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Rheumatology›Condition·Updated Jun 27, 2026·v1

Osteoarthritis

Osteoarthritis is a chronic joint disorder characterized by cartilage loss, bone remodeling, and synovitis, most commonly affecting the knee, hip, and hand. Evaluation relies on the classic triad: age >50, activity-related pain, and morning stiffness <30 minutes. Radiographs confirm the diagnosis and guide staging (Kellgren-Lawrence grade). Management begins with exercise, weight loss, and NSAIDs; intra-articular therapies (corticosteroids, PRP) are second-line options. Joint replacement is definitive for end-stage disease. Key pitfalls: over-reliance on opioids, repeated steroid injections, and failure to refer for timely arthroplasty.

High Evidence174 references·5,475 words·22 min read·v1
osteoarthritisdegenerative joint diseaseknee arthritiship arthritisjoint replacementNSAIDsintra-articular therapyKellgren-Lawrenceexercise therapy

Quick Reference

RxDrug of choiceNaproxen 500 mg twice daily (or ibuprofen 600-800 mg three times daily) for symptom relief; paracetamol (acetaminophen) 1000 mg three times daily as first-line if NSAIDs are contraindicated.
AltAlternativesTopical diclofenac gel 1% (knee/hand OA); tramadol 50-100 mg every 4-6 hours (max 400 mg/day); intra-articular corticosteroids (triamcinolone acetonide 40 mg knee); intra-articular hyaluronic acid (Synvisc 16 mg/2 mL × 3); leukocyte-rich PRP (3 mL knee, 1-2 sessions).
⊘AvoidStrong opioids for long-term use; glucosamine/chondroitin (OARSI and ACR recommend against); treadmill incline walking in patellofemoral OA; repeated intra-articular corticosteroids every 3 months (↑ risk of cartilage loss).
DxTest of choiceWeight-bearing anteroposterior and lateral radiographs with Kellgren-Lawrence grading; MRI for equivocal cases or preoperative planning (assess cartilage loss, meniscal extrusion, bone marrow lesions).
ScKey scoreKellgren-Lawrence grade (0-4) for radiographic severity; WOMAC or KOOS/HOOS for symptoms and function; NRS/VAS for pain; SPPB for physical function.
→When to referSevere persistent pain and functional loss despite 6 months of conservative therapy (→ arthroplasty); suspected avascular necrosis or subchondral insufficiency fracture (urgent orthopaedics); declining function (→ physiatry).
Exercise, weight loss, and NSAIDs are the pillars of OA management. Intra-articular corticosteroids and PRP provide second-line options. Joint replacement is definitive for end-stage disease. Avoid opioids and unproven supplements.
Osteoarthritis (OA) is the most prevalent joint disorder, characterized by progressive cartilage loss, subchondral bone remodeling, and synovitis. It is a leading cause of disability worldwide, with the knee and hip most commonly affected. Diagnosis is clinical and radiographic, with MRI reserved for equivocal cases or surgical planning. Management centers on exercise, weight loss, NSAIDs, and joint replacement for end-stage disease. The goal of this page is to provide a comprehensive, actionable framework for clinicians managing OA in daily practice.

Overview and Recommendations

Background

  • •Osteoarthritis is the most common joint disorder globally, affecting over 32.5 million adults in the United States alone and representing the leading indication for total knee and hip arthroplasty. OA is a whole-joint disease involving dynamic processes, cartilage degradation, subchondral bone remodeling, and low-grade synovial inflammation, not merely 'wear and tear.'
  • •Primary OA is idiopathic, age-related, and typically involves the knee, hip, hand, and spine. Secondary OA arises from predisposing factors such as joint trauma, congenital anomalies (e.g., developmental dysplasia of the hip), metabolic disorders (hemochromatosis), or inflammatory arthritis (rheumatoid arthritis sequelae). Recognizing this distinction guides targeted prevention and treatment.
  • •The 'four phenotypes' model (inflammatory, metabolic, mechanical, and aging) is replacing the historical primary/secondary dichotomy, reflecting the heterogeneity in pathophysiology and treatment response. For instance, metabolic OA is associated with the metabolic syndrome and shows a distinct pain profile and response to weight loss.
  • •Despite the absence of a disease-modifying OA drug (DMOAD), the paradigm has shifted toward early detection and phenotype-driven intervention, including structured exercise, targeted biomechanical therapy, and joint replacement at the optimal time point.
  • •Knee OA accounts for roughly 80% of the total OA disability burden, with the medial tibiofemoral compartment most commonly affected (10:1 ratio over lateral). Hip OA is the second most common large-joint OA, often associated with cam-type femoroacetabular impingement and altered femoral anteversion.
  • •Osteoarthritis imposes a substantial socioeconomic burden: direct costs (joint replacement, medications) and indirect costs (lost work productivity, early retirement) exceed $140 billion annually in the U.S. Prognostic stakes are high, untreated symptomatic knee OA reduces quality of life more than cardiovascular disease.

Evaluation

  • •Suspect OA in any patient over 50 with insidious-onset, activity-related joint pain that improves with rest, morning stiffness lasting <30 minutes, and no significant inflammatory features (redness, warmth, prolonged stiffness). The Knee injury and Osteoarthritis Outcome Score (KOOS) and Hip disability and Osteoarthritis Outcome Score (HOOS) are validated patient-reported outcome measures for baseline assessment and monitoring.
  • •Ask about weight-bearing activities (walking, stairs, standing) that worsen pain, and nocturnal pain that may indicate advanced disease with bone marrow lesions. Inquire about prior joint injury, occupation, sports history, and family history of OA or joint replacement.
  • •Examine the affected joint for crepitus on active/passive motion, bony enlargement (Heberden's nodes at the DIP, Bouchard's nodes at the PIP), limited range of motion, and varus or valgus deformity at the knee. Perform the patellofemoral compression test for anterior knee pain.
  • •Assess gait, alignment (e.g., varus thrust in knee OA), and muscle strength, particularly the quadriceps in knee OA and gluteus medius in hip OA. Measure body mass index (BMI ≥ 25 increases risk 3- to 4-fold).
  • •Order weight-bearing anteroposterior and lateral radiographs of the affected joint. In the knee, a Rosenberg view (flexed PA) better visualizes posterior compartment joint space narrowing. The Kellgren-Lawrence (KL) grading system (0-4) is the standard: KL grade ≥2 (definite osteophyte and possible joint space narrowing) defines radiographic OA.
  • •Joint space width <2 mm in the medial compartment is considered severely narrowed; asymmetrical narrowing favors OA over inflammatory arthritis. In the hip, joint space narrowing occurs superolaterally in primary OA (axial/posteromedial in secondary). The center-edge angle of Wiberg ≤20° suggests dysplasia-associated OA.
  • •MRI is not routinely indicated for OA diagnosis but is reserved for: (1) suspected meniscal or ligamentous injury with mechanical symptoms (locking, instability), (2) atypical presentation (rapid progression, inflammatory features), (3) preoperative planning for joint-preserving surgery (osteotomy, cartilage repair). Key MRI findings: cartilage loss <1.5 mm, meniscal extrusion >3 mm, subchondral bone marrow lesions (BMLs).
  • •CT is valuable for preoperative planning: measures femoral anteversion (normal 10-15°), tibial slope (mean 10.2° in Korean OA), glenoid version, and acetabular coverage. CT is also first-line for detecting occult fractures that may mimic OA flares.
  • •Laboratory tests are not diagnostic but help exclude inflammatory arthritis: check ESR, CRP, rheumatoid factor, anti-CCP. Synovial fluid analysis (WBC <2000 cells/μL, predominantly mononuclear) is indicated if inflammatory arthritis is suspected (e.g., gout, pseudogout).
  • •Diagnostic criteria: The ACR criteria for knee OA include knee pain plus at least 3 of the following: age >50, stiffness <30 min, crepitus, bony tenderness, bony enlargement, no palpable warmth. For hip OA: hip pain plus internal rotation <15° and flexion ≤115° (or ESR ≤45 mm/hr if internal rotation >15°).
  • •Assess functional status with the Short Physical Performance Battery (SPPB) and the Western Ontario and McMaster Universities Arthritis Index (WOMAC) as part of the initial evaluation.
  • •Also consider: avascular necrosis (often younger, with corticosteroid/alcohol use, MRI shows subchondral collapse), subchondral insufficiency fracture (acute pain, elderly, MRI shows low-signal band), and neuropathic arthropathy (Charcot joint, marked deformity with loss of sensation).

Management

  • •First-line management: structured land-based exercise (aerobic, resistance, balance) at least 150 min/week, combined with self-management education and weight loss (target 5-10% body weight if BMI >25). Refer to a physiotherapist if unsure how to prescribe an individualised home program.
  • •Paracetamol (acetaminophen) 1000 mg three times daily is the first-line oral analgesic; limit total daily dose to 3000 mg. However, efficacy is modest (NNT=16 for pain relief) and there is little anti-inflammatory effect.
  • •Use oral NSAIDs as more effective alternatives (naproxen 500 mg twice daily, ibuprofen 600-800 mg three times daily). Lowest effective dose for the shortest duration; all are equivalent. Gastroprotection with a PPI (e.g., omeprazole 20 mg daily) is recommended for patients at risk of GI bleeding (age >65, prior ulcer, concurrent anticoagulant/aspirin).
  • •Topical NSAIDs (diclofenac gel 1% four times daily) are first-line for knee and hand OA in patients >75 or with CV/renal contraindications to oral NSAIDs. Mild systemic absorption; avoid on broken skin.
  • •Tramadol 50-100 mg every 4-6 hours as needed (max 400 mg/day) is a third-line option in patients who are not candidates for NSAIDs or joint replacement. The 2020 OARSI guidelines conditionally recommend it, only if other therapies have failed.
  • •Intra-articular corticosteroids: Triamcinolone acetonide 40 mg (knee) or 20-40 mg (hip); onset of effect 2-7 days, duration 4-8 weeks. A single dose can improve pain and swelling. Avoid repeated injections (every 3 months) as evidence suggests possible cartilage volume loss with frequent use.
  • •Intra-articular hyaluronic acid (HA): For knee OA, a single course of 3 weekly injections (e.g., Synvisc, 16 mg/2 mL) or a single high-molecular-weight injection (Gel-One, 30 mg/3 mL). Evidence is moderate for short-term (12-24 weeks) pain relief; the NNT for meaningful improvement is about 5.
  • •Leukocyte-rich platelet-rich plasma (PRP): 3 mL to the knee, 1-2 sessions; superior to placebo for pain reduction at 12 months (NNT=5). Contraindicated for patients on antiplatelet therapy or with active infection. The Knee Society does not recommend combination with HA over PRP alone.
  • •Initiate quadriceps-strengthening exercises for knee OA (avoiding high-impact loading). In patients with varus knee OA, consider lateral wedge insoles to reduce medial compartment load, though their effect on symptoms is small.
  • •Refer for total knee arthroplasty (TKA) or total hip arthroplasty (THA) when there is severe, persistent pain unresponsive to non-operative treatment, functional limitation, and radiographic end-stage disease (bone-on-bone appearance). Typical thresholds: WOMAC pain score >50/100, walking distance <400 meters. TKA and THA are the most effective treatments for end-stage OA.
  • •For patients with hip OA, if not a surgical candidate or pre-arthritic, consider cooled radiofrequency ablation (CRFA) of the genicular nerves (knee) or periarticular nerves (hip). This provides 6-12 months of pain relief by neurolysis. A diagnostic block (local anesthetic) should be performed first to confirm pain source.
  • •Avoid: Strong opioids (guidelines recommend against long-term use due to risk of addiction, falls, and overdose); treadmill incline walking in patellofemoral OA; glucosamine and chondroitin (guidelines recommend against due to lack of efficacy over placebo).
  • •For cervical facet OA with radicular pain, consider facet joint injections (0.5 mL of bupivacaine 0.5% + 20 mg methylprednisolone) under fluoroscopy. For lumbar facet OA, radiofrequency denervation can provide 6-12 months of relief if diagnostic blocks are positive.
  • •When to refer: urgent referral to orthopaedics if suspected avascular necrosis (hip), subchondral insufficiency fracture, or rapidly progressive OA (destruction within 6-12 months). Refer to a physiatrist for comprehensive rehabilitation when function is declining despite 6 weeks of conservative care.
  • •Post-arthroplasty management: Continue optimal medical management if other joints are affected. For TKA, weight-bearing as tolerated with a walker for the first 6 weeks; physical therapy focuses on gaining range of motion (goal: 0-90° at 6 weeks). Venous thromboembolism prophylaxis (aspirin 325 mg twice daily for 10-14 days, or rivaroxaban 10 mg daily for 14 days if high-risk) is standard.
  • •Monitoring: At each visit, assess pain (using the visual analog scale, VAS, 0-10), function (WOMAC, KOOS/HOOS), and adverse effects from medications (renal function, liver function, bleeding). In patients on long-term NSAIDs, check renal function (eGFR) and serum potassium every 3-6 months.
  • •Escalation: If pain remains moderate (VAS 4-6) after 8 weeks of first-line therapy (exercise + weight loss + NSAIDs), consider intra-articular therapy (corticosteroid or PRP). If pain is severe (VAS 7-10) and end-stage OA is present, refer for arthroplasty. If the patient declines surgery, consider tramadol or NSAID combined with physical therapy.
  • •Novel agents: Disease-modifying OA drugs are not approved. Sprifermin (recombinant human FGF-18) has shown modest cartilage thickness increase in Phase II trials but is not yet approved. Investigational agents target Wnt signaling, catabolic enzymes (ADAMTS-5, MMP-13), and TRPV1 antagonism.

Board Review — High Yield

  • •Kellgren-Lawrence grade, The standard radiographic OA staging system; grade ≥2 (definite osteophyte and possible joint space narrowing) defines radiographic OA.
  • •Medial tibiofemoral compartment, Most common site of knee OA due to carrying 60-70% of load; varus malalignment accelerates progression; joint space width <2 mm is severely narrowed.
  • •Heberden's nodes, Bony enlargement at the DIP; associated with nodal OA; reflects osteophyte formation; Bouchard's nodes are at the PIP.
  • •Cam-type femoroacetabular impingement, Alpha angle >55° at femoral head-neck junction; causes premature hip OA; more common in males.
  • •Meniscal extrusion >3 mm, A key MRI finding in accelerated knee OA; associated with cartilage loss and subchondral bone marrow lesions.
  • •Synovial fluid WBC <2000 cells/μL, Distinguishes OA from inflammatory arthritis (<2000 usually mononuclear).
  • •Total knee/hip arthroplasty, The most effective treatment for end-stage OA; signs: nocturnal pain, rest pain, bone-on-bone radiographic appearance.
  • •Intra-articular corticosteroids, Triamcinolone acetonide 40 mg (knee), 20-40 mg (hip); effect in 2-7 days, lasts 4-8 weeks. Avoid every-3-month use due to risk of cartilage loss.
  • •Exercise and weight loss, First-line therapy for OA; 5-10% weight loss in overweight patients produces clinically meaningful pain reduction; structured exercise (aerobic + resistance) improves function.
  • •OARSI 2020 guidelines, Strongly recommend exercise, weight loss, NSAIDs, topical NSAIDs; conditionally recommend tramadol, PRP; strongly recommend against glucosamine and chondroitin.

Deep Dive — Evidence Details

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