- Accumulation of precipitated crystals in and around joint spaces causing acute or chronic symptoms
- Monosodium urate crystals (gout) most common; others include calcium pyrophosphate dihydrate (CPPD-pseudogout), basic calcium phosphate (BCP) crystals (calcium hydroxyapatite and calcium oxalate); lipid and immunoglobulin crystals (rare)
- Intra-articular crystals initiate an immune response and neutrophil phagocytosis with the subsequent release inflammatory factors.
- Joint aspiration is the gold-standard for diagnosis.
- Uncontrolled disease may lead to chronic joint changes and disability.
- Most treatments are aimed at decreasing crystal-induced inflammation.
- Gout: 4% of U.S. adults >20 years with lifetime incidence of gout, men > women (1)
- CPPD (pseudogout), hydroxyapatite, and calcium oxalate, men = women (2)
- Highest prevalence of gout is 7% in men >65 years (3).
- Prevalence of other crystal arthropathies not well defined
Etiology and Pathophysiology
- High levels of crystal-forming molecules precipitate in synovium and synovial fluid.
- Inflammatory response is initiated, attracting neutrophils to the synovial tissues.
- Subsequent phagocytosis of crystals releases cascade of additional inflammatory factors (IL-1β).
- Gout: hyperuricemia prerequisite to monosodium urate crystal formation
- CPPD: excessive local production of extracellular inorganic pyrophosphate from chondrocytes
- BCP/hydroxyapatite: normal part of bone metabolism, crystallization seen in associated tissue damage associated with elderly joints
- Calcium oxalate: crystallization in patients with hyperoxalemia or end-stage renal disease
- Genetics play a role in hyperuricemia and familial CPPD disease.
- Clinical application of genetic studies limited
- Age >40 years (gout); age >60 years (CPPD)
- Dehydration, alcohol consumption, obesity (gout)
- Chronic renal disease
- Underlying arthritic disease, joint trauma
- Parathyroid disease
- Calcium, phosphorus, or magnesium derangements
Commonly Associated Conditions
- CPPD (also called chondrocalcinosis)
- Mostly idiopathic
- Hereditary CPPD
- Tissue damage
- Parathyroid, calcium, or phosphorus disorders
- Calcium oxalate
- Excessive ascorbic acid intake
- Renal failure
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