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Chondrocalcinosis

Deposition of calcium pyrophosphate dihydrate crystals in joint tissue causes acute and chronic inflammatory joint disease. The acute form is called Pseudo-gout.

Aetiology

  • Hereditary (Autosomal dominant)
  • Idiopathic
  • Associated with various metabolic disorders

Incidence

  • Affects males and females equally
  • Usually more than 50 years
  • Increased incidence with increased age
  • 3 - 5% of population have CPPD deposition in the knee at autopsy
  • Seen in 40% of patients with haemochromatosis or hyperparathyroidism

Clinically

  • Presents with acute gout-like episode in about 30%
  • Attack develops over 12 - 36 hours and persists for 1 - 2 weeks
  • 5% have pseudo-rheumatoid appearance
  • 50% goon to chronic disease with progressive joint degeneration (ordinary degenerative osteoarthritis or degenerative spondylosis)
  • The remainder remain asymptomatic
  • Knee is usual site (accounts for ~ 50%), but other larger joints may be affected
  • Inflammation of one or more joints, lasting several days and usually less severe than gout.
  • May present in association with true gout
  • Seldom affects the great toe
  • Diagnosis confirmed by positively birefringent crystals in synovial fluid (Gout negative)
  • Chronic chondrocalcinosis is usually asymptomatic, but may lead to poly-articular osteoarthritis
  • X-Rays:
    • Calcification of articular cartilage and fibro-cartilaginous structures (menisci, TFCC, symphysis pubis, intervertebral discs)
    • Punctate, or linear densities in articular hyaline cartilage or fibro-cartilage
    • Fine calcified line separate from the subchondral plate in hyaline cartilage
    • In fibro-cartilage, thick irregular densities 
    • Tendon calcifications are linear and indicate development of degenerative changes

Investigations

  • Synovial fluid is inflammatory with 50 - 500 cells /mm³ (degenerative arthritis is usually non inflammatory)
  • Need to exclude associated diseases
    • Gout
    • Hyperuricaemia
    • Diabetes mellitis
    • Haemochromatosis
    • Ochronosis
    • Hyperparathyroidism
    • Wilsons disease
    • Acromegaly
    • Hyperphosphatasia
    • Hypothyroidism
    • Degenerative joint disease

Pathology

  • Initial site of crystal formation is believed to be in the articular cartilage around chondrocytes, which are then extruded into the joint and cause inflammatory reaction
  • Commoner in aged and abnormal cartilage, therefore often associated with other arthritidies
  • Cause of crystal shedding believed to be a sudden change in the ionic calcium and pyrophosphate equilibrium in cartilage, e.g. acute injury, illness, operation or inflammatory arthritis
  • Often precedes and assumed to predispose to the development of OA
  • About 1/3 associated with intervertebral disc calcification
  • CPPD crystals are short blunt rods, which are weakly birefringent under compensated polarised light in contrast to the strongly negative birefringence of urate crystals

Differential Diagnosis

  • Hyperparathyroidism : hypercalcaemia and subperiosteal erosion's
  • Haemochromatosis : degenerative, progressive arthritis of finger joints with calcification in multiple joints on X-Ray and associated with intervertebral disc calcification
  • Ochronosis (IBEM; due to absence of homogentisic acid oxidase) : presents around the 4th decade with pain and stiffness of large joints and the spine, intervertebral disc calcification and ankylosis
  • Homogentisic acid in urine : turns black when left standing

Treatment

  • Rest
  • Anti-inflammatory therapy (NSAIDs, corticosteroid injection)
  • Chronic chondrocalcinosis appears to be irreversible
  • Treatment for secondary OA

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