsteoarthritis (OA)Rheumatoid arthritis (RA)
Basic pathologyDegenerative joint disease with progressive loss of articular cartilage and bony remodelingChronic systemic autoimmune inflammatory synovitis causing cartilage and bone destruction
Usual ageUsually older adults, often >50 yearsAny age, commonly 30-50 years; females more affected
Risk factorsAge, obesity, prior injury, repetitive joint loading, malalignmentFemale sex, family history, smoking, autoimmune predisposition
OnsetInsidious, slowly progressiveInsidious but may progress over weeks to months
Joint distributionOften asymmetric; weight-bearing and mechanically stressed jointsTypically symmetric polyarthritis
Common jointsKnees, hips, cervical/lumbar spine, first CMC, DIP and PIP jointsMCP, PIP, wrists, MTP joints, cervical spine
DIP involvementCommon, with Heberden nodesUsually spared
First CMC jointFrequently affectedUsually spared
MCP jointsUsually sparedCharacteristically involved
Hip involvementCommonLess common than small-joint disease
Type of painWorse with activity/use; relieved by rest initiallyWorse after rest or inactivity; improves with gentle movement
Morning stiffnessBrief, usually <30 minutesProlonged, typically >1 hour
SwellingHard, bony enlargement; little true synovitisSoft, boggy, warm synovial swelling
CrepitusCommonNot a prominent early feature
Systemic featuresAbsentMay have fatigue, low-grade fever, weight loss, anemia, extra-articular disease
DeformitiesBony enlargement, reduced movement; usually lateUlnar deviation, swan-neck deformity, boutonniere deformity, Z-thumb, subluxation
Extra-articular manifestationsNoneRheumatoid nodules, interstitial lung disease, pleuritis, pericarditis, scleritis, vasculitis, neuropathy
Inflammatory markersUsually normalESR and CRP often elevated
Rheumatoid factorNegativeOften positive, but not diagnostic alone
Anti-CCP antibodyNegativeMore specific for RA; predicts erosive disease
Synovial fluidNon-inflammatory: usually <2,000 WBC/mm³Inflammatory: usually 2,000-50,000 WBC/mm³, predominantly neutrophils
X-ray findingsNon-uniform joint-space narrowing, osteophytes, subchondral sclerosis, subchondral cystsUniform joint-space narrowing, marginal erosions, periarticular osteopenia, soft-tissue swelling, deformity
Main treatment principleReduce pain, maintain function, address biomechanics and weightStart early disease-modifying therapy to prevent irreversible erosions and disability
Drugs commonly usedTopical/oral NSAIDs if appropriate, paracetamol has limited benefit, intra-articular corticosteroid for selected jointsDMARDs such as methotrexate first-line, often with short-term glucocorticoid bridge; biologic/targeted DMARDs if needed
Role of surgeryJoint replacement for severe end-stage diseaseSynovectomy or joint replacement for advanced damaged joints, after disease control

Key exam points

  • OA is mechanical and degenerative: pain increases with use, stiffness is short-lived, and X-ray shows osteophytes and subchondral sclerosis.
  • RA is inflammatory and autoimmune: symmetric small-joint involvement, morning stiffness >1 hour, systemic manifestations, and X-ray shows marginal erosions and periarticular osteopenia.
  • OA commonly affects DIP joints and first CMC. RA characteristically affects MCP, PIP, and wrist joints, while DIP joints are usually spared.
  • RA needs early DMARD treatment, particularly methotrexate unless contraindicated. NSAIDs relieve symptoms but do not prevent erosions.
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