Calcium crystal effects on the cells of the joint: implications for pathogenesis of disease.

H S Cheung

Journal: Current opinion in rheumatology 2000;12(3):223-7

PMID: 10803753

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Abstract

In the past three years, there has been considerable progress in delineating the mechanism of calcium-containing crystal-induced cell activation: (1) the identification of Ca2+ influx and p42/44 mitogen-activated protein kinase activation as the signal transduction pathways; (2) induction of nuclear transcription factors of cyclic adenosine monophosphate (cAMP) response element binding protein, activator protein-1, and nuclear factor kappaB; (3) the differential role of crystal endocytosis and dissolution in crystal-induced metalloproteinase synthesis and mitogenesis; (4) crystal upregulation of matrix metalloproteinases, including MMP-13 but downregulation of tissue inhibitor of metalloproteinase-1 and -2, thus magnifying the degenerative effect of crystals. Phosphocitrate, a specific inhibitor of biologic effect of calcium crystals, reverses the degenerative effects of crystals.

Address: Geriatric Research Education and Clinical Center, Miami Veterans Affairs Medical Center and Division of Rheumatology and Immunology, University of Miami School of Medicine, FL, USA. [email protected]

DOI: 10.1097/00002281-200005000-00012

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MeSH Terms: Calcium Phosphates, Calcium Pyrophosphate, Chondrocalcinosis, Collagenases, Crystallization, Cyclic AMP Response Element-Binding Protein, Humans, Joints, Matrix Metalloproteinase 13, Mitogen-Activated Protein Kinase 1, NF-kappa B, Protein Kinase C, Signal Transduction, Transcription Factor AP-1, Transcription Factors, Up-Regulation