Definition and epidemiology
Osteoarthritis (OA) is a degenerative joint disease characterized by breakdown of articular cartilage, subchondral bone remodeling, and secondary synovial inflammation. It is the leading cause of chronic joint pain and disability worldwide.
- Most common joint disease globally, affecting a substantial proportion of adults over age 60
- Prevalence rises steadily with age; radiographic evidence is far more common than symptomatic disease
- Knee OA is the most frequent symptomatic site, followed by hip and hand OA
- More common in women after menopause, particularly for hand and knee OA
- Primary (idiopathic) OA has no identifiable underlying cause; secondary OA results from a prior joint insult
- Pain worsens with use, improves with rest — opposite pattern to inflammatory arthritis
- Morning stiffness lasts under 30 minutes, unlike RA (over 1 hour)
- Heberden nodes = DIP, Bouchard nodes = PIP
- Classic X-ray findings: joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts
- Inflammatory markers (ESR/CRP) are typically normal
- Spares MCP joints and wrists, unlike rheumatoid arthritis
- First-line treatment is weight loss and exercise, not medication
- Synovial fluid WBC count is non-inflammatory, generally under 2000/microL
Etiology and risk factors
OA results from an imbalance between cartilage breakdown and repair, driven by mechanical and biochemical factors.
Non-modifiable risk factors
- Age (strongest risk factor)
- Female sex
- Genetic predisposition (especially hand OA)
- Prior joint trauma or surgery
Modifiable risk factors
- Obesity (increases load on weight-bearing joints and promotes systemic inflammation via adipokines)
- Repetitive joint use or occupational stress (e.g., kneeling, heavy lifting)
- Joint malalignment (varus/valgus deformity)
- Muscle weakness around the joint
Secondary causes
- Prior fracture or ligamentous injury
- Inflammatory arthritis (e.g., rheumatoid arthritis) causing joint damage
- Metabolic/crystal disease (hemochromatosis, ochronosis, gout, CPPD)
- Congenital or developmental joint abnormalities (e.g., hip dysplasia)
Pathophysiology
OA was once considered purely a 'wear and tear' process, but it is now understood as an active disease involving the whole joint.
- Chondrocytes initially attempt repair but eventually produce degraded, weaker extracellular matrix
- Progressive loss of proteoglycans and collagen type II leads to cartilage fibrillation and thinning
- Subchondral bone responds with sclerosis and formation of osteophytes (bony outgrowths) at joint margins
- Low-grade synovial inflammation contributes to pain and further cartilage breakdown
- Loss of cartilage reduces joint space, increasing bone-on-bone friction and mechanical pain
- Unlike inflammatory arthritis, systemic inflammatory markers are typically normal or only mildly elevated
Clinical features
OA presents with a gradual, insidious onset of joint symptoms, typically asymmetric and limited to a few joints.
Symptoms
- Joint pain that worsens with activity and improves with rest
- Morning stiffness that is brief, usually lasting less than 30 minutes (contrasts with rheumatoid arthritis)
- Stiffness after inactivity ('gelling phenomenon')
- Reduced range of motion and functional limitation over time
Signs
- Crepitus on joint movement
- Bony enlargement: Heberden nodes (DIP joints) and Bouchard nodes (PIP joints) in hand OA
- Joint line tenderness, effusion (usually mild), and malalignment in advanced disease
- Reduced range of motion with pain at extremes
Commonly affected joints
- Knees, hips, hands (DIP, PIP, first CMC joint), cervical and lumbar spine, first MTP joint
- Classically spares the MCP joints and wrists (helpful distinction from rheumatoid arthritis)
Diagnosis
OA is primarily a clinical diagnosis, supported by imaging when needed; laboratory testing is used mainly to exclude other causes.
Clinical diagnosis
- Based on characteristic history and exam findings in a patient over 45 with activity-related joint pain and no prominent inflammatory features
Imaging
- Plain radiographs are first-line and may show the classic findings:
| Radiographic feature | Description |
|---|---|
| Joint space narrowing | Due to cartilage loss |
| Osteophytes | Bony spurs at joint margins |
| Subchondral sclerosis | Increased bone density beneath cartilage |
| Subchondral cysts | Fluid-filled lesions in subchondral bone |
- MRI is not routinely needed but can assess soft tissue and early cartilage changes in select cases
Laboratory tests
- Not required for diagnosis; used to exclude inflammatory or crystal arthropathies when the presentation is atypical
- Inflammatory markers (ESR, CRP) and rheumatoid factor are typically normal
- Synovial fluid, if sampled, shows a non-inflammatory profile (WBC count generally under 2000/microL)
Differential diagnosis
- Rheumatoid arthritis — symmetric, small joint (MCP, wrist) involvement, prolonged morning stiffness over 1 hour, elevated inflammatory markers, positive RF/anti-CCP
- Gout — acute, severely painful monoarticular attacks, classically first MTP joint, negatively birefringent crystals
- Pseudogout (CPPD) — acute monoarthritis, chondrocalcinosis on imaging, positively birefringent rhomboid crystals
- Psoriatic arthritis — associated skin/nail changes, dactylitis, DIP involvement with distinct radiographic pattern
- Septic arthritis — acute, hot, swollen joint with fever, requires urgent synovial fluid analysis
- Fibromyalgia — diffuse pain and tender points without structural joint damage or radiographic changes
Management
Management follows a stepwise approach per major guidelines (ACR, OARSI, NICE), beginning with non-pharmacologic measures.
Non-pharmacologic (first-line, for all patients)
- Patient education about the chronic, generally slowly progressive nature of OA
- Weight loss in overweight/obese patients, which reduces load on weight-bearing joints
- Structured exercise programs: strengthening, low-impact aerobic activity, and range-of-motion exercises
- Physical therapy and assistive devices (canes, braces, orthotics) as needed
Pharmacologic
- Topical NSAIDs are preferred for knee/hand OA, especially in older adults, to limit systemic exposure
- Oral NSAIDs for inadequate response, used at the lowest effective dose with attention to GI, renal, and cardiovascular risk
- Acetaminophen may provide modest benefit and is sometimes used, though guidelines increasingly favor NSAIDs when not contraindicated
- Intra-articular corticosteroid injections for short-term relief of flares, particularly knee OA
- Duloxetine may be considered as an adjunct for chronic knee OA pain
- Glucosamine/chondroitin and hyaluronic acid injections lack consistent evidence of benefit; recommendations vary by society and are generally not routinely endorsed
- Opioids are discouraged and reserved for refractory cases due to limited benefit and significant risk
Surgical
- Total joint arthroplasty (knee or hip replacement) for severe disease with significant pain and functional limitation refractory to conservative therapy
- Osteotomy may be considered in select younger patients with malalignment
Complications and prognosis
- Progressive joint deformity, instability, and loss of function
- Chronic pain impacting mobility, independence, and quality of life
- Increased fall risk in elderly patients with lower limb OA
- Secondary muscle atrophy and deconditioning around affected joints
- OA is generally slowly progressive but non-fatal; course varies widely between individuals
- Joint replacement surgery has excellent outcomes for pain relief and function in end-stage disease, particularly hip and knee
Heberden's = 'H' is for 'High up' (closer to fingertip, DIP); Bouchard's is proximal (PIP), between Heberden's and the hand.
Practice questions
1. A 62-year-old woman presents with bilateral hand pain that has worsened gradually over 3 years. She notes stiffness in the morning lasting about 10 minutes that resolves quickly. Examination reveals bony enlargement of the distal interphalangeal joints bilaterally with mild tenderness but no warmth or erythema. ESR and CRP are within normal limits. Which of the following is the most likely diagnosis?
2. A 68-year-old man with a BMI of 34 presents with chronic right knee pain that worsens with walking and improves with rest. X-ray shows joint space narrowing, osteophytes, and subchondral sclerosis. He has already tried acetaminophen with minimal relief and has no history of peptic ulcer disease or renal impairment. Which of the following is the most appropriate next step in management?
3. A 70-year-old woman with long-standing knee osteoarthritis undergoes arthrocentesis for a swollen knee. Synovial fluid analysis reveals a WBC count of 800/microL with no crystals seen under polarized light. Which of the following best characterizes this synovial fluid finding?
Frequently asked questions
What causes osteoarthritis?
Osteoarthritis is caused by progressive breakdown of articular cartilage that outpaces the joint's repair capacity, leading to bone remodeling and osteophyte formation. Risk factors include aging, obesity, joint trauma, repetitive mechanical stress, and genetic predisposition. It can also develop secondarily after joint injury, inflammatory arthritis, or metabolic conditions like hemochromatosis.
What are the first symptoms of osteoarthritis?
The earliest symptoms are usually joint pain and stiffness that occur with activity and improve with rest, often in the knees, hips, or hand joints. Morning stiffness is typically brief, lasting less than 30 minutes. Patients may also notice mild joint swelling, crepitus (a grating sensation), and gradual loss of flexibility over months to years.
How is osteoarthritis diagnosed?
Osteoarthritis is diagnosed clinically based on a typical history of activity-related joint pain in a patient usually over 45, combined with exam findings like crepitus and bony enlargement. Plain X-rays support the diagnosis by showing joint space narrowing, osteophytes, and subchondral sclerosis. Blood tests are not needed to diagnose OA but help rule out inflammatory arthritis when the picture is unclear.
Is osteoarthritis curable?
No, osteoarthritis is not curable, but it is very manageable, and many people maintain good function for years with the right approach. Treatment focuses on reducing pain and preserving joint function through weight loss, exercise, and medications. In advanced, refractory cases, joint replacement surgery can effectively eliminate pain and restore mobility.
Osteoarthritis vs rheumatoid arthritis — what is the difference?
Osteoarthritis is a degenerative, mechanical joint disease with activity-related pain, brief morning stiffness, and normal inflammatory markers, while rheumatoid arthritis is a systemic autoimmune disease with symmetric small joint inflammation, prolonged morning stiffness over an hour, and elevated inflammatory markers. RA typically involves the MCP joints and wrists, which OA characteristically spares. RA also requires immunosuppressive treatment, unlike OA.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: M19
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.