Prognosis

Pseudogout is an inflammatory arthropathy, with acute and chronic forms, caused by the deposition of calcium pyrophosphate dihydrate (CPPD) crystals in synovial structures. Chondrocalcinosis (calcified cartilage seen on radiographs), found in the majority of pseudogout patients, was first recognized in 1957 by Zitnan and Sitaj. McCarty in 1962 defined the relationship of intrasynovial CPPD crystals to chondrocalcinosis. The prevalence of pseudogout is not known. However, 8% of all people older than 60 years have radiographic evidence of chondrocalcinosis. The prevalence of chondrocalcinosis increases with age to involve as many as 28% of the population in the ninth decade. The mode of inheritance of CPPD is unsettled. However, an autosomal dominant pattern has been described in some populations in which disease begins in early adulthood, progresses rapidly, and is polyarticular.

I. Pathogenesis. Aging, osteoarthritis, genetic defects, and certain metabolic disorders are thought to induce abnormalities in cartilage that enhance deposition of CPPD crystals. Crystals are shed into the joint and undergo phagocytosis by leukocytes. The release lysosomal enzymes results in an acute inflammatory response. If inflammation persists, the cellular infiltrate of the synovium changes to a mononuclear pattern with fibroblastic proliferation in the chronic form of the disease.

Diseases associated with CPPD include hyperparathyroidism, hemochromatosis, hypophosphatasia, hypomagnesemia, gout, neuropathic arthropathy, and osteoarthritis. The association of CPPD with hypothyroidism is controversial. Diabetes has been shown not to be linked with pseudogout.

Osteoarthritis and chondrocalcinosis are both common disorders, and their exact relationship has not been established. It is possible that chrondrocalcinosis is a disease marker for certain cartilage changes in osteoarthritis.

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