Production of cytokines, vascular endothelial growth factor, matrix metalloproteinases, and tissue inhibitor of metalloproteinases 1 by tenosynovium demonstrates its potential for tendon destruction in rheumatoid arthritis

Jain, Abhilash; Nanchahal, Jagdeep; Troeberg, Linda; Green, Patricia; Brennan, Fionula M.

doi:10.1002/1529-0131(200108)44:8<1754::aid-art310>3.0.co;2-8

Cited by 82 publications

(48 citation statements)

References 17 publications

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“…This is consistent with an immunopathologic picture of early RA, in which inflammatory change within the tenosynovium mirrors that of the synovial membrane, as shown by Jain et al (4). In our cohort, erosions were identified adjacent to tendinitis/ tenosynovitis in only half of patients at baseline, but in 92% at 6 years.…”

Section: Discussionsupporting

confidence: 92%

“…An important complication is tendon rupture, which has been related both to invasion of the tendon by tenosynovial pannus and fraying of the tendon against eroded bone margins (2,3). Studies of invasive tenosynovium have revealed high levels of matrix metalloproteinases, proinflammatory cytokines, and angiogenic factors, indicating a propensity for damage to neighboring tissues (4). The importance of ongoing tenosynovial inflammation in promoting tendon rupture has been confirmed by observations that prophylactic dorsal tenosynovectomy can prevent this complication in many patients (5).…”

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confidence: 99%

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Magnetic resonance imaging evidence of tendinopathy in early rheumatoid arthritis predicts tendon rupture at six years

McQueen¹,

Beckley²,

Crabbe³

et al. 2005

Arthritis & Rheumatism

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Objective. To determine whether magnetic resonance imaging (MRI) evidence of tendinopathy in early rheumatoid arthritis (RA) could be used to predict the course of tendon involvement in later disease and specifically the risk of tendon rupture.Methods. The occurrence, pattern, and progression of tendinopathy were studied prospectively over 6 years in a cohort of patients who had presented with RA. Of 42 patients enrolled, full MRI and clinical data were available for 31 at 6 years. MRI scans of the dominant wrist were scored for tendinopathy by 2 radiologists using a validated system. These data were compared with MRI synovitis, erosion scores, and disease activity measures. Prognostic factors for tendon inflammation and rupture were sought.Results. Thirty-four patients (81%) had MRI evidence of tendinopathy at baseline, falling to 59% at 1 year and 68% at 6 years. The most commonly affected site was the extensor carpi ulnaris. MRI tendinopathy and synovitis scores were correlated at baseline (r ‫؍‬ 0.37, P ‫؍‬ 0.01) and 1 year (r ‫؍‬ 0.45, P ‫؍‬ 0.003) but not at 6 years (r ‫؍‬ 0.11, P ‫؍‬ 0.5). The strongest predictor of the 6-year tendinopathy score was the 1-year tendinopathy score ( Conclusion. MRI can be used to quantify tendinopathy at the wrist in RA patients. High scores in early disease were predictive of tendon rupture in a small group of patients, but further studies are required to determine whether this has clinical relevance.Tendinopathy involving the extensor tendons of the wrist is observed in 50-64% of patients with rheumatoid arthritis (RA) (1). An important complication is tendon rupture, which has been related both to invasion of the tendon by tenosynovial pannus and fraying of the tendon against eroded bone margins (2,3). Studies of invasive tenosynovium have revealed high levels of matrix metalloproteinases, proinflammatory cytokines, and angiogenic factors, indicating a propensity for damage to neighboring tissues (4). The importance of ongoing tenosynovial inflammation in promoting tendon rupture has been confirmed by observations that prophylactic dorsal tenosynovectomy can prevent this complication in many patients (5). However, the decision to perform surgery is usually made in established cases of RA once

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Magnetic resonance imaging evidence of tendinopathy in early rheumatoid arthritis predicts tendon rupture at six years

McQueen¹,

Beckley²,

Crabbe³

et al. 2005

Arthritis & Rheumatism

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“…Several of the actions of TNF␣ are also mediated indirectly through the modulation of IL-1 expression, which then has many other downstream effects (7). In a number of concurrent studies, TNF␣ has been shown to induce the expression of multiple proteolytic enzymes, including matrix metalloproteinases (MMPs) 1, 3, and 9, which have been associated with destruction of the cartilage extracellular matrix (8)(9)(10). It is presently believed that most of the actions of TNF␣ affect the synovium and that many of the pathologic effects of TNF␣ are exerted through the stimulation of hypertrophic pannus formation, which is then invasive and destructive to the articular cartilage surface.…”

mentioning

confidence: 99%

Tumor necrosis factor α activation of the apoptotic cascade in murine articular chondrocytes is associated with the induction of metalloproteinases and specific pro‐resorptive factors

Cho¹,

Lehmann²,

Edgar³

et al. 2003

Arthritis & Rheumatism

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Objective. Tumor necrosis factor ␣ (TNF␣) blockade provides substantive reduction of the symptoms of rheumatoid arthritis (RA). While the biologic actions of TNF␣ have been well characterized in immune and synovial cells, which are known to be major contributors to the progression of cartilage destruction in RA, the current studies were designed to assess the direct effects of TNF␣ on chondrocytes.Methods. We examined the expression of several groupings of messenger RNA (mRNA) that define key biologic pathways that have previously been associated with either the general actions of TNF␣ or cartilage destruction, in murine articular chondrocytes isolated from wild-type mice and TNF␣ receptor-null (p55/ p75 ؊/؊ ) mice. Results. TNF␣ induced the expression of multiple mRNA that facilitate apoptosis and lead to apoptosisinduced cell death. The induction of apoptosis was accompanied by the increased expression of several factors involved in the regulation of skeletal tissue proteolysis and resorption. Quantitative increases from 2-fold to >10-fold were seen for inducible nitric oxide synthase, matrix metalloproteinase 3, macrophage colony-stimulating factor, and osteoprotegerin mRNA expression. The dependence of the induction of these mRNA on TNF␣ was confirmed by comparison with the effects of TNF␣ on chondrocytes isolated from receptornull mice.Conclusion. These findings demonstrate that TNF␣ alters the expression of a complex array of genes within murine chondrocytes that contribute to the destruction of joint surfaces, independent of its actions on synovial and immune cells. Further studies are needed to clarify the biologic actions of TNF␣ in human cartilage cells.

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“…In patients with stable established RA in a previous study, we also observed reduced tendon stiffness compared with controls of similar physical fitness (Matschke V et al: unpublished observations). RA is known to cause synovial inflammation and hypertrophy of tendon sheaths and on occasion, synovial tissue infiltration of the tendon itself (12). However, the PT does not have a tendon sheath.…”

Section: Discussionmentioning

confidence: 99%

Adverse changes in tendon–muscle physiology and physical function caused by an isolated acute rheumatoid knee effusion: A case study

Matschke

Thom

Lemmey

et al. 2011

Arthritis Care & Research

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Production of cytokines, vascular endothelial growth factor, matrix metalloproteinases, and tissue inhibitor of metalloproteinases 1 by tenosynovium demonstrates its potential for tendon destruction in rheumatoid arthritis

Cited by 82 publications

References 17 publications

Magnetic resonance imaging evidence of tendinopathy in early rheumatoid arthritis predicts tendon rupture at six years

Magnetic resonance imaging evidence of tendinopathy in early rheumatoid arthritis predicts tendon rupture at six years

Tumor necrosis factor α activation of the apoptotic cascade in murine articular chondrocytes is associated with the induction of metalloproteinases and specific pro‐resorptive factors

Adverse changes in tendon–muscle physiology and physical function caused by an isolated acute rheumatoid knee effusion: A case study

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