Calcium Pyrophosphate Deposition Disease (CPPD) (Pseudogout)

EULAR recommendations for calcium pyrophosphate deposition. Part II: Management. Published: 2011.

Article Last Updated:12/07/2026

Pseudogout

Note on terminology:

Calcium pyrophosphate deposition disease (CPPD) is the umbrella term for the condition where calcium pyrophosphate crystals form and deposit in joint tissues
Chondrocalcinosis refers to the physical finding of calcium pyrophosphate crystals in the hyaline or fibrocartilage (on X-ray)
Pseudogout refers to acute CPPD

Causes and Risk Factors

CPPD is characterised by the deposition of calcium pyrophosphate crystals within the joint, which then triggers an inflammatory immune response

Risk factors: ^[Ref]

Genetic factors (e.g. mutations in ANKH and ENPP1 genes)
Advanced age (30-50% of patients are >85 y/o)
Pre-existing osteoarthritis
Metabolic and endocrine conditions
- Hypomagnesaemia
- Hyperparathyroidism
- Haemochromatosis

Clinical Features

There are 2 main clinical subtypes of CPPD: ^[Ref]

Clinical subtype	Clinical features
Acute CPPD (pseudogout)	Possible triggers include physical trauma and surgical procedures Sudden onset of acute monoarticular / oligoarticular arthritis: Severe hot, red, swollen joint pain – mimicking a gout attack The severe joint pain can temporarily restrict movement and limit daily activities Involved joint Knee – most common It also frequently affects the wrists and hips Attacks are generally self-limiting, lasting 7-10 days
Chronic CPPD (pseudo-rheumatoid arthritis)	Presents as chronic, symmetrical, and deforming polyarthritis Patient may present with persistent joint inflammation or recurrent acute flares that mimic rheumatoid arthritis Most commonly involves the wrists and metacarpal joints Tenosynovitis is common and can lead to carpal tunnel syndrome or cubital tunnel syndrome

Clinical subtype

Clinical features

Acute CPPD (pseudogout)

Possible triggers include physical trauma and surgical procedures

Sudden onset of acute monoarticular / oligoarticular arthritis:

Severe hot, red, swollen joint pain – mimicking a gout attack
The severe joint pain can temporarily restrict movement and limit daily activities
Involved joint
- Knee – most common
- It also frequently affects the wrists and hips

Attacks are generally self-limiting, lasting 7-10 days

Chronic CPPD (pseudo-rheumatoid arthritis)

Presents as chronic, symmetrical, and deforming polyarthritis

Patient may present with persistent joint inflammation or recurrent acute flares that mimic rheumatoid arthritis
Most commonly involves the wrists and metacarpal joints
Tenosynovitis is common and can lead to carpal tunnel syndrome or cubital tunnel syndrome

Investigation and Diagnosis

^[Ref]

Imaging

1st line: X-ray

Typical finding: chondrocalcinosis
- A thin, linear or punctate calcification within cartilage, often seen parallel to the articular surface
- In the knee: calcification of the menisci or within the articular cartilage
- In the wrist: calcification of the triangular fibrocartilage complex
However, X-rays only have a ~40% sensitivity for detecting clinically significant CPPD

Synovial fluid analysis

Joint aspiration for synovial fluid analysis is the gold standard test

Appearance: cloudy, yellow
Viscosity: reduced
WBC count and differential: 2,000 – 50,000 cells/µL with polymorph (neutrophil) predominance
Microscopy: rhomboid-shaped calcium pyrophosphate crystals with weak positive birefringence
Gram stain / culture: -ve
Glucose: normal

Synovial fluid microscopy in crystal arthropathy

Gout (monosodium urate crystals): needle-shaped crystals with negative birefringence
Pseudogout (calcium pyrophosphate crystals): rhomboid-shaped with positive birefringence (pseudogout = positive)

Blood tests

Since CPPD can be triggered by underlying metabolic conditions, a metabolic panel is recommended:

Calcium, magnesium and phosphate levels
Iron studies (to screen for haemochromatosis – esp. in younger patients)
TSH and PTH levels
Serum urate levels (to exclude gout)

Management

There are currently no approved disease-modifying therapies to stop or reverse the deposition of calcium pyrophosphate crystals.

Clinical subtype	Management
Acute CPPD (pseudogout)	Initial management: local treatment (esp. for monoarticular or oligoarticular attacks) Apply ice Rest the joint Joint aspiration + intra-articular corticosteroid injection Local treatment is typically sufficient to resolve the flare. If ineffective, consider systemic treatment: 1st line: oral NSAIDs or low-dose colchicine 2nd line: corticosteroids (oral / IM / IV) or ACTH injection
Chronic CPPD	1st line: oral NSAIDs and/or low-dose colchicine 2nd line: low-dose oral corticosteroids 3rd line: methotrexate 4th line: hydroxychloroquine

Clinical subtype

Management

Acute CPPD (pseudogout)

Initial management: local treatment (esp. for monoarticular or oligoarticular attacks)

Apply ice
Rest the joint
Joint aspiration + intra-articular corticosteroid injection

Local treatment is typically sufficient to resolve the flare. If ineffective, consider systemic treatment:

1st line: oral NSAIDs or low-dose colchicine
2nd line: corticosteroids (oral / IM / IV) or ACTH injection

Chronic CPPD

1st line: oral NSAIDs and/or low-dose colchicine
2nd line: low-dose oral corticosteroids
3rd line: methotrexate
4th line: hydroxychloroquine

References

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Calcium Pyrophosphate Deposition Disease (CPPD) (Pseudogout)

Pseudogout

Causes and Risk Factors

Clinical Features

Investigation and Diagnosis

Management

References

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