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Health condition · Clinically reviewed

Calcium crystal diseases, pseudogout, basic calcium phosphate and the rarer causes.

Not gout, not always osteoarthritis. A family of crystal arthropathies with distinctive tests, a clear treatment ladder and often a treatable underlying cause.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against EULAR, BSR and peer-reviewed rheumatology sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK practice on CPPD, basic calcium phosphate disease and rarer crystal arthropathies.

Key facts

Calcium crystal diseases at a glance.

The essentials, in plain English - the main crystal types, the classic sites and how they are diagnosed and treated in the UK today.

  • What it is

    A family of non-urate crystal arthropathies driven by calcium-containing crystals depositing in cartilage, tendon or joint fluid.

  • CPPD (pseudogout)

    Calcium pyrophosphate dihydrate crystals cause chondrocalcinosis on X-ray and can trigger acute pseudogout attacks.

  • Basic calcium phosphate

    Hydroxyapatite drives calcific tendinitis, acute periarthritis and Milwaukee shoulder syndrome.

  • Rarer causes

    Oxalate arthritis (primary or secondary), cholesterol crystal effusions and calcium carbonate deposition all exist.

  • Key test

    Synovial fluid aspiration and polarised microscopy remain the gold standard, alongside plain X-ray and ultrasound.

  • Treatable

    Acute attacks settle with NSAIDs, colchicine or steroid; chronic disease responds to prophylaxis and treating the underlying cause.

Why this guide matters

The three ideas that shape the plan.

Calcium crystal diseases are common, often missed and frequently mislabelled. The three points below shape everything else on this page.

  • Aspiration remains the gold standard

    Synovial fluid microscopy under polarised light is what separates CPPD from gout, and both from sepsis.

  • Find and fix the driver

    Haemochromatosis, hyperparathyroidism, low magnesium, Wilson disease and hypophosphatasia can all be treated.

  • Attacks respond to a familiar ladder

    NSAIDs, colchicine and intra-articular steroid handle most acute pseudogout and BCP attacks safely.

How the diagnosis is made

From hot joint to a clear plan.

The steps a UK GP, rheumatologist or emergency clinician will normally follow, in order - so you know what to expect and why.

  1. 01

    Assessing

    History and joint pattern

    Sudden monoarticular pain in knee, wrist or shoulder points to pseudogout; chronic large-joint pain with rapid destruction suggests Milwaukee shoulder.

  2. 02

    Assessing

    Examination

    Hot, swollen, tender joint with reduced range of movement. Look for signs of underlying metabolic disease such as haemochromatosis or hyperparathyroidism.

  3. 03

    Assessing

    Rule out sepsis

    A hot joint is septic arthritis until proven otherwise. Aspirate early and send fluid for urgent Gram stain, culture and cell count.

  4. 04

    Confirming

    Synovial fluid microscopy

    Polarised light reveals positively birefringent rhomboid CPPD crystals or negatively birefringent needle-shaped urate. BCP needs alizarin red stain or electron microscopy.

  5. 05

    Confirming

    Imaging

    X-ray for chondrocalcinosis in menisci, triangular fibrocartilage of the wrist and hyaline cartilage. Ultrasound may show hyperechoic deposits within cartilage.

  6. 06

    Preparing

    Metabolic bloods

    Calcium, phosphate, PTH, magnesium, ferritin and iron studies, urate, ALP, inflammatory markers and a rheumatology screen to look for a treatable driver.

  7. 07

    Preparing

    Specialist referral

    Refractory, destructive or unusual disease warrants rheumatology and, where relevant, orthopaedic or metabolic bone input.

Typical timeline: an acute attack settled within days, with a clearer chronic plan over the next few weeks.

Symptoms

What calcium crystal disease actually looks like.

From an out-of-the-blue hot knee to a slowly failing shoulder - the patterns to recognise and the features that mean it is time to escalate.

  • Acute pseudogout attack

    Sudden monoarticular pain, swelling and a hot joint, often in the knee or wrist. Mimics gout and septic arthritis.

  • Chronic pyrophosphate arthropathy

    Pseudo-OA with grumbling knee, wrist or MCP pain and radiographic chondrocalcinosis.

  • Pseudo-RA and pseudo-neuropathic

    A polyarticular inflammatory pattern or rapidly destructive joint change can mimic rheumatoid or Charcot arthritis.

  • Calcific tendinitis

    Basic calcium phosphate deposits in tendon, most often the supraspinatus, causing sudden severe shoulder pain.

  • Milwaukee shoulder syndrome

    Destructive rotator cuff arthropathy in elderly women with a haemorrhagic effusion and rapid glenohumeral destruction.

  • Acute periarthritis

    Painful, hot periarticular inflammation from BCP deposition, often around the shoulder, hip or finger joints.

  • Oxalate arthritis

    Envelope-shaped bipyramidal crystals in primary hyperoxaluria or dialysis patients, causing chronic joint pain and effusion.

  • Red flag - hot joint

    Any single hot, swollen joint needs urgent aspiration to exclude septic arthritis before assuming a crystal cause.

Treatment

How calcium crystal diseases are treated in the UK.

Settle the attack, prevent the next one and treat the underlying driver. For destructive disease, orthopaedics joins the plan.

  • NSAIDs

    First-line for acute pseudogout and calcific tendinitis where kidney function, GI risk and cardiac risk allow.

  • Colchicine

    500 microgram once or twice daily for acute attacks and for prophylaxis in recurrent CPPD, adjusted for renal function.

  • Intra-articular steroid

    Rapid relief in a single inflamed joint once sepsis is excluded, ideally under ultrasound guidance in larger joints.

  • Oral or IM steroid

    A short course for polyarticular flares or where NSAIDs and colchicine are contraindicated.

  • Hydroxychloroquine or methotrexate

    Steroid-sparing options for chronic inflammatory CPPD and pseudo-RA presentations.

  • IL-1 or IL-6 inhibitors

    Anakinra, canakinumab and emerging tocilizumab data for refractory CPPD, used under specialist rheumatology guidance.

  • Barbotage and shockwave

    Ultrasound-guided needling and extracorporeal shockwave therapy for symptomatic calcific tendinitis alongside physiotherapy.

  • Joint replacement

    Total hip or knee replacement for advanced destructive arthropathy that no longer responds to medical care.

The pathway

A stepped approach - from acute attack to long-term control.

  1. Step 1

    Exclude sepsis by aspiration, then treat the acute attack with NSAIDs, colchicine or intra-articular steroid.

  2. Step 2

    Screen for and treat the driver - haemochromatosis, hyperparathyroidism, low magnesium, Wilson or hypophosphatasia.

  3. Step 3

    Prophylactic colchicine 500 microgram once or twice daily for recurrent CPPD attacks.

  4. Step 4

    Steroid-sparing options - hydroxychloroquine or methotrexate for chronic inflammatory disease.

  5. Step 5

    IL-1 inhibitors anakinra or canakinumab for refractory CPPD - specialist-led and evidence still emerging.

  6. Step 6

    Barbotage, shockwave and physiotherapy for calcific tendinitis; joint replacement for advanced destructive arthropathy.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and specialist rheumatology society standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP or rheumatologist knows your joints, imaging and bloods and can tell you which parts apply to you. If in doubt, get seen.

  • EULAR. Recommendations for calcium pyrophosphate deposition (CPPD) - diagnosis and management.

  • ACR/EULAR 2023 classification criteria for CPPD.

  • British Society for Rheumatology (BSR). Guidance on crystal arthropathies.

  • NICE CKS. Gout and pseudogout.

  • Rheumatology reviews on basic calcium phosphate disease and Milwaukee shoulder syndrome.

Red flags

When calcium crystal disease needs urgent attention.

Most crystal arthritis is manageable in primary care and rheumatology clinics. These are the situations that need same-day or same-week specialist input.

  • Hot single joint

    Assume septic arthritis until aspiration and cultures exclude it, even when crystals are eventually found.

  • Rapidly destructive shoulder

    Milwaukee shoulder syndrome in an older woman with a haemorrhagic effusion needs urgent orthopaedic and rheumatology input.

  • Systemic features

    Fever, rigors, sweats or weight loss alongside joint disease demand a sepsis and malignancy work-up before labelling as crystal disease.

  • Young patient with CPPD

    CPPD under 55 warrants screening for haemochromatosis, hyperparathyroidism, hypomagnesaemia, hypophosphatasia, Wilson disease and familial CPPD.

  • Renal impairment on colchicine

    Colchicine accumulates in kidney disease and interacts with clarithromycin and statins; dose reduce and check for red-flag myopathy.

  • Steroid injection into a septic joint

    Never inject a joint you have not aspirated first when infection is possible - it can seed catastrophic sepsis.

  • Oxalate crystals on aspiration

    Consider ethylene glycol poisoning, primary hyperoxaluria, short bowel syndrome or advanced renal failure and refer urgently.

  • Neurological features with Wilson

    Younger CPPD with tremor, dysarthria or liver disease should trigger caeruloplasmin testing and hepatology referral.

  • Post-parathyroidectomy flare

    Acute pseudogout is well described after parathyroid surgery - warn patients and have a rescue plan.

Living with it

A treatable condition, with a clear ladder.

Four things that make the biggest difference day to day - early relief, prevention where attacks recur, treating the driver and protecting joint function.

A quiet reminder

A hot joint deserves a fresh look, not just a repeat script.

If pain patterns change, joints start to fail or attacks become more frequent, ask for a rheumatology review rather than pushing on.

  1. 01 Pacing

    Rest, ice and early relief

    Ice, rest and starting an anti-inflammatory promptly shortens most acute pseudogout attacks and calcific tendinitis flares.

  2. 02 Prevent

    Low-dose colchicine as prophylaxis

    500 microgram once or twice daily can prevent recurrent CPPD attacks when the joints keep flaring.

  3. 03 Treat cause

    Fix what is driving it

    Venesection for haemochromatosis, parathyroidectomy for hyperparathyroidism and magnesium replacement can quieten CPPD.

  4. 04 Move

    Physiotherapy protects joints

    Guided rehabilitation after a calcific tendinitis flare or a Milwaukee shoulder episode preserves function and reduces relapse.

Frequently asked

Everything we get asked about calcium crystal diseases.

Quick answers on pseudogout, Milwaukee shoulder, the underlying metabolic causes and modern treatment options.

  • What are calcium crystal diseases?

    A family of non-urate crystal arthropathies caused by calcium-containing crystals depositing in cartilage, tendon or joint fluid. The main forms are calcium pyrophosphate dihydrate (CPPD or pseudogout) disease, basic calcium phosphate (hydroxyapatite) disease, oxalate arthritis, cholesterol crystal effusions and calcium carbonate deposition.

  • How is pseudogout diagnosed?

    Joint aspiration and polarised light microscopy show positively birefringent rhomboid CPPD crystals. X-rays often show chondrocalcinosis in the menisci, triangular fibrocartilage of the wrist or hyaline cartilage, and ultrasound may show hyperechoic deposits within cartilage. Septic arthritis must be excluded first with Gram stain, cell count and culture.

  • How does pseudogout differ from gout?

    Both cause sudden hot swollen joints, but the crystals differ. Gout produces negatively birefringent needle-shaped monosodium urate crystals and often affects the big toe. Pseudogout produces positively birefringent rhomboid CPPD crystals and more often affects the knee, wrist or shoulder in older adults.

  • What is Milwaukee shoulder syndrome?

    A destructive shoulder arthropathy driven by basic calcium phosphate crystals, seen mainly in elderly women. There is rotator cuff failure, a large often haemorrhagic effusion and rapid glenohumeral joint destruction. Management combines symptom control, physiotherapy and consideration of shoulder surgery.

  • What conditions make CPPD more likely?

    Ageing and osteoarthritis are the strongest associations. Others include haemochromatosis, primary hyperparathyroidism, hypomagnesaemia, hypophosphatasia, Wilson disease and familial CPPD. Young patients with CPPD should be screened for these treatable drivers.

  • How is refractory CPPD treated?

    When NSAIDs, colchicine and steroids are not enough, options include hydroxychloroquine, methotrexate and IL-1 blockade with anakinra or canakinumab. Emerging evidence supports tocilizumab in selected refractory cases. These decisions are made in specialist rheumatology clinics.

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