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Arthritis — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Updated: 2026-07-06
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Quick Facts

Type
Musculoskeletal joint disease (inflammatory or degenerative)
Specialist
Rheumatologist; Orthopaedic Surgeon for surgical management
Key Treatment
OA: paracetamol, NSAIDs, physiotherapy, joint replacement. RA: methotrexate, biologics (adalimumab, etanercept)
Prevalence
Affects over 350 million people worldwide; osteoarthritis is the most common joint disease; rheumatoid arthritis affects 1% of the global population

What Is Arthritis?

Arthritis is not a single disease but an umbrella term encompassing over 100 conditions affecting joints and surrounding tissues. The two most prevalent forms are osteoarthritis (OA) — a degenerative joint disease characterised by cartilage breakdown and bone remodelling, most common in the elderly — and rheumatoid arthritis (RA) — a systemic autoimmune disease causing synovial inflammation, joint destruction, and extra-articular manifestations. Other significant forms include psoriatic arthritis, ankylosing spondylitis, gout, and juvenile idiopathic arthritis. Arthritis affects over 350 million people worldwide and is the leading cause of disability in developed nations. OA affects 10-15% of adults over 60 and virtually all adults over 75 on imaging. RA affects approximately 1% of the global population, with a 3:1 female predominance.

Causes & Risk Factors

Osteoarthritis: age (the strongest risk factor — OA is progressive with advancing age), female sex (greater risk after menopause from oestrogen decline), obesity (each kilogram of excess weight places approximately 4 kg of force on the knee), previous joint injury, repetitive occupational joint loading, joint malalignment, and genetic predisposition. Rheumatoid arthritis: autoimmune — autoreactive T and B cells, anti-citrullinated protein antibodies (ACPA/anti-CCP) and rheumatoid factor (RF) are pathogenic; genetic risk (HLA-DRB1 shared epitope); environmental triggers including cigarette smoking (strongest modifiable RA risk factor — doubles risk), female hormones, periodontitis (Porphyromonas gingivalis), gut microbiome dysbiosis, and viral triggers (EBV, Parvovirus B19). Gout: hyperuricaemia from uric acid overproduction or underexcretion (diet high in purines, fructose, alcohol; diuretics; renal insufficiency).

Symptoms & Signs

Osteoarthritis: joint pain worsening with activity and relieved by rest, morning stiffness lasting under 30 minutes (distinguishes from inflammatory arthritis where it exceeds 30 minutes-1 hour), crepitus (grating sensation), restricted range of motion, bony enlargement (Heberden's nodes at DIP joints, Bouchard's nodes at PIP joints in finger OA), and joint deformity in advanced disease. Most commonly affected joints: knees, hips, hands, and lumbar spine. Rheumatoid arthritis: symmetrical small joint polyarthritis (MCPs, PIPs — hands, wrists, feet), prolonged morning stiffness (over 1 hour — a key diagnostic feature), soft synovial swelling, warmth and tenderness; systemic features — fatigue, weight loss, fever; extra-articular manifestations — rheumatoid nodules, serositis (pleuritis, pericarditis), interstitial lung disease, scleritis, secondary Sjogren's syndrome, and vasculitis in severe RA.

How Arthritis Is Diagnosed

Osteoarthritis: clinical diagnosis based on history and examination; confirmed by X-ray showing joint space narrowing, osteophyte formation, subchondral sclerosis, and cysts. MRI is not routinely required but detects early OA, cartilage defects, and meniscal pathology. Rheumatoid arthritis: 2010 ACR/EULAR classification criteria use joint involvement, serology (RF, anti-CCP antibodies — anti-CCP has 95% specificity and is more specific than RF), acute phase reactants (CRP, ESR), and symptom duration. Anti-CCP positive and RF positive ('seropositive RA') predicts more erosive disease. X-ray hands and feet: juxta-articular osteoporosis, joint space narrowing, erosions (later sign). Ultrasound detects synovitis and erosions earlier than X-ray. Blood tests: FBC (normocytic anaemia of chronic disease), ESR/CRP (elevated in active RA), LFTs and renal function (before treatment). Gout: serum urate (may be normal during acute attack), joint aspiration showing negatively birefringent monosodium urate crystals under polarised light microscopy (gold standard).

Treatment Options

Osteoarthritis: paracetamol (first-line for mild OA), topical NSAIDs (diclofenac gel — first-line for knee/hand OA; fewer systemic side effects), oral NSAIDs (ibuprofen, naproxen — with PPI gastroprotection), intra-articular corticosteroid injections (short-term pain relief 4-8 weeks), intra-articular hyaluronic acid injections (modest evidence), physiotherapy (muscle strengthening, aerobic exercise), weight loss (highly effective for knee OA — 10% weight loss reduces pain by 50%), and joint arthroplasty (knee and hip replacement — highly effective for end-stage OA with 90-95% patient satisfaction at 10 years). Rheumatoid arthritis: treat-to-target strategy aiming for remission or low disease activity (DAS28 score below 2.6). csDMARDs: methotrexate (15-25 mg/week oral or subcutaneous — anchor drug), sulfasalazine, hydroxychloroquine (combination triple therapy is effective). Biologics: TNF inhibitors (adalimumab, etanercept, infliximab), IL-6 receptor antagonists (tocilizumab), B-cell depletion (rituximab), T-cell costimulation blockade (abatacept). JAK inhibitors (tofacitinib, baricitinib, upadacitinib) — oral targeted synthetic DMARDs. Low-dose prednisolone as bridging therapy. Gout: acute attack — colchicine 500 mcg TDS, NSAIDs, or prednisolone; urate-lowering therapy: allopurinol (target uric acid below 360 micromol/L).

Complications

Rheumatoid arthritis: progressive joint erosion and destruction causing permanent deformity (swan-neck and boutonnière deformity of fingers, Z-deformity of thumb, ulnar deviation of MCPs) and functional disability in 50% of untreated patients within 10 years. RA doubles the risk of myocardial infarction — cardiovascular disease is the leading cause of excess mortality, driven by chronic synovial inflammation accelerating atherosclerosis and endothelial dysfunction. Extra-articular RA complications include interstitial lung disease (ILD — affects 10-20% and may be progressive and fatal), rheumatoid vasculitis, scleritis, secondary Sjogren's syndrome, cervical spine instability (atlantoaxial subluxation risking spinal cord compression), and anaemia of chronic disease. Biologic therapy increases infection susceptibility — TNF inhibitors reactivate latent tuberculosis (mandatory TB screening before initiation). Gout complications include tophi formation (urate crystal deposits in joints, bursae, and kidneys), gouty nephropathy, and obstructive urolithiasis. Osteoarthritis end-stage causes severe joint deformity (valgus/varus knee), complete loss of joint space, and inability to mobilise without joint replacement. Depression affects 30-40% of patients with chronic arthritis.

Prevention & Lifestyle Management

For osteoarthritis: maintain healthy weight (the single most effective intervention for knee and hip OA risk), engage in regular low-impact exercise (swimming, cycling — strengthens periarticular muscles without joint loading), protect joints from injury (proper technique in sports, ergonomic workplace adjustments), avoid repetitive high-impact activities. For rheumatoid arthritis: smoking cessation is the most important modifiable risk factor — quitting smoking reduces RA risk by 30-50% and improves response to treatment in established disease. For gout: reduce dietary purines (red meat, shellfish, organ meats, beer), limit alcohol (particularly beer), increase hydration, lose weight, switch from thiazide diuretics if possible, and take urate-lowering therapy consistently — lifelong allopurinol prevents gout flares and tophus formation.

When to See a Doctor

Consult a doctor for joint pain or swelling lasting more than 6 weeks, especially if associated with morning stiffness exceeding 30-60 minutes, warmth, symmetrical involvement, or systemic symptoms such as fatigue and weight loss — these features suggest inflammatory arthritis requiring urgent rheumatology assessment and early treatment. In rheumatoid arthritis, the window of opportunity for preventing joint damage is in the first 3-6 months — early DMARD treatment substantially changes the disease trajectory. For suspected gout (acute severe monoarthritis with red, hot, swollen joint), see a doctor within 24-48 hours as early treatment shortens acute attack duration. Alert your rheumatologist immediately for any new redness, swelling, or warmth in a prosthetic joint — these symptoms may indicate periprosthetic joint infection requiring urgent surgical management.

Frequently Asked Questions

Osteoarthritis (OA) is a degenerative 'wear and tear' disease caused by breakdown of joint cartilage and bone remodelling over time, most common in older adults (particularly over 50), affecting weight-bearing joints (knees, hips) and the hands. Morning stiffness lasts less than 30 minutes. It is not a systemic inflammatory disease. Rheumatoid arthritis (RA) is a systemic autoimmune disease where the immune system attacks the synovial lining of joints, causing inflammation, cartilage destruction, and bone erosion. It predominantly affects small joints symmetrically, morning stiffness lasts over 1 hour, and it is associated with fatigue, raised inflammatory markers (CRP, ESR), and autoantibodies (rheumatoid factor, anti-CCP). RA can affect multiple organ systems beyond the joints.
Rheumatoid arthritis cannot currently be cured, but modern treat-to-target strategies achieve remission — complete or near-complete resolution of symptoms and inflammation — in over 50% of patients. Early aggressive treatment with methotrexate and biologics prevents joint damage and preserves function for decades. Sustained remission on treatment allows some patients to taper or discontinue biologics, but most require ongoing treatment. Untreated or poorly controlled RA leads to progressive joint destruction, disability, and increased cardiovascular mortality. The goal is normal function and quality of life, which is achievable for the majority with contemporary treatment.
Joint replacement (arthroplasty) is highly effective for end-stage OA unresponsive to conservative management, but it is not the only option. Before surgery, optimise non-surgical management: weight loss (most impactful for knee OA), physiotherapy and muscle strengthening, regular low-impact exercise, oral and topical analgesics (paracetamol, NSAIDs), intra-articular corticosteroid or hyaluronic acid injections, and activity modification. Surgery is considered when pain significantly impairs daily activities, sleep, and quality of life despite 3-6 months of optimal non-surgical treatment. Total knee and hip arthroplasty have excellent long-term outcomes — 90%+ implant survival at 10-15 years.
Biologic DMARDs (TNF inhibitors, IL-6 antagonists, B-cell depletion) have over 20 years of post-marketing safety data and are generally well-tolerated for long-term use. Key risks include: increased susceptibility to infections (particularly respiratory infections, reactivation of latent tuberculosis — TB screening is mandatory before starting TNF inhibitors); risk of lymphoma (modestly increased but confounded by RA disease activity itself); injection site or infusion reactions; and rarely, drug-induced lupus or demyelinating disease with TNF inhibitors. JAK inhibitors have additional concerns regarding cardiovascular events and thrombosis in older patients with cardiovascular risk factors. The benefits of effective RA control (preventing joint destruction, reducing cardiovascular risk from chronic inflammation) generally outweigh treatment risks when patients are properly screened and monitored.

References

  1. NICE Guideline NG100 — Osteoarthritis: Care and Management, 2022
  2. NICE Guideline NG100 — Rheumatoid Arthritis in Adults: Management, 2023
  3. Smolen JS et al. — EULAR Recommendations for the Management of Rheumatoid Arthritis, Annals of the Rheumatic Diseases, 2023
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Last updated: 2026-07-06

Important: This information is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider for diagnosis and treatment.

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