2000
DOI: 10.1053/joca.1999.0292
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Tumor necrosis factor alpha can contribute to focal loss of cartilage in osteoarthritis

Abstract: Variations in chondrocyte TNF-R expression occur in OA cartilage in vivo. TNFalpha at concentrations produced by OA synovium in vitro, can degrade cartilage matrix. In most OA supernatants sTNF-R concentrations were insufficient to abrogate the effects of TNFalpha. Thus conditions exist in some OA knees for TNFalpha to contribute to focal loss of cartilage.

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Cited by 91 publications
(71 citation statements)
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“…It has been implicated in the inhibition of 1,25-D stimulated extracellular matrix protein synthesis [34] and the activation of catabolic MAP kinase pathways in articular chondrocytes [10], which can lead to focal loss of cartilage glycosaminoglycans [46]. Despite this we found no evidence that TNFα is involved in cartilage destruction in OC/OA.…”
Section: Discussioncontrasting
confidence: 64%
See 1 more Smart Citation
“…It has been implicated in the inhibition of 1,25-D stimulated extracellular matrix protein synthesis [34] and the activation of catabolic MAP kinase pathways in articular chondrocytes [10], which can lead to focal loss of cartilage glycosaminoglycans [46]. Despite this we found no evidence that TNFα is involved in cartilage destruction in OC/OA.…”
Section: Discussioncontrasting
confidence: 64%
“…Systemic levels of TNFα were unaltered in OA lesion affected pigs compared to unaffected controls. However, local production of TNFαis known to be important in the destruction of cartilage in osteoarthritis [46] and future studies should consider measuring concentrations of TNFα in the synovial fluid of affected joints.…”
Section: Discussionmentioning
confidence: 99%
“…As inhibition of the target antigen in synovium or psoriatic skin is necessary for induction of the pharmacological effect, antibody penetration into these compartments is a critical requirement for therapeutic efficacy. The importance of suppression of cytokines such as TNF, interleukin (IL)-17, and IL-12/23 in synovium during treatment of RA has recently been demonstrated, and the role of the synovial membrane expression of these cytokines as predictive of joint damage and disease progression is now well established (78)(79)(80)(81)(82). In line with these observations, effective inhibition of cytokines such as IL-17 and TNF allows rapid control of the inflammatory manifestations of RA and retards cartilage and bone destruction.…”
Section: Biodistribution Of Marketed Antibodiesmentioning
confidence: 99%
“…43 We observed that the NO donor Noc-12 (2.5 to 25 mol/L), and the peroxynitrite generator Sin-1 (1 to 10 mol/L) 44 shared the ability of IL-1 to induce TGase activity in cultured normal knee meniscal cells, although Noc-12 and Sin-1 were less effective than IL-1 at inducing TGase activity (Figure 7). Tumor necrosis factor (TNF)-␣, which also acts on chondrocytes, 45,46 stimulated increased TGase activity in cultured normal knee meniscal cells (Figure 7). In contrast, TGF-␤ did not induce TGase activity under these conditions (Figure 7).…”
Section: Mechanism Of Induction Of Tgase Activity By Il-1mentioning
confidence: 99%