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

Arthritis is an umbrella term for over 100 distinct conditions that share the common feature of joint inflammation, causing pain, swelling, stiffness, and impaired function. The two most prevalent types are: osteoarthritis (OA) — a degenerative joint disease characterised by progressive loss of articular cartilage, subchondral bone remodelling, osteophyte formation, and synovial inflammation, affecting 528 million people globally (7.6% of the world population) and the most common joint disease worldwide; and rheumatoid arthritis (RA) — a chronic systemic autoimmune disorder in which immune activation drives synovial inflammation (synovitis), pannus formation, and progressive articular cartilage and bone erosion, affecting approximately 18 million people worldwide and being a major contributor to work disability. Other clinically significant forms include: gout (monosodium urate crystal deposition arthritis — the most common inflammatory arthritis in men, affecting 1-4% of adults in developed countries); psoriatic arthritis (seronegative inflammatory arthritis in 20-30% of psoriasis patients); ankylosing spondylitis (axial spondyloarthropathy involving sacroiliac joints and spine); reactive arthritis (following genitourinary or gastrointestinal infections); septic arthritis (joint infection — medical emergency); lupus arthritis; and juvenile idiopathic arthritis (JIA — the most common paediatric rheumatological condition). Arthritis is the leading cause of disability in the United States and other developed countries, affecting over 350 million people globally across all age groups.

Osteoarthritis: OA results from an imbalance between cartilage breakdown and repair — driven by mechanical stress on degraded cartilage, subsequent chondrocyte apoptosis, proteolytic enzyme (MMP, aggrecanase) release, and low-grade synovial inflammation — ultimately leading to full-thickness cartilage loss, subchondral bone exposure, osteophyte formation, and joint space narrowing visible on X-ray. Key risk factors include advanced age (the strongest risk factor), obesity (each 5 kg weight loss reduces knee OA risk by 50%), previous joint injury, female sex (particularly post-menopausal, suggesting hormonal influence), repetitive occupational joint loading, and genetic predisposition (TGF-β pathway genes). Rheumatoid arthritis: RA is an autoimmune disease in which autoreactive T-cells (HLA-DRB1*04 'shared epitope') and B-cells (producing anti-citrullinated protein antibodies/ACPA and rheumatoid factor/RF) drive persistent synovial inflammation; major environmental triggers include smoking (doubles RA risk and worsens outcomes), gut and oral microbiome dysbiosis (Porphyromonas gingivalis periodontal bacteria implicated), hormonal factors (pregnancy remission, postpartum flare, female predominance 3:1), and early-life infections. Gout: caused by hyperuricaemia (serum urate above 360 mcmol/L) from overproduction (rare — HGPRT enzyme deficiency) or, more commonly, underexcretion (90%) of uric acid — driven by dietary purines (organ meats, shellfish, red meat, fructose), alcohol (especially beer), obesity, chronic kidney disease, diuretics (thiazide/loop), and genetic variants (SLC2A9, ABCG2). Septic arthritis: haematogenous bacterial seeding (Staphylococcus aureus most common; Neisseria gonorrhoeae in sexually active young adults; Streptococcus species) causes joint destruction within hours to days without urgent treatment.

Osteoarthritis symptoms develop insidiously over years: deep, aching joint pain worsening with weight-bearing activity and relieved by rest (late-stage OA causes rest and night pain — a sign of severe disease); brief morning stiffness typically under 30 minutes (distinguishing OA from inflammatory arthritis); crepitus (audible or palpable grinding sensation within the joint from roughened articular surfaces); bony enlargement and deformity — Heberden's nodes (distal interphalangeal joints) and Bouchard's nodes (proximal interphalangeal joints) in hand OA; reduced range of motion; antalgic gait (limping to offload affected joint); and eventual functional impairment — difficulty climbing stairs, rising from a chair, or walking distances. Most commonly affected joints: knees (tricompartmental or medial predominantly), hips, hands, first carpometacarpal joint (thumb base — causing 'square hand' deformity), spine (facet joint spondylosis), and first metatarsophalangeal joint (hallux valgus risk). Rheumatoid arthritis typically presents with symmetrical polyarthritis of small joints (metacarpophalangeal, proximal interphalangeal joints of hands, metatarsophalangeal joints of feet — 'MCP/PIP' distribution), wrists, elbows, and knees; prolonged morning stiffness over 1 hour (reflecting overnight accumulation of inflammatory mediators); joint warmth, redness, and boggy swelling from synovitis; systemic features in active disease: fatigue (profound — often a dominant complaint), low-grade fever, and unintentional weight loss; anaemia of chronic disease; and in severe RA — rheumatoid nodules (subcutaneous nodules on pressure points — olecranon, fingers), vasculitis, pleuritis, scleritis. Gout presents as acute severe monoarthritis — often developing overnight to maximum intensity within 12-24 hours: excruciating pain (often described as the worst pain experienced), redness, swelling, and warmth — most classically in the first MTP joint (big toe — podagra — in 50% of first attacks) but also ankle, midfoot, wrist, or knee. Septic arthritis: single hot, swollen joint with fever and marked systemic toxicity — requires emergency aspiration and IV antibiotics.

Osteoarthritis: diagnosis is predominantly clinical (characteristic history, typical distribution) confirmed by plain radiography — X-ray findings include joint space narrowing (cartilage loss), osteophytes (bony outgrowths at joint margins), subchondral sclerosis (increased bone density beneath cartilage), and subchondral cysts; there is often poor correlation between X-ray severity and symptoms (up to 40% of severe X-ray OA is asymptomatic). MRI is more sensitive for early cartilage changes, meniscal tears, bone marrow oedema, and ligament injuries but is not required for routine OA diagnosis. Rheumatoid arthritis: the 2010 ACR/EULAR classification criteria allocate points for joint count and distribution (0-5 points), seropositivity — rheumatoid factor (RF) and anti-cyclic citrullinated peptide/anti-CCP antibodies (0-3 points; high-positive anti-CCP carries highest specificity and is associated with more erosive disease), elevated acute-phase reactants (CRP/ESR — 0-1 point), and symptom duration above 6 weeks (1 point); score of 6 or more confirms RA. Early erosions in RA may be detected by MRI or ultrasound (active synovitis shows vascularity on power Doppler) before X-ray changes — ultrasound is increasingly used in rheumatology clinics. FBC (anaemia of chronic disease), LFTs (before DMARD prescribing), HBV/HCV and TB screening (before biologics). Gout: serum uric acid is elevated in 90%+ of gout cases — but can be normal during an acute attack; definitive diagnosis by joint aspiration showing negatively birefringent needle-shaped monosodium urate crystals under polarised light microscopy; ultrasound shows 'double contour sign' on cartilage surface from urate deposition. Septic arthritis: urgent joint aspiration (synovial fluid — turbid, WBC above 50,000/mm3, predominantly neutrophils) with Gram stain and culture; blood cultures in all cases; X-ray baseline; ESR, CRP, and WBC elevated.

Osteoarthritis treatment: non-pharmacological first — patient education, therapeutic exercise (especially quadriceps strengthening for knee OA — the most evidence-based OA intervention), weight loss (5% body weight reduction reduces knee pain by 50%), physiotherapy, hydrotherapy, walking aids, orthotics (medial wedge insoles for lateral knee OA), and activity modification. Pharmacological: topical NSAIDs (diclofenac gel) and topical capsaicin (first-line for knee/hand OA with fewer systemic effects); oral paracetamol (limited evidence for regular use — recent trials show modest benefit only); oral NSAIDs (naproxen, ibuprofen, celecoxib) — effective but carry GI, cardiovascular, and renal risks; intra-articular corticosteroid injections (IA CS — short-term pain relief for 4-12 weeks; limit to 4 per year per joint to avoid cartilage degradation). Duloxetine (60 mg/day) reduces central sensitisation-driven pain in OA. Joint arthroplasty (hip replacement — 95%+ 10-year implant survival; knee replacement — 90%+ at 10 years) for end-stage OA with failed conservative management. Rheumatoid arthritis: treat-to-target strategy — aim for remission (DAS28 below 2.6) or low disease activity (DAS28 below 3.2) within 3-6 months of diagnosis. First-line: methotrexate (7.5-25 mg/week — 'anchor DMARD') — take with folic acid 5 mg weekly to reduce toxicity; may be combined with sulfasalazine (SSZ) and hydroxychloroquine (HCQ) — 'triple therapy' highly effective. Biologics when DMARDs fail: TNF-alpha inhibitors (adalimumab SC fortnightly, etanercept SC weekly, certolizumab, golimumab); anti-IL-6 (tocilizumab, sarilumab); anti-CD20 (rituximab); CTLA-4Ig (abatacept). JAK inhibitors — baricitinib 2-4 mg/day, tofacitinib 5 mg BD, upadacitinib — oral targeted therapies (note cardiovascular/VTE risk monitoring requirements). Short bridging courses of prednisolone 7.5-15 mg/day are appropriate for acute flares or while DMARDs take effect. Gout: acute attack — colchicine 500 mcg three times daily (or 1 mg then 0.5 mg one hour later) or NSAIDs (indomethacin, naproxen) for 5-7 days; IA corticosteroid injection for large joint. Urate-lowering therapy (ULT): allopurinol 100-900 mg/day (xanthine oxidase inhibitor — titrate to serum urate target below 360 mcmol/L, or below 300 mcmol/L with tophi); febuxostat 80-120 mg/day if allopurinol intolerant; begin ULT during an attack only if already established. Provide colchicine or NSAID prophylaxis for the first 3-6 months of ULT initiation. Lesinurad (uricosuric) for refractory cases.

Untreated RA leads to joint erosion and destruction within 1-2 years — causing permanent deformities (ulnar deviation, boutonniere, swan-neck deformities of the fingers, volar subluxation of wrists), loss of function, and disability. RA also increases cardiovascular risk 2-fold through chronic systemic inflammation. Atlantoaxial subluxation (C1-C2 instability) is a rare but life-threatening complication of severe RA with spinal cord compression risk. Untreated OA progresses to bone-on-bone articulation requiring joint replacement. Uncontrolled gout leads to tophus formation (urate crystal deposits in soft tissues, tendons, and joints), chronic gouty arthropathy with joint destruction, and kidney stones and urate nephropathy. All forms of arthritis, if inadequately treated, cause significant disability, clinical depression, and reduced life expectancy from comorbid cardiovascular disease and immobility.

Maintain a healthy BMI — even 5% weight loss significantly reduces knee OA pain and slows disease progression by reducing joint load. Exercise regularly with low-impact activities (swimming, cycling, walking, aquatic therapy) to strengthen joint-supporting muscles and maintain cartilage nutrition without excessive mechanical stress. Avoid smoking — a major modifiable risk factor for RA (doubles risk and worsens outcomes) and accelerates OA progression. For gout prevention: limit alcohol (especially beer and spirits), reduce purine-rich foods (red meat, organ meats, shellfish, anchovies), avoid high-fructose corn syrup beverages, stay well hydrated (2-3 L/day), and maintain urate-lowering therapy adherence (most gout flares are from ULT non-adherence). Protect joints from injury — wear appropriate footwear, avoid repetitive high-impact activities, and seek prompt treatment for sports injuries. Early diagnosis and treat-to-target therapy in RA prevents irreversible joint damage and long-term disability.

See your GP for: persistent joint pain, stiffness, or swelling lasting more than 6 weeks, morning stiffness lasting more than 30 minutes (suggesting inflammatory arthritis), joint warmth or redness, or significant functional limitation. Seek urgent assessment for: a single hot, swollen joint with fever — this may be septic arthritis (joint infection — a medical emergency requiring urgent joint aspiration and IV antibiotics). See a rheumatologist promptly for suspected rheumatoid arthritis — early treatment within weeks of symptom onset dramatically reduces joint damage. See a doctor for: joint pain in a child (juvenile idiopathic arthritis), sudden severe joint pain in a gout-prone patient, or any joint symptoms following a tick bite (Lyme arthritis). Do not self-medicate arthritis long-term with over-the-counter NSAIDs without medical assessment.