Effect of synthetic calcium pyrophosphate and hydroxyapatite crystals on the interaction of human blood mononuclear cells with chondrocytes, synovial cells, and fibroblasts

Dayer, Jean‐Michel; Evêquoz, V.; Zavadil-Grob, Carolyn; Grynpas, Marc D.; Cheng, Pei‐Tak; Schnyder, J.; Trechsel, U.; Fleisch, H.

doi:10.1002/art.1780301208

Cited by 46 publications

(19 citation statements)

References 32 publications

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“…Immune complexes composed of self-associated IgG rheumatoid factor have been shown to induce the release of IL-1 by monocytes (52), raising the question whether immune complexes can alter directly IL-6 production. We have already demonstrated that the crystals associated with inflammatory arthropathies (urate, pyrophosphate, and hydroxyapatite) can induce IL-6 production (Guerne, P. A., unpublished results), and it will be of interest to determine whether this effect is direct or mediated by IL-1 (53,54). Lipopolysaccharide has been shown to increase serum IL-6 activity in vivo (55) and in cultures of human fibroblasts (56), monocytes (19), and endothelial cells in vitro (Jirik, F., et al, manuscript submitted).…”

Section: Methodsmentioning

confidence: 98%

Synovium as a source of interleukin 6 in vitro. Contribution to local and systemic manifestations of arthritis.

Guerne

Zuraw²,

Vaughan³

et al. 1989

J. Clin. Invest.

473

171

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Synovial inflammation is often associated with systemic changes, such as increased levels of acute phase proteins and hypergammaglobulinemia, which cannot be explained by the cytokines described in synovial fluids and synoviocyte secretions. Interleukin 6 (IL-6) has recently been characterized as a mediator of multiple inflammatory responses. This cytokine promotes T and B lymphocyte growth and differentiation, and acute phase protein synthesis. We therefore examined IL-6 production by human synoviocytes and its presence in synovial fluids. In vitro, synoviocytes spontaneously released IL-6, which was increased by IL-1 and tumor necrosis factor-a. Synoviocyte-derived IL-6 activity was able to induce hybridoma-plasmacytoma proliferation, and immunoglobulin and acute-phase protein synthesis. The synovial fluids from patients with diverse arthropathies contained IL-6 activity, but higher levels were present in inflammatory arthropathies than in osteoarthritis. These results demonstrate that synoviocytes are a potent source of IL-6, which can contribute to important manifestations of inflammatory arthropathies.

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Section: Methodsmentioning

confidence: 98%

Synovium as a source of interleukin 6 in vitro. Contribution to local and systemic manifestations of arthritis.

Guerne

Zuraw²,

Vaughan³

et al. 1989

J. Clin. Invest.

473

171

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“…This hypothesis was tested by determining whether calcium crystals could activate cells to secrete metalloproteinases. Upon adding natural and synthetic BCP, and CPPD crystals to cultured synoviocytes, collagenase activity in the ambient media was significantly augmented in a dose-related fashion over untreated cultures [17,25,39]. It has been shown that metalloproteinase induction and secretion also occur in human fibroblasts in response to BCP crystals.…”

Section: Induction Of Metalloproteinases By Calcium-containing Crystalsmentioning

confidence: 86%

“…It was concluded that PC inhibits disease progression in MPA when given before disease is established [20]. It has been shown that calcium crystals can activate a wide variety of cell types, including chondrocytes [21], fibroblasts [22], synoviocytes [23] and immune cells [24][25][26], which are likely to contribute to the pathologic response. The remainder of this review, however, will focus mainly on the underlying mechanisms by which calcium crystals activate mitogenesis and metalloproteinase induction in fibroblasts, and fibroblast-like cells.…”

Section: Multi-author Review Articlementioning

confidence: 99%

“…BCP crystals can substitute for PDGF as a competence growth factor in vitro [10]. BCP crystals and PDGF exert similar biologic effects on cultured cells, such as stimulation of PGE 2 production via the phospholipase A 2 /cyclo-oxygenase pathway, activation of phospholipase C and inositol phospholipid hydrolysis [27], and induction of collagenase and neutral protease synthesis [25,28]. Proto-oncogenes c-fos and c-myc are induced with similar kinetics [29,30].…”

Section: Mitogenic Effects Of Calcium-containing Crystalsmentioning

confidence: 99%

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Calcium and disease: molecular determinants of calcium crystal deposition diseases

Misra¹

2000

CMLS, Cell. Mol. Life Sci.

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Deposition of basic calcium phosphate (hydroxyapatite, octacalcium phosphate and tricalcium phosphate) (BCP) and crystalline calcium pyrophosphate dihydrate (CPPD) is associated with a variety of aging-related pathologies, including osteoarthritis, cartilage degeneration and pseudogout. These diseases of calcium deposition serve as some of the best-studied examples of how calcium-regulated changes in gene expression can directly lead to pathogenic consequences. Tissue damage can result when crystals stimulate cells to release matrix-degrading molecules or secrete cytokines that stimulate the release of matrix-degrading molecules. Exposure of cultured cells to crystals induces expression of cellular proto-oncogenes such as c-fos, c-myc and c-jun, by a calcium-dependent mechanism, and this response can be blocked by a potential therapeutic compound, phosphocitrate. Activation of the c-fos and c-jun genes is directly involved in expression of metalloproteinases such as collagenase and stromelysin, suggesting that crystal-mediated activation of these genes is directly involved in pathogenesis. In this review recent advances in the molecular mechanisms responsible for crystal-mediated cell activation are discussed.

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“…CPPD and BCP are much less potent stimulators of IL-1 [31]. Human monocytes stimulated with BCP and CPPD crystals secreted an IL-1-like factor that stimulated fibroblasts and chondrocytes to produce collagenase and PGE 2 [32].…”

Section: In Vitro Biologic Effects Of Calcium-containing Crystalsmentioning

confidence: 98%

The role of crystals in articular tissue degeneration

Cheung

1999

Curr Rheumatol Rep

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The deposition of calcium-containing crystals in articular tissues is probably an underrecognized event. Clinical observations indicate that exaggerated and uniquely distributed cartilage degeneration is associated with these deposits. Perhaps the most compelling argument favoring a role for crystals in causing osteoarthritis stems from their in vitro effects on articular tissues. In this short review, we will discuss the fact that crystals can cause the degeneration of articular tissues in 2 separate pathways. In the "Direct" pathway, crystals directly induce fibroblast-like synoviocytes to proliferate and produce metalloproteinases and prostaglandins. The other "Paracrine pathway" involves the interaction between crystals and macrophages/monocytes, which leads to synthesis and release of cytokines that can reinforce the action of crystals on synoviocytes and induce chondrocytes to secrete enzymes, eventually causing the degeneration of articular tissues.

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Effect of synthetic calcium pyrophosphate and hydroxyapatite crystals on the interaction of human blood mononuclear cells with chondrocytes, synovial cells, and fibroblasts

Cited by 46 publications

References 32 publications

Synovium as a source of interleukin 6 in vitro. Contribution to local and systemic manifestations of arthritis.

Synovium as a source of interleukin 6 in vitro. Contribution to local and systemic manifestations of arthritis.

Calcium and disease: molecular determinants of calcium crystal deposition diseases

The role of crystals in articular tissue degeneration

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