作者: MARK FAHEY , ELIZABETH MITTON , EMILY MUTH , ANN K. ROSENTHAL
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摘要: Calcium pyrophosphate dihydrate crystals (CPPD) occur commonly in osteoarthritic joints. At the time of knee replacement for osteoarthritis, example, 60% synovial fluids possess either CPPD and/or hydroxyapatite-like basic calcium phosphate crystals. (1) (2) Although role these is not completely understood, they likely contribute to joint damage. Clinically, their presence predicts increased damage and rapid destruction cartilage. (3) In vitro, induce production proteases catabolic cytokines from cells chondrocytes. (4) While no specific therapies this form pathologic mineralization currently exist, intra-articular corticosteroids are widely used clinically both osteoarthritis calcium-crystal deposition diseases. (5) Corticosteroids, including dexamethasone (Dxm), steroid hormones with a broad range physiologic pharmacologic effects. Pharmacologic effects on vary depending route administration. While systemic corticosteroid administration may reduce bone mineralization, (6) have been associated tissue mineralization. (7) This has reproduced as repeated injections methylprednisolone resulted articular calcifications rabbit (8) Previous work fetal chondrocytes other cell types suggested that Dxm increase by altering chondrocyte phenotype. (9, 10) However, little known about mammalian cartilage mineralization. CPPD crystal formation relatively unique actors involved fully delineated, key participants process identified. pericellular matrix facilitated extracellular organelles, vesicles. (11) Excess quantities ATP (12) or its metabolite (13) elaborated abnormal resemble hypertrophic responsible bone. (14) addition, abnormalities matrix, characterized levels osteopontin (15) high activities protein cross-linking transglutaminase enzymes (16), also formation. Two enzymes, type II factor XIIIA, well chondrocytes, (17) latter play particularly important formation. The purpose current investigation was determine effect investigate mechanism effect.