Oligoarthritis and polyarthritis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The first task is to prove inflammation. Distinguish soft synovial swelling from bony enlargement, oedema and tenderness without swelling. Map every symptomatic and asymptomatic joint, including wrists, MCP, PIP, DIP, feet and large joints. Note tendon sheaths, entheses and whole-digit swelling. A concise phenotype such as 'eight-week symmetrical MCP and PIP synovitis with sparing of DIP joints' is more useful than 'polyarthralgia'.

Tempo narrows cause. Hours to days suggests infection, crystals or viral disease; weeks suggests rheumatoid, reactive or connective-tissue disease; longstanding episodic attacks suggest palindromic or crystal disease. Add exposure, medicine and family history. In older patients, polymyalgia rheumatica causes girdle symptoms without true peripheral weakness, while RS3PE produces pitting oedema with synovitis and should prompt age-appropriate assessment for alternatives.

Investigations follow the phenotype. Baseline FBC, renal and liver tests, CRP and ESR assess inflammation and treatment safety. RF and anti-CCP are appropriate when rheumatoid arthritis is suspected; ANA and extractable antibodies require systemic clues. Urinalysis is a cheap organ screen when connective-tissue disease or vasculitis is plausible. Imaging identifies baseline damage or occult synovitis but should not delay referral.

Initial care balances urgency, diagnostic clarity and symptom control. Treat sepsis immediately, avoid indiscriminate corticosteroids before infection is excluded, and provide proportionate analgesia. Early rheumatology assessment enables prompt DMARD treatment for persistent inflammatory arthritis. Give explicit safety-netting for fever, breathlessness, chest pain, eye pain, weakness, sensory change or reduced urine output.

Key points

Oligoarthritis involves a small number of joints and polyarthritis a broader multi-joint pattern, but count swollen joints rather than relying on the patient's word 'all over'.
Define onset, duration, symmetry, small- versus large-joint distribution, axial disease, enthesitis, dactylitis and whether inflammation is additive, migratory or episodic.
Examine skin, scalp, nails, eyes, mouth, lymph nodes and relevant cardiopulmonary, abdominal and neurological systems because extra-articular findings often decide the differential.
Persistent synovitis warrants rheumatology referral even with normal CRP, negative rheumatoid factor and normal early radiographs.
A very hot single joint, bacteraemia risk or systemic toxicity cannot be explained away by an otherwise convincing polyarthritis pattern; aspirate the suspicious joint.
Use infection and travel history to select tests for parvovirus, hepatitis, HIV or sexually transmitted infection; indiscriminate viral panels create false leads.
ANA is not a screening test for nonspecific joint pain, and a positive result without compatible systemic features may not represent connective-tissue disease.
Document functional loss, work, pregnancy plans, vaccination and infection risk early because these shape treatment urgency and safe DMARD choice.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Autoimmune synovitis

Rheumatoid arthritis, psoriatic arthritis and connective-tissue diseases cause persistent immune-mediated inflammation across characteristic joint and extra-articular distributions.

Infection and post-infection inflammation

Viral infection, disseminated bacterial infection and reactive arthritis can cause acute or subacute multi-joint symptoms through direct or immune-mediated mechanisms.

Crystal, degenerative and systemic disease

Polyarticular crystal flares, nodal osteoarthritis, endocrine disease, malignancy and medicine effects can mimic a primary inflammatory rheumatic disorder.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Synovial immune activation
Activated immune cells and cytokines expand synovium, recruit inflammatory effusions and produce pain, warmth, stiffness and progressive articular injury.
2
Patterned tissue involvement
Disease-specific targeting of small joints, entheses, axial structures or periarticular tissue creates distributions that meaningfully change the diagnostic probability.
3
Systemic inflammatory effects
Persistent inflammation drives fatigue, anaemia, thrombosis and organ manifestations, while pain and inactivity accelerate weakness and cardiovascular risk.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Rheumatoid distribution

Symmetrical MCP, PIP, wrist and MTP synovitis with prolonged stiffness and reduced squeeze supports rheumatoid arthritis; DIP-predominant disease suggests another explanation.

Spondyloarthritis distribution

Asymmetric lower-limb arthritis, enthesitis, dactylitis, psoriasis, uveitis, inflammatory bowel disease or inflammatory axial pain defines a different therapeutic pathway.

Systemic autoimmune pattern

Rash, ulcers, Raynaud phenomenon, sicca, serositis, cytopenia, proteinuria, haematuria or neuropathy should trigger targeted connective-tissue and vasculitic assessment.

Infectious patternRed flag

Fever, rash, exposure, immunosuppression, endocarditis risk or one destructive joint among several painful joints raises infection and requires urgent cultures and sampling.

Non-inflammatory polyarthralgia

Diffuse tenderness without synovitis, brief stiffness and stable function may reflect osteoarthritis, hypermobility, endocrine disease or pain amplification, but warrants planned reassessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Structured joint count and full-system examinationFirst step
Why
Confirm synovitis, define distribution and find disease-defining extra-articular features.
Interpretation and limitations
Tenderness alone is nonspecific. Record swollen joints, dactylitis, entheses, skin and nail findings, axial features and organ signs that redirect urgency.
02
FBC, CRP, ESR, renal and liver profile plus urinalysis
Why
Assess inflammatory burden, cytopenia, organ involvement and a baseline for future treatment.
Interpretation and limitations
Normal markers do not exclude inflammatory arthritis. Protein, blood or casts in urine with systemic features require urgent renal and autoimmune evaluation.
03
RF and anti-CCP antibodies
Why
Refine prognosis and probability when rheumatoid arthritis is clinically suspected.
Interpretation and limitations
Anti-CCP is more specific than RF, but neither is diagnostic alone and seronegative rheumatoid arthritis remains a clinical possibility.
04
Phenotype-directed infection and autoimmune tests
Why
Test plausible viral, reactive, connective-tissue or vasculitic mechanisms rather than ordering a blanket panel.
Interpretation and limitations
Interpret every positive result using pre-test probability, titre or pattern, timing and confirmatory tests; incidental antibodies should not override examination.
05
Radiography, ultrasound or MRI
Why
Document damage, confirm uncertain synovitis and assess axial, entheseal or deep-joint disease.
Interpretation and limitations
Ultrasound can show synovial hypertrophy and Doppler activity; MRI may show occult inflammation, but neither replaces the clinical and longitudinal phenotype.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Rheumatoid arthritis

Persistent symmetrical small-joint synovitis, prolonged morning stiffness and anti-CCP antibodies support rheumatoid arthritis, although seronegative disease remains possible.

Spondyloarthritis spectrum

Psoriasis, dactylitis, enthesitis, inflammatory back pain, uveitis or inflammatory bowel disease suggests axial or peripheral spondyloarthritis.

Viral or reactive arthritis

Abrupt onset after fever, rash, hepatitis, diarrhoea or genitourinary infection supports an infectious or post-infectious process, interpreted with exposure-specific testing.

Connective-tissue or vasculitic disease

Raynaud phenomenon, photosensitive rash, ulcers, sicca symptoms, neuropathy, renal abnormalities or cytopenias require a systemic autoimmune differential.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Systemically unwellFind infection or organ threat firstFirst stepPolyarthritis with fever, shock, focal hot joint, renal change, visual symptoms, neuropathy or cardiopulmonary involvement.

1Stabilise physiology, obtain blood cultures and organ-directed tests, and aspirate any disproportionately inflamed accessible joint before antimicrobial treatment when safely possible.
2Contact the appropriate acute specialty and rheumatology; begin sepsis or organ-protection treatment according to the responsible pathway rather than awaiting a complete antibody panel.
3Trend physiology and organ function while microbiology and targeted immune tests return, revising the diagnosis when response or distribution is discordant.

02Persistent synovitisRefer before serology settles the labelObjective swelling persists or recurs across several joints without immediate instability.

1Document onset, swollen-joint distribution, morning stiffness, function and extra-articular features; request baseline bloods and rheumatoid serology when appropriate.
2Refer promptly through rheumatology even when tests are normal, and avoid delaying for radiographic erosions or repeated primary-care observation.
3Use a reviewed analgesic plan and functional support; if bridging corticosteroid is considered, exclude infection and agree dose, duration and reassessment with the treating pathway.

03No synovitis todayPreserve uncertainty and reviewSymptoms suggest episodic inflammation but examination shows no current swelling or red-flag organ feature.

1Clarify attack timing, photographs, previous records, rash, infection and medicine exposure, and examine for enthesitis, dactylitis, nodal change and hypermobility.
2Select only tests supported by the history, recognising that broad low-prevalence serology increases false positives and anxiety.
3Arrange review during a flare or after a defined interval, with urgent return advice for a hot joint, systemic illness, eye pain, weakness or renal symptoms.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Erosive joint damage

Uncontrolled synovitis can destroy cartilage and bone, rupture tendons and cause fixed deformity, disability and loss of work or independence.

Extra-articular organ injury

Inflammatory arthritis may involve eye, lung, heart, skin, kidney, nerve or bowel, with prognosis determined by more than the joint count.

Treatment and cardiovascular burden

Persistent inflammation and immobility increase cardiovascular and thrombotic risk; corticosteroids add infection and metabolic harms, while other immunosuppression can increase infection risk without structured prevention and monitoring.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record swollen and tender joints separately and use the same anatomical map at review.
Track functional tasks, stiffness duration, fatigue, weight and extra-articular symptoms alongside pain.
Follow FBC, renal, liver, urine and inflammatory-marker abnormalities to resolution or specialist handover.
Confirm urgent and routine referrals have been received and ensure the patient knows how to report deterioration.
Review analgesic, NSAID and corticosteroid exposure for gastrointestinal, renal, cardiovascular, metabolic and infection harms.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Distribution has diagnostic weight

MCP–PIP symmetry, DIP involvement, dactylitis, enthesitis and lower-limb asymmetry each shift probability more than a nonspecific positive inflammatory marker.

Arthralgia is not synovitis

Pain without objective swelling may precede disease, but labelling it arthritis creates false certainty and exposes patients to unnecessary immunosuppression.

One joint can be different

A patient with established inflammatory arthritis can still develop septic arthritis, gout or fracture in a single newly hot joint.

Urinalysis changes urgency

Microscopic blood and protein with systemic inflammatory features can reveal organ-threatening immune disease before creatinine rises substantially.

Steroids alter the evidence

Empirical corticosteroids may rapidly improve several disorders while masking infection and reducing later diagnostic signs, so use a defined, reviewed indication.

11Common pitfallsFrequent interpretation and management errors.

01
Counting painful regions rather than objectively swollen joints.
02
Delaying rheumatology referral until RF, anti-CCP or radiographs become positive.
03
Calling a positive ANA the cause of joint pain without compatible systemic features.
04
Failing to aspirate one unusually hot joint because the patient already has a rheumatic diagnosis.
05
Ignoring pregnancy plans, vaccination and latent infection risk until after immunosuppression is proposed.