Disease relevance of Chondrocalcinosis

• The activation of human neutrophils by monosodium urate and calcium pyrophosphate dihydrate crystals is believed to play a critical role in the pathogenesis of arthritides such as acute gout and pseudogout, respectively [1].
• Release of prostaglandin E2 (PGE2), 6-keto-PGF1 alpha, leukotriene B4 (LTB4), and LTC4 was measured in supernatants of synovial tissue, cartilage, and bone incubates from patients with osteoarthritis, active rheumatoid arthritis (RA), inactive RA, and pseudogout [2].
• Chondrocalcinosis and polymyalgia rheumatica in carpal tunnel syndrome [3].
• The synovial manifestations in the first patient included recurrent episodes of acute arthritis due to calcium pyrophosphate dihydrate crystal deposition and, later, chronic synovitis with radiologically evident chondrocalcinosis [4].
• Acute pseudogout (calcium pyrophosphate dihydrate deposition disease [CPPD disease]) developed in two patients with chronic renal failure [5].

High impact information on Chondrocalcinosis

• The metabolic and genetic factors leading to deposition of calcium pyrophosphate crystals in cartilage of patients with chondrocalcinosis are not well understood [6].
• Crystal-induced arthropathy. Gout and pseudogout [7].
• Chondrocalcinosis simulating ankylosing spondylitis [8].
• Colchicine, a drug used specifically in the treatment of gout and pseudogout, inhibited microcrystal-induced tyrosine phosphorylation, while beta- and gamma-lumicolchicine were without effect [1].
• Letter: Probenecid in chondrocalcinosis articularis [9].

Chemical compound and disease context of Chondrocalcinosis

• Thus, radiographically typical chondrocalcinosis may be due to calcium oxalate [10].
• OBJECTIVE: Monosodium urate monohydrate (MSU) and calcium pyrophosphate dihydrate (CPPD) crystals cause acute gout and pseudogout, respectively [11].
• Microscopic examination of the volar carpal ligament and the flexor synovial tendon sheath failed to reveal histologic signs of chondrocalcinosis [12].
• Acute pseudogout following intra-articular injection of high molecular weight hyaluronic acid [13].
• There was no statistically significant relation for gender, meniscectomy, injury, uric acid concentration, chondrocalcinosis, smoking, and occupation related factors, except possibly standing [14].

Biological context of Chondrocalcinosis

• Refinement of the chromosome 5p locus for familial calcium pyrophosphate dihydrate deposition disease [15].
• It was analyzed as a potential positional candidate gene for calcium pyrophosphate dihydrate deposition disease, and in several unrelated families, sequence variants were identified that segregated with the calcium pyrophosphate dihydrate deposition disease phenotype among affected members [16].
• Cell counts were higher in RA and pseudogout compared to OA and CPA, and in active compared to inactive RA [17].

Anatomical context of Chondrocalcinosis

• Increased pyrophosphate in fibroblasts and lymphoblasts from patients with hereditary diffuse articular chondrocalcinosis [6].
• Increased synovial interleukin-8 and interleukin-6 levels in pseudogout associated with granulocyte colony-stimulating factor [18].
• Higher levels of 5NT activity occurred in synovial fluid from osteoarthritic joints than from joints of patients with gout, pseudogout, or rheumatoid arthritis [19].
• Chondrocytes that accumulate proteoglycans and inorganic pyrophosphate in the pathogenesis of chondrocalcinosis [20].
• Because acute gout and pseudogout appear to be dependent on interleukin-8 (IL-8)-induced neutrophil ingress, this study was undertaken to define and compare how MSU and CPPD crystals stimulate IL-8 messenger RNA (mRNA) expression in mononuclear phagocytes [11].

Gene context of Chondrocalcinosis

• Mutations in ANKH cause chondrocalcinosis [21].
• MMP-1 activity was increased in pseudogout and injury groups over control levels, whereas MMP-3 activity was increased only in the pseudogout group [22].
• This paper examines the extent to which understanding of six of the principle disorders of connective tissue: the glycosaminoglycan storage diseases, ankylosing spondylitis, rheumatoid arthritis, systemic lupus erythematosus, chondrocalcinosis, and osteoarthrosis, has progressed during the past ten years [23].
• Thirty members of a Tunisian family with hereditary chondrocalcinosis were typed for HLA-A, B, and DR antigens: 7 affected and 23 unaffected subjects in three consecutive generations [24].
• Carpal tunnel syndrome in chondrocalcinosis of the wrist. Clinical and histologic study [12].

Analytical, diagnostic and therapeutic context of Chondrocalcinosis

• Synovial membrane histopathology in the differential diagnosis of rheumatoid arthritis, gout, pseudogout, systemic lupus erythematosus, infectious arthritis and degenerative joint disease [25].
• It is concluded that there is good evidence to associate hypophosphatasia, hypomagnesemia, and hyperparathyroidism with chondrocalcinosis and acute attacks of "pseudogout." Meta-analysis also suggests a small but significant association between hypothyroidism and chondrocalcinosis [26].
• In an additional 12 patients, the diagnosis of pseudogout was made in patients who suffered from acute arthritis after parathyroidectomy that relieved the primary hyperparathyroidism [27].
• Diagnosis of calcium pyrophosphate dihydrate deposition disease by fine needle aspiration biopsy: a case report [28].
• Pseudogout associated with primary hyperparathyroidism: management in the immediate postoperative period for prevention of acute pseudogout attack [29].

References