Bone resorption by cells isolated from rheumatoid synovium.

Chang, J S; Quinn, J; A, Demazière; Bulstrode, C.; Francis, M. J. O.; Duthie, Robert B.; Athanasou, N A

doi:10.1136/ard.51.11.1223

Cited by 45 publications

(24 citation statements)

References 28 publications

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“…Rheumatologists unanimously agree that the prevention of early erosions is one of the primary targets of treatment. However, the precise relationships between synovial inflammation and cartilage damage and subsequent or simultaneous macrophage and osteoclast activation and the development of erosive changes remain obscure (48). And, the controversy about the effect of DMARDs on radiologic progression of disease continues.…”

Section: Discussionmentioning

confidence: 99%

Sulfasalazine in early rheumatoid arthritis. A 48‐week double‐blind, prospective, placebo‐controlled study

Hannonen

Möttönen

Hakola

et al. 1993

Arthritis & Rheumatism

120

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Objective. To investigate the efficacy and tolerability of sulfasalazine (SSZ) in the treatment of early rheumatoid arthritis (RA). Methods. Eighty patients (symptomatic disease < 12 months) were randomly assigned to treatment with SSZ or placebo for 48 weeks. Clinical, laboratory, and scintigraphic data were used to determine the effects of treatment. Results. SSZ was superior to placebo in reducing the laboratory features of inflammation, the clinical parameters of disease activity, as well as the scintigraphic activity in the joints. Furthermore, fewer erosive changes developed in the joints of patients receiving active treatment, but the difference between treatment groups did not reach statistical significance. Conclusion. SSZ is effective in the treatment of RA, and its onset of action is rapid. The results support the view that SSZ retards the development of joint erosions. However, like other conventional disease‐modifying antirheumatic drugs, its remission‐inducing ability is insufficient.

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Section: Discussionmentioning

confidence: 99%

Sulfasalazine in early rheumatoid arthritis. A 48‐week double‐blind, prospective, placebo‐controlled study

Hannonen

Möttönen

Hakola

et al. 1993

Arthritis & Rheumatism

120

View full text Add to dashboard Cite

show abstract

“…Cytokines that have been implicated in degenerative joint disease are interleukin-1 (Chang et al, 1986(Chang et al, , 1992Goldring et al, 1988;Verschure and Van, 1990;Davies et al, 1992), tumor necrosis factor (Campbell et al, 1990a,b;Pickvance et al, 1993), interleukin-6 (Bender et al, 1990), andinterleukin-8 (DeMarco et al, 1991;Elford and Cooper, 1991). Collectively, these cytokines increase fibrocartilage degradation by stimulating the synthesis of matrix-degrading enzymes by local cell populations.…”

Section: Temporomandibular Joint Diseasementioning

confidence: 99%

Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

Haskin

Milam²,

Cameron

1995

Critical Reviews in Oral Biology & Medicine

136

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ABSTRACT:The wide range of disease prevalences reported in epidemiological studies of temporomandibular degenerative joint disease reflects the fact that diagnoses are frequently guided by the presence or absence of non-specific signs and symptoms. Treatment is aimed at alleviating the disease symptoms rather than being guided by an understanding of the underlying disease processes. Much of our current understanding of disease processes in the temporomandibular joint is based on the study of other articular joints. Although it is likely that the molecular basis of pathogenesis is similar to that of other joints, additional study of the temporomandibular joint is required due to its unique structure and function. This review summarizes the unique structural and molecular features of the temporomandibular joint and the epidemiology of degenerative temporomandibular joint disease. As is discussed in this review, recent research has provided a better understanding of the molecular basis of degenerative joint disease processes, including insights into: the regulation of cytokine expression and activation, arachidonic acid metabolism, neural contributions to inflammation, mechanisms of extracellular matrix degradation, modulation of cell adhesion in inflammatory states, and the roles of free radicals and heat shock proteins in degenerative joint disease. Finally, the multiple cellular and molecular mechanisms involved in disease initiation and progression, along with factors that may modify the adaptive capacity of the joint, are presented as the basis for the rational design of new and more effective therapy.

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“…In this region, the bone trabeculae had also largely disappeared, coinciding with the radiological appearance of a radiolucent band. Most of the infiltrating cells appeared mononuclear, rather than osteoclastic, but such cells have bone-resorbing properties [24]; Safranin O staining showed that the articular cartilage has also lost most of its proteoglycan, a sign of proteinase attack. These mononuclear cells had failed to penetrate the adjoining cartilage, which appeared comparatively normal using van Gieson's stain, although somewhat thinned: in parallel, radiography showed that a thin radiodense rim external to the radiolucent band was still present.…”

Section: Evidence That the Triplet Feature Reflects Joint Pathologymentioning

confidence: 99%

Visualisation of subchondral erosion in rat monoarticular arthritis by magnetic resonance imaging

et al. 1995

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High-resolution magnetic resonance imaging (MRI) was used to investigate antigen-induced monoarticular arthritis (AIMA) in the rat. In sagittal, spin-echo images of the knee, characteristic parallel bands, in the order dark-light-dark, were consistently observed 5-8 days after arthritis induction; the bands ran concentric with, and just beneath, the femoral and tibial articular surfaces. Concurrent radiology, histology and MRI (chemical shift-selective imaging and contrast enhancement with magnetisation transfer and gadolinium) established that the phenomenon reflected subchondral erosion, not artefact. The outer hypointense band corresponded to calcified cartilage underlying the articular surface. The central hyperintense band reflected inflammatory matrix displacing normal haematopoietic tissue immediately subchondrally; here, trabecular bone had mostly disappeared, but adjacent articular cartilage, although under attack and lacking proteoglycan, appeared structurally normal. The inner hypointense band reflected deeper, truncated trabeculae within inflammatory matrix, layered with pallisading osteoblast-like cells. This study exemplifies the power of MRI for revealing localised joint pathology non-invasively, and shows that rat AIMA shares many pathological features with arthritis in human beings.

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Bone resorption by cells isolated from rheumatoid synovium.

Cited by 45 publications

References 28 publications

Sulfasalazine in early rheumatoid arthritis. A 48‐week double‐blind, prospective, placebo‐controlled study

Sulfasalazine in early rheumatoid arthritis. A 48‐week double‐blind, prospective, placebo‐controlled study

Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

Visualisation of subchondral erosion in rat monoarticular arthritis by magnetic resonance imaging

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