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

Arthritis pain is chronic or recurrent pain arising from joints affected by one of over 100 different types of arthritis — conditions characterised by joint inflammation, degeneration, or immune-mediated damage. The two most prevalent forms are osteoarthritis (OA) — a degenerative joint disease characterised by progressive cartilage loss, bone remodelling (osteophyte formation), and synovial inflammation — and rheumatoid arthritis (RA) — a chronic autoimmune synovitis driven by T-cell and B-cell mediated inflammation with joint destruction, systemic involvement, and extra-articular manifestations. Other common arthritides causing chronic pain include gout (uric acid crystal deposition), psoriatic arthritis, ankylosing spondylitis, reactive arthritis, and systemic lupus erythematosus. Arthritis pain has multiple mechanisms: nociceptive (from inflamed synovium, stretched joint capsule, and bone erosion), central sensitisation (amplified pain processing — particularly in fibromyalgia and widespread OA), and neuropathic components (from nerve compression in spinal arthritis). Effective management requires identifying the type of arthritis, the pain mechanism, and the functional impact.

Osteoarthritis (OA): primary risk factors include advancing age (the most important — OA prevalence rises steeply after 45), female sex (particularly after menopause — hormonal protection is lost), obesity (mechanical loading on weight-bearing joints and systemic adipokine-driven inflammation — each kg of weight loss reduces knee loading by 4 kg per step), previous joint injury (post-traumatic OA — ACL tear, meniscal injury, intra-articular fracture), occupational joint loading (kneeling, squatting), and family history (hereditary forms). OA most commonly affects the knees, hips, hands (DIP, PIP, and carpometacarpal joints), and spine. Rheumatoid arthritis (RA): an autoimmune condition of unknown aetiology — genetic predisposition (HLA-DRB1 shared epitope alleles — conferring 3-5x risk), smoking (the strongest environmental risk factor — doubles RA risk and worsens severity), female sex (3:1 female predominance), age 30-60 most common at onset, and prior infections (triggering molecular mimicry). Seropositivity (positive rheumatoid factor and/or anti-CCP antibodies) confers more severe disease. Gout: hyperuricaemia from purine-rich diet (red meat, seafood, organ meats), alcohol excess (particularly beer — xanthine oxidase-inducing), diuretics (thiazide, loop — reduce urate excretion), and underlying renal impairment.

Osteoarthritis pain: activity-related pain and stiffness — typically worse after physical activity or prolonged inactivity ('start-up stiffness' under 30 minutes on waking), improving with gentle movement; crepitus (cracking, grinding sensation on joint movement); joint enlargement from osteophytes and effusion; reduced range of motion; and bony tenderness. Advanced OA: rest pain, nocturnal pain, muscle wasting around the joint, and varus/valgus deformity (knee). No systemic features (normal inflammatory markers). Rheumatoid arthritis pain: symmetrical polyarthritis affecting small joints of the hands and feet (MCP, PIP, MTP joints) and large joints; prolonged early morning stiffness (above 1 hour — distinguishes RA from OA); joint swelling, warmth, and tenderness; fusiform (spindle-shaped) PIP joint swelling; and rheumatoid nodules (subcutaneous nodules over extensor surfaces — 20% of RF-positive patients). Systemic features: fatigue, weight loss, low-grade fever. Extra-articular manifestations: interstitial lung disease, pericarditis, vasculitis, episcleritis, Felty's syndrome. Gout: acute sudden onset (hours) of exquisite monoarticular pain — most commonly the first metatarsophalangeal joint (podagra), but also ankle, knee, wrist; joint red, hot, swollen, exquisitely tender to touch (even bedsheet contact is painful); tophi (urate deposits in cartilage, bursae, soft tissues) in chronic tophaceous gout.

Clinical assessment: detailed joint history (onset, distribution, duration of morning stiffness, triggers, pattern of joint involvement — symmetrical/asymmetrical, large/small joints), functional assessment (HAQ — Health Assessment Questionnaire), and pain scores (NRS 0-10 or VAS). Blood tests: FBC, ESR, CRP (elevated in inflammatory arthritis — RA, gout; normal in OA); rheumatoid factor (RF — positive in 70-80% of RA; also positive in other conditions — low specificity); anti-CCP antibodies (ACPA — 95% specific for RA — the most specific RA antibody; positive 10-15 years before clinical RA onset); serum uric acid (elevated in gout — but can be normal during an acute attack); ANA screen and anti-dsDNA (SLE); HLA-B27 (ankylosing spondylitis — 95% positive). X-rays: OA — joint space narrowing, osteophytes, subchondral sclerosis, cysts; RA — periarticular osteopenia, joint erosions (marginal bone destruction), and joint space narrowing. MRI: superior for early RA erosions, synovitis, bone marrow oedema, and soft tissue assessment; identifies meniscal pathology in knee OA. Ultrasound-guided aspiration: joint aspiration (arthrocentesis) and synovial fluid analysis — crystals (urate — negatively birefringent needles under polarised light for gout; calcium pyrophosphate — weakly positive birefringent rhomboidal crystals for CPPD/pseudogout), cell count (above 50,000 white cells/mL suggests septic arthritis requiring emergency treatment). Ultrasound: detects synovitis (power Doppler), erosions, and enthesitis in early RA and psoriatic arthritis.

Osteoarthritis — non-pharmacological (first-line): exercise (land and water-based — strengthens periarticular muscle, improves proprioception, reduces pain — NICE recommends as first-line regardless of OA severity); weight loss (every 1 kg lost reduces knee symptoms and progresses more slowly); physiotherapy and occupational therapy (joint protection, adaptive equipment, insoles for knee OA); pacing and self-management education; TENS (transcutaneous electrical nerve stimulation — provides temporary relief). OA pharmacological: topical NSAIDs (diclofenac gel — knee and hand OA — effective with low systemic absorption); oral NSAIDs (ibuprofen, naproxen — effective but GI, renal, and cardiovascular risks; use lowest dose for shortest duration; add PPI gastroprotection); paracetamol (limited efficacy for OA alone — 2023 evidence suggests modest benefit; used regularly not PRN); intra-articular corticosteroid injection (provides 4-8 weeks analgesia for effusive joints — do not repeat more than 3-4 times per year); intra-articular hyaluronate (Synvisc, Durolane — some evidence for knee OA; modest short-term benefit). Surgical: unicompartmental or total knee replacement (TKR), total hip replacement (THR) — highly effective for severe OA not responding to conservative management; excellent long-term outcomes (implant survival 90-95% at 15-20 years). Rheumatoid arthritis: treat-to-target approach — suppress disease activity to clinical remission (DAS28 below 2.6) or low disease activity. DMARDs: methotrexate (7.5-25 mg weekly — first-line; requires folate supplementation, liver and FBC monitoring); combination DMARDs (MTX + sulfasalazine + hydroxychloroquine); leflunomide and sulfasalazine alternatives. Biologics (for inadequate DMARD response): TNF inhibitors (etanercept, adalimumab, certolizumab — SC injection); IL-6 inhibitors (tocilizumab, sarilumab); abatacept (T-cell co-stimulation blocker); rituximab (B-cell depletion — for RA seropositive). JAK inhibitors (tofacitinib, baricitinib, upadacitinib — oral): effective, rapid-onset; cardiovascular and VTE safety monitoring required. Gout acute treatment: high-dose NSAIDs (naproxen 750mg then 500mg 8-hourly); colchicine 500 mcg 2-4 times daily; prednisolone 30-40mg for 5 days if NSAIDs contraindicated. Urate-lowering therapy (ULT — allopurinol, starting low 100mg, titrating to target serum urate below 360 µmol/L; febuxostat alternative) for patients with recurrent gout (2 or more attacks per year), tophi, or renal impairment.

Inadequately controlled arthritis causes progressive physical, psychological, and social deterioration. Joint destruction: uncontrolled inflammatory arthritis (rheumatoid arthritis, psoriatic arthritis) causes irreversible joint erosion — cartilage loss, bone erosion, and synovial joint destruction visible on X-ray — leading to deformities (swan-neck, boutonnière deformities in RA), loss of grip strength, and functional disability. Extra-articular complications of RA include rheumatoid vasculitis, interstitial lung disease (pulmonary fibrosis), pericarditis, secondary Sjögren's syndrome, and significantly increased cardiovascular disease risk (RA patients have 1.5–2 times the cardiovascular mortality of age-matched controls, driven by chronic systemic inflammation). Gout, if untreated, leads to chronic tophaceous gout — urate crystal deposits in soft tissues (tophi on the ears, Achilles tendons, and fingers), chronic tophaceous arthritis causing joint deformity, and urate nephropathy causing chronic kidney disease. Septic arthritis (bacterial joint infection) — a feared complication that can arise in the context of immunosuppressive DMARD therapy — causes rapid cartilage destruction if not diagnosed and treated within 24–48 hours. Chronic pain leads to significant psychological sequelae: depression (present in 20–30% of patients with chronic arthritis), anxiety, severe sleep disruption, and social isolation. Medications used to manage arthritis also carry their own complications: long-term NSAIDs carry GI (peptic ulcer, GI bleeding), renal, and cardiovascular risks; long-term corticosteroids cause osteoporosis, avascular necrosis, hypertension, diabetes, and adrenal suppression; biologics and DMARDs increase infection susceptibility.

Arthritis prevention and disease modification require sustained lifestyle change. Weight management: maintaining a healthy BMI (below 25 kg/m2) is the most impactful modifiable risk factor for knee OA — obesity dramatically accelerates OA progression and gout risk. Regular low-impact exercise: swimming, cycling, water aerobics, Tai Chi — maintain joint range of motion, strengthen periarticular muscles, and reduce pain without high impact loading. Joint protection: avoid activities causing significant repetitive joint loading at work (employer reasonable adjustments), use joint protection techniques (occupational therapy), and promptly treat traumatic joint injuries to prevent post-traumatic OA. Gout prevention: dietary purine reduction (limit red meat, organ meats, shellfish, and alcohol — particularly beer), increase hydration, and take prescribed urate-lowering therapy (allopurinol) regularly as prescribed — do not stop ULT during acute attacks. RA prevention: smoking cessation — smoking is the strongest modifiable risk factor for RA development and worsens disease severity and erosive progression in established RA. Early RA treatment: initiate DMARDs as soon as diagnosis is confirmed — early treat-to-target approach prevents joint damage and disability (the 'window of opportunity' — early, aggressive treatment induces sustained remission in a substantial proportion of patients).

See a GP for joint pain lasting more than 6 weeks, particularly if accompanied by swelling, warmth, or morning stiffness exceeding 30 minutes. Early rheumatology referral is essential: inflammatory arthritis symptoms (symmetrical small joint pain and swelling, prolonged morning stiffness, positive RF or anti-CCP antibodies) should be referred urgently to rheumatology within 3 weeks — delayed treatment leads to irreversible joint damage (NICE RA quality standard). Seek immediate emergency care for: a single acutely hot, swollen, extremely tender joint (especially if associated with fever) — septic arthritis (bacterial joint infection) is an orthopaedic emergency requiring same-day aspiration and IV antibiotics; delay of even 24 hours causes permanent joint destruction. Refer urgently for: rapidly progressive joint destruction, new neurological symptoms with joint disease (cervical myelopathy in RA), and systemic features (unexplained weight loss, fever, night sweats) — exclude malignancy or systemic vasculitis.