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Role of interleukin-17 in cartilage and bone destruction in rheumatoid arthritis.

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Differential roles of nitric oxide and oxygen radicals in chondrocytes affected by osteoarthritis and rheumatoid arthritis.

Mazzetti I, Grigolo B, Pulsatelli L, Dolzani P, Silvestri T, Roseti L, Meliconi R, Facchini A.

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Differences in nitric oxide production by superficial and deep human articular chondrocytes: implications for proteoglycan turnover in inflammatory joint diseases.

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IL-17 derived from juxta-articular bone and synovium contributes to joint degradation in rheumatoid arthritis.

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Basic fibroblast growth factor accelerates matrix degradation via a neuro-endocrine pathway in human adult articular chondrocytes.

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IL-18 is produced by articular chondrocytes and induces proinflammatory and catabolic responses.

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Cartilage destruction by matrix degradation products.

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Anti-interleukin-1 and anti-CD44 interventions producing significant inhibition of cartilage destruction in an in vitro model of cartilage invasion by rheumatoid arthritis synovial fibroblasts.

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Reduced cartilage proteoglycan loss during zymosan-induced gonarthritis in NOS2-deficient mice and in anti-interleukin-1-treated wild-type mice with unabated joint inflammation.

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The increased synthesis of inducible nitric oxide inhibits IL-1ra synthesis by human articular chondrocytes: possible role in osteoarthritic cartilage degradation.

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