Joint Pain (Arthralgia) — Causes, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Joint pain (arthralgia — from Greek arthron, joint, and algos, pain) refers to discomfort, aching, or soreness within a joint, with or without associated inflammation. It is one of the most prevalent symptoms in primary care, affecting people of all ages, and can involve any synovial joint in the body. Joint pain may arise from the joint itself — cartilage, synovium, subchondral bone, capsule, or ligaments — or may be referred from adjacent structures. The most common causes worldwide are osteoarthritis (the leading cause in adults over 50), rheumatoid arthritis, gout, and post-viral arthralgia. However, joint pain is a symptom of over 100 conditions spanning degenerative, inflammatory, crystalline, infective, metabolic, and neoplastic disorders. The clinical distinction between arthralgia (pain only) and arthritis (pain with objective signs of inflammation — swelling, warmth, restricted movement, erythema) is critical: arthritis implies active joint inflammation requiring specific investigation and treatment, while arthralgia may be mechanical or systemic. The number of joints affected (monoarthritis — one joint; oligoarthritis — 2-4 joints; polyarthritis — five or more joints) and the pattern of involvement are key diagnostic clues. Osteoarthritis alone affects approximately 300 million people globally (WHO 2023) and is the leading cause of disability in older adults. Timely identification of the underlying cause is essential — some causes, such as septic arthritis or crystal arthropathy, require urgent intervention, while most inflammatory arthropathies benefit significantly from early disease-modifying treatment.

Degenerative: osteoarthritis (OA) — the most common cause in adults over 45; characterised by progressive articular cartilage degradation, subchondral bone sclerosis, osteophyte formation, and synovial inflammation; risk factors include age, obesity (each additional kg above ideal body weight increases knee OA risk by 5-fold), previous joint injury, occupational loading, female sex (especially after menopause), and genetic predisposition. Inflammatory arthritis: rheumatoid arthritis (RA) — autoimmune synovitis (synovial membrane inflammation), symmetric, affecting small joints of hands and feet first; driven by anti-citrullinated protein antibodies (ACPA/anti-CCP — 70% sensitivity, 97% specificity) and rheumatoid factor (RF); progressive joint destruction without DMARD therapy. Psoriatic arthritis (PsA) — 20-30% of psoriasis patients; spondylarthritis pattern with dactylitis (sausage digit), enthesitis (heel pain), and sacroiliitis. Ankylosing spondylitis — axial spondylarthritis (HLA-B27 positive in 90%); predominant sacroiliac and spinal joint involvement. Crystal arthropathy: gout (monosodium urate crystals) — attacks of acute severe joint pain, typically the first metatarsophalangeal joint (podagra), knee, or ankle; triggered by hyperuricaemia, alcohol, purines, dehydration, diuretics; pseudogout (calcium pyrophosphate crystals — CPPD) — predilection for wrist and knee. Infective: septic arthritis (bacterial joint infection — Staphylococcus aureus most common; Neisseria gonorrhoeae in sexually active young adults) — medical emergency; reactive arthritis (post-infective — Chlamydia, Salmonella, Yersinia, Campylobacter, and Shigella); viral arthralgia (parvovirus B19, Ross River virus, chikungunya, COVID-19). Systemic: systemic lupus erythematosus (SLE), sarcoidosis, lyme disease, haemochromatosis, hypothyroidism, hypermobility spectrum disorder (Ehlers-Danlos syndrome).

Joint pain characteristics: location (specific joint or diffuse), quality (aching, sharp, burning, throbbing), severity (VAS score 0-10), timing (constant or episodic, nocturnal or activity-related), aggravating and relieving factors, pattern of onset (sudden — gout or septic arthritis; gradual — OA or RA), and morning stiffness duration (below 30 minutes — OA; above 60 minutes — inflammatory arthritis). Osteoarthritis: pain is activity-related, relieved by rest; minimal or no morning stiffness (below 30 minutes); bony swelling, crepitus, restricted range of motion, deformity (varus deformity in medial compartment knee OA; Heberden's nodes at DIP joints, Bouchard's nodes at PIP joints in hand OA). Rheumatoid arthritis: symmetric small joint polyarthritis (MCPs, PIPs, wrists, MTPs); significant morning stiffness above 60-90 minutes; soft tissue swelling, boggy synovium; fatigue, weight loss, low-grade fever; later: ulnar deviation, swan-neck deformity, boutonniere deformity, rheumatoid nodules. Gout: acute monoarthritis with exquisite tenderness (bedsheet intolerance), erythema, warmth, and swelling; resolution over 7-14 days without treatment; chronic tophaceous gout — monosodium urate deposits (tophi) in soft tissue (ear helix, Achilles tendon, bursa). Septic arthritis: acute monoarthritis with fever, rigors, severe pain, extreme tenderness, inability to move the joint — medical emergency.

History and physical examination: pattern of joint involvement, inflammatory vs. mechanical features, duration, associated systemic features (rash, eye involvement, GI symptoms, urethritis), family history, medications (diuretics worsen gout), and occupation. Blood tests: full blood count (anaemia of chronic disease in RA; leucocytosis in septic arthritis and gout); CRP and ESR (elevated in inflammatory arthritis and infection — typically normal or minimally raised in OA); rheumatoid factor (RF — present in 70% of RA but also in other conditions); anti-CCP antibodies (highly specific for RA — 97% specificity); uric acid (elevated above 360 micromol/L confirms hyperuricaemia — supports gout, though gout can occur with normal urate during acute attack); ANA (screening for SLE; anti-dsDNA for specificity); HLA-B27 (ankylosing spondylitis — positive in 90%); Lyme serology (ELISA then Western blot in endemic areas). Imaging: X-ray (joint space narrowing, osteophytes, subchondral sclerosis in OA; periarticular erosions and osteoporosis in RA; chondrocalcinosis in CPPD); MRI (most sensitive for early synovitis, bone marrow oedema, cartilage and ligament integrity, sacroiliitis — excellent for assessing RA and spondylarthritis activity); ultrasound (synovitis, effusion, enthesitis — Doppler mode shows increased vascularity in active synovitis; guides joint aspiration and injection). Joint aspiration (arthrocentesis): synovial fluid analysis — cell count (WBC above 50,000/mm3 — septic arthritis; 2000-75,000 — inflammatory; below 2000 — non-inflammatory), microscopy (gram stain and culture for infection; polarised light microscopy for crystals — negatively birefringent needle-shaped urate crystals in gout; positively birefringent rhomboid-shaped calcium pyrophosphate crystals in pseudogout).

Treatment is entirely directed by the underlying cause. Osteoarthritis: non-pharmacological (core treatment): aerobic exercise and strength training (the most evidence-based intervention — reduces pain and improves function more than analgesics alone; NICE-endorsed); weight loss (5-10% weight reduction in obese OA patients reduces knee pain by 50%; each kg of weight loss reduces knee joint load by 4 kg); physiotherapy (quadriceps strengthening, gait assessment, aids); patient education. Pharmacological: paracetamol 1 g four times daily (limited evidence in OA but widely used); topical NSAIDs (diclofenac 1% gel — first-line for knee OA; fewer systemic side effects); oral NSAIDs (ibuprofen, naproxen, diclofenac — effective for pain and function but GI, renal, and cardiovascular risks limit use in older patients; co-prescribe a PPI); intra-articular corticosteroid injections (triamcinolone or methylprednisolone — rapid but temporary relief, typically 4-12 weeks; not more than 3-4 times per year); intra-articular hyaluronic acid (viscosupplementation — modest benefit). Surgery: partial or total joint replacement (arthroplasty — knee and hip TJR are among the most cost-effective procedures in medicine; 95% 10-year implant survival). Rheumatoid arthritis: early DMARD initiation is critical — treat-to-target strategy (DAS28 remission target); methotrexate (MTX) 7.5-25 mg weekly (first-line DMARD — folic acid 5 mg weekly to reduce toxicity); add hydroxychloroquine, sulfasalazine for triple therapy; biologic DMARDs (anti-TNF: adalimumab, etanercept; anti-IL-6: tocilizumab, sarilumab; anti-CD20: rituximab; JAK inhibitors: baricitinib, upadacitinib — for inadequate response to MTX). Gout: acute attack: colchicine 500 mcg two-three times daily (first-line — inhibits neutrophil phagocytosis) or NSAIDs; corticosteroids for those unable to tolerate both. Long-term urate-lowering therapy: allopurinol (100-300 mg/day — titrated to target serum urate below 360 micromol/L, below 300 in tophaceous gout); febuxostat for allopurinol-intolerant patients. Septic arthritis: inpatient emergency treatment — IV antibiotics (flucloxacillin 2 g four times daily or vancomycin; adjust based on cultures) and urgent surgical joint washout — delay causes permanent joint destruction.

Untreated or inadequately managed joint pain leads to significant complications depending on the underlying cause. Osteoarthritis: progressive joint space narrowing and destruction leading to severe functional limitation, inability to walk stairs or perform daily activities, and requirement for joint replacement surgery; loss of independence in elderly patients. Rheumatoid arthritis: if untreated, progressive joint destruction and deformity within 2 years; extra-articular complications including rheumatoid nodules, interstitial lung disease (ILD — 10-20% of RA patients), pericarditis, peripheral neuropathy, Felty's syndrome (splenomegaly and neutropenia), and a 1.5-2-fold increased cardiovascular risk. Gout: chronic tophaceous gout — urate tophi depositing in soft tissues, tendons, and bursa causing chronic pain, deformity, and tendon rupture; urate nephropathy and nephrolithiasis (uric acid kidney stones) impairing renal function; cardiovascular disease risk associated with hyperuricaemia. Septic arthritis: without prompt treatment (within 6-12 hours of presentation), permanent cartilage destruction, joint stiffness (ankylosis), and osteomyelitis develop in over 50% of untreated cases; haematogenous spread causing septicaemia and multi-organ failure. Inflammatory arthritis: disability, loss of employment, depression (30-50% prevalence in chronic inflammatory arthritis), and reduced life expectancy if cardiovascular and other systemic complications are not managed.

Maintaining a healthy body weight is the most impactful preventable measure for osteoarthritis — obesity is the strongest modifiable risk factor for knee and hip OA; each kg of weight reduction decreases knee joint loading by 4 kg. Regular low-impact aerobic exercise (swimming, cycling, walking) maintains joint health, cartilage nutrition, and periarticular muscle strength without excessive joint loading — NICE recommends exercise as core OA treatment regardless of age or comorbidities. Avoid repetitive joint overloading in occupation or sport — use ergonomic equipment, joint protection techniques, and appropriate footwear. For gout prevention: maintain serum urate below 360 micromol/L with allopurinol or febuxostat; reduce dietary purines (red meat, organ meats, shellfish, beer) and alcohol (especially beer and spirits); stay well hydrated (2-3 litres daily — reduces urate crystallisation); avoid diuretics and low-dose aspirin where possible (both raise serum urate); and achieve a healthy weight (obesity raises serum urate through increased urate production and reduced excretion). For rheumatoid arthritis and other inflammatory arthropathies: early DMARD initiation (within 3 months of symptom onset) significantly reduces long-term joint damage and disability — the 'window of opportunity' concept underpins the NICE recommendation for urgent rheumatology referral (within 3 weeks) for suspected inflammatory arthritis. Annual cardiovascular risk assessment for all inflammatory arthritis patients — cardiovascular disease is the leading cause of excess mortality in RA.

Seek emergency care immediately for: acute severe joint pain with fever, rigors, marked swelling, and inability to move the joint — possible septic arthritis (joint infection), which is a medical emergency requiring same-day joint aspiration, IV antibiotics, and surgical washout within hours to prevent permanent joint destruction. This is particularly urgent in patients with prosthetic joints (prosthetic joint infection requires emergency specialist review). See a GP urgently (within 24-48 hours) for: any single hot, swollen, extremely tender joint (red joint) — to exclude septic arthritis and gout requiring urgent aspiration and treatment; acute joint pain in a person taking immunosuppressant medications (steroids, biologics, chemotherapy) — septic arthritis risk is significantly elevated. See a GP within 1-2 weeks for: new joint pain persisting beyond 2 weeks; morning stiffness lasting over 30 minutes with joint swelling (possible inflammatory arthritis — early DMARD therapy significantly improves outcomes); joint pain with a rash (possible SLE, psoriatic arthritis, or viral arthritis); or joint pain with eye inflammation (uveitis — associated with spondylarthritis and JIA). Request urgent rheumatology referral (within 3 weeks — NICE guidance) for suspected early inflammatory arthritis with morning stiffness, symmetric small joint involvement, and raised inflammatory markers — delay in diagnosis and DMARD treatment leads to irreversible joint erosion.