Read more about this disease, some with Classification – Types – Signs and symptoms – Genetics – Pathophysiology – Diagnosis – Screening – Prevention – Treatment and management – Cures and much more, some including pictures and video when available.
Calcium pyrophosphate deposition disease (CPPD) is a rheumatologic disorder with varied clinical manifestations due to precipitation of calcium pyrophosphate dihydrate crystals in the connective tissues. It is more commonly known by alternative names that specify certain clinical or radiographic findings, although neither is synonymous with CPPD. Pseudogout refers to the clinically evident acute synovitis with red, tender, and swollen joints that may resemble gouty arthritis (a similar condition with joint deposition of monosodium urate crystals). Chondrocalcinosis[1][2], on the other hand, refers to the radiographic evidence of calcification in hyaline and/or fibrocartilage. Pyrophosphate arthropathy is a term that may refer to either of the above.[3] Statistically, the interphalangeal joints are the most commonly affected.[1]
CPDD crystal deposition disease is a polyarticular arthritis (i.e. it leads to an inflammation of several joints in the body), although it can initially present as monoarticular (i.e. confined to just one joint).[4] CPDD crystals tend to form within articular tissues.[4] Although, in theory, any joint may be affected, the knees, wrists, and hips are the statistically the most commonly attributed areas.[2] In rare case, pseuogout may affect the spinal canal and cause myelopathy.[5] The exact pathology of CPDD is unknown, although increased adenosine triphosphate (the molecule used as energy currency in all animals) breakdown, which results in increased pyrophosphate levels in joints, is thought to be a method of crystal development.[2] There is some recent evidence suggesting that the gene ANKH is involved in crystal-related inflammatory reactions and inorganic phosphate transport.[2] Excessive calcium (due to hypomagnesemia) has a potential relationship with chondrocalcinosis, and magnesium supplementation may reduce or alleviate symptoms.[6]
Patients usually present with inflammation of one or more joints often resulting in pain in the affected joint(s).[2] Hyperparathyroidism, hemochromatosis, hypophosphatemia and renal osteodystrophy are often also associated with chondrocalcinosis.[2] In some cases, traumatic arthritis has resulted in chondrocalcinosis.[2][4] In general, the white blood cell count is raised[2]. Rarely, patients may also present with signs of carpal tunnel syndrome.[2]
Radiography has a large role to play in the diagnosis of chondrocalcinosis with radiographs, CT scans, MRIs, ultrasound and nuclear medicine all having a part.[1] CT scans and MRIs show calcific masses (usually within the ligamentum flavum or joint capsule) however radiography is more successful.[1] As with most conditions, chondrocalcinosis can present with similarity to other diseases such as ankylosing spondylitis or gout.[1][2] Arthrocentesis, or removing synovial fluid from the affected joint, is perfomed to test the synovial fluid for the calcium pyrophosphate crystals that are present in CPDD
Treatment for asymptomatic chondrocalcinosis is not advised to prevent end-organ damage.[2] For acute pseudogout, intra-articular corticosteroid injection, systemic corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), or occasionally, high-dose colchicine.[2] NSAIDs are generally administered in low doses to help prevent chondrocalcinosis, however in an acute attack is already occurring, higher doses are administered.[2] Research into surgical removal of calcifications is underway, however this still remains an experimental procedure.[2]
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