Osteoarthritis (OA) is the most common chronic joint disorder and the leading cause of musculoskeletal disability worldwide. It is a progressive degenerative disease of synovial joints characterized by loss of articular cartilage, remodeling of subchondral bone, osteophyte formation, synovial inflammation, capsular fibrosis, and weakness of periarticular muscles. Although traditionally considered a "wear-and-tear" disease, current evidence demonstrates that osteoarthritis is a whole-joint disorder involving mechanical, inflammatory, metabolic, biochemical, and genetic factors.

The disease usually develops gradually, affecting one or a few joints, and results in chronic pain, stiffness, reduced mobility, and functional limitation.

Epidemiology

• Most common form of arthritis worldwide.

• Prevalence increases with advancing age.

• More common in women after the age of 50 years.

• Knee and hip osteoarthritis are major causes of disability.

• Obesity is one of the strongest modifiable risk factors.

Etiology

Osteoarthritis is multifactorial and results from an imbalance between cartilage breakdown and repair.

Primary osteoarthritis develops without an identifiable cause.

Secondary osteoarthritis may result from:

• Previous joint trauma

• Congenital joint abnormalities

• Inflammatory arthritis

• Obesity

• Metabolic disorders

• Crystal arthropathies

• Avascular necrosis

• Septic arthritis

Pathophysiology

Osteoarthritis develops when mechanical stress, ageing, genetic susceptibility, and metabolic factors disrupt the normal balance between cartilage degradation and repair. Chondrocytes become activated and release inflammatory cytokines and matrix-degrading enzymes, particularly matrix metalloproteinases, which progressively break down collagen and proteoglycans within the articular cartilage. As cartilage becomes thinner and loses its shock-absorbing capacity, increased mechanical load is transferred to the underlying subchondral bone, leading to sclerosis, cyst formation, and bone remodeling. Marginal osteophytes develop as an adaptive response to joint instability, while mild synovial inflammation contributes to pain and stiffness. Progressive structural changes ultimately result in joint deformity, reduced range of motion, muscle weakness, and chronic disability.

Risk factors

• Increasing age

• Female sex

• Obesity

• Previous joint injury

• Occupational overuse

• Repetitive mechanical stress

• High-impact sports

• Family history

• Muscle weakness

• Joint malalignment

• Diabetes mellitus

• Metabolic syndrome

Commonly affected joints

• Knee

• Hip

• Cervical spine

• Lumbar spine

• Distal interphalangeal (DIP) joints

• Proximal interphalangeal (PIP) joints

• First carpometacarpal joint (thumb base)

• First metatarsophalangeal joint

Clinical presentation

Symptoms usually develop gradually over months or years.

Pain

• Joint pain aggravated by activity

• Pain relieved by rest

• Pain worsening toward the end of the day

• Weight-bearing pain

• Mechanical pain

Stiffness

• Morning stiffness lasting less than 30 minutes

• Stiffness after periods of inactivity ("gelling phenomenon")

Functional symptoms

• Reduced joint mobility

• Difficulty walking

• Difficulty climbing stairs

• Difficulty rising from a chair

• Reduced grip strength

• Limping

Mechanical symptoms

• Crepitus

• Locking

• Joint instability

• Giving way

Physical examination

• Bony enlargement

• Joint line tenderness

• Reduced range of motion

• Crepitus

• Mild joint effusion

• Varus or valgus deformity

• Muscle wasting

Characteristic deformities

• Heberden's nodes (DIP joints)

• Bouchard's nodes (PIP joints)

• Squaring of the thumb base

• Genu varum

Diagnostic criteria

Diagnosis is primarily clinical and supported by imaging.

Typical features include:

• Age greater than 45 years

• Activity-related joint pain

• Morning stiffness lasting less than 30 minutes

• Crepitus

• Bony enlargement

• Restricted movement

• Absence of systemic inflammatory features

The American College of Rheumatology (ACR) clinical classification criteria for knee osteoarthritis support the diagnosis when knee pain is present together with at least three of the following:

• Age over 50 years

• Morning stiffness less than 30 minutes

• Crepitus

• Bony tenderness

• Bony enlargement

• No palpable warmth of the joint

Investigations

Laboratory investigations

Laboratory tests are usually normal and are mainly performed to exclude inflammatory arthritis.

• Complete blood count (CBC)

• Erythrocyte sedimentation rate (ESR)

• C-reactive protein (CRP)

• Rheumatoid factor (RF) when indicated

• Anti-cyclic citrullinated peptide antibody (anti-CCP) when inflammatory arthritis is suspected

Synovial fluid analysis

Performed when diagnosis is uncertain or infection/crystal arthritis is suspected.

Typical findings:

• Clear or slightly yellow fluid

• Non-inflammatory

• White blood cell count generally below 2,000/mm³

• Negative Gram stain and culture

Imaging

Plain X-ray (first-line investigation)

Typical findings include:

• Joint space narrowing

• Marginal osteophytes

• Subchondral sclerosis

• Subchondral cysts

• Bone deformity

CT scan

Useful for complex joints and surgical planning.

MRI

Useful for:

• Early cartilage damage

• Meniscal injuries

• Ligament pathology

• Bone marrow lesions

Diagnostic arthroscopy

May be considered in selected cases when diagnosis remains uncertain or when treating associated intra-articular pathology.

Differential diagnosis

• Rheumatoid arthritis

• Gout

• Calcium pyrophosphate deposition disease

• Septic arthritis

• Psoriatic arthritis

• Avascular necrosis

• Meniscal injury

• Bursitis

Management

Treatment aims to:

• Relieve pain

• Improve function

• Slow disease progression

• Maintain independence

• Improve quality of life

Non-pharmacological management

First-line management includes:

• Patient education

• Weight reduction in overweight or obese patients

• Regular low-impact exercise

• Physiotherapy

• Muscle strengthening exercises

• Range-of-motion exercises

• Transcutaneous electrical nerve stimulation (TENS)

• Joint protection strategies

• Activity modification

• Walking aids such as crutches or walkers for severe disease

• Crepe bandages or braces during symptomatic periods

• Appropriate footwear

Pharmacological treatment

Oral NSAIDs

Ibuprofen

• 400 mg orally immediately, then 200 mg orally every 8 hours for 7–14 days.

OR

Diclofenac sodium

• 50 mg orally every 8 hours for 7–14 days.

OR

Meloxicam

• 7.5–15 mg orally every 12–24 hours for 7–14 days.

OR

Dexketoprofen trometamol

• 12.5 mg orally every 4–6 hours

or

• 25 mg orally every 8 hours for 7–14 days.

Topical NSAIDs

Diclofenac gel

• Apply every 12 hours for 2 weeks.

OR

Ketoprofen gel

• Apply every 12 hours for 2 weeks.

Gastroprotection

Patients receiving prolonged NSAID therapy should receive gastroprotection when indicated.

Options include:

Omeprazole

• 20 mg orally once daily

OR

Pantoprazole

• 40 mg orally once daily

OR

Esomeprazole

• 40 mg orally once daily

OR

Lansoprazole

• 30 mg orally once daily for 2–4 weeks.

Additional analgesia

Tramadol

• 50 mg orally every 8 hours for 7–14 days.

OR

Tramadol + paracetamol

• 550 mg orally every 8 hours for 14 days.

OR

Ibuprofen + paracetamol

• 900 mg orally every 8 hours for 14 days.

Oral corticosteroid

Prednisolone

• 5–10 mg orally once daily according to clinical response.

Intra-articular injections

For patients with persistent symptoms despite conservative treatment.

Methylprednisolone

• 80 mg/mL for large joints.

• 40 mg/mL for small joints.

• Repeat every 2–12 weeks.

• Maximum four injections per year for up to two years.

OR

Triamcinolone

• 80 mg/mL for large joints.

• 40 mg/mL for small joints.

• Repeat every 2–12 weeks.

• Maximum four injections per year for up to two years.

OR

Betamethasone

• 12 mg/mL for large joints.

• 6 mg/mL for small joints.

• Repeat every 2–12 weeks.

• Maximum four injections annually for up to two years.

These injections may be administered together with:

1% Lignocaine

• 1–2 mL intra-articularly.

AND

Hyaluronic acid

• 16 mg intra-articularly once weekly for three consecutive weeks.

Nutritional supplements

Evidence for supplements remains variable; however, according to the current STG:

Glucosamine sulfate 1500 mg + Chondroitin sulfate 1200 mg

• Fixed-dose combination orally once daily with meals for 3–6 months.

Surgical management

Surgery is indicated for advanced disease causing severe pain, deformity, or major functional limitation despite optimal conservative treatment.

Procedures include:

• High tibial osteotomy for varus deformity of the knee

• Fibular osteotomy for medial compartment degeneration of the knee

• Total joint replacement (arthroplasty)

• Joint fusion (arthrodesis) for limb salvage

• Excisional arthroplasty

For patients who are poor surgical candidates, consider:

• Peripheral nerve block

• Radiofrequency ablation for pain management

Rehabilitation

• Progressive strengthening exercises

• Aerobic exercise

• Balance training

• Occupational therapy

• Joint protection techniques

• Assistive devices where required

• Home exercise programme

Monitoring and follow-up

Patients should be reviewed every 2–4 weeks initially to evaluate:

• Pain severity

• Functional improvement

• Medication adverse effects

• Disease progression

• Need for escalation of therapy

• Suitability for surgical referral

Long-term monitoring should include assessment of:

• Weight management

• Exercise adherence

• Radiographic progression where indicated

• Cardiovascular and gastrointestinal risks associated with NSAID use

Complications

• Chronic pain

• Progressive joint deformity

• Muscle wasting

• Functional disability

• Falls

• Reduced mobility

• Depression

• Loss of independence

• Need for joint replacement

Prognosis

Osteoarthritis is a chronic progressive disease with a variable rate of progression. Many patients maintain good function with lifestyle modification, exercise, weight reduction, and appropriate pharmacological therapy. Early conservative management can significantly reduce pain and delay disease progression. Advanced disease may ultimately require joint-preserving surgery or total joint replacement to restore mobility and quality of life.