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At least 1,531 records · Page 85Linked to original sources
PubMed1997

Effect of interleukin 1 and leukaemia inhibitory factor on chondrocyte metabolism in articular cartilage from normal and interleukin-6-deficient mice: role of nitric oxide and IL-6 in the suppression of proteoglycan synthesis.

We studied the role of IL-6 and nitric oxide (NO) in IL-1 and leukaemia inhibitory factor (LIF) induced suppression of proteoglycan synthesis. Cartilage explants of patellae and femoral heads were incubated with IL-1 or LIF. Conditioned media were analysed for IL-6 activity (B9-assay) and NO content (Griess). Proteoglycan synthesis was assessed using [35S]sulfate incorporation. IL-1 dose dependently induced IL-6 synthesis and neutralizing IL-6 with antibodies did not reduce proteoglycan synthesis suppression, neither in explants nor in isolated chondrocytes. IL-6 independence was confirmed using cartilage from IL-6 deficient mice. IL-1 significantly increased NO release in normal and IL-6 deficient chondrocytes and addition of the NO synthase inhibitor, N(G)-monomethyl-L-arginine markedly alleviated proteoglycan synthesis suppression. LIF also induced proteoglycan synthesis suppression in cartilage from normal and IL-6 deficient mice, but the suppression was neither accompanied by nor dependent on NO release. Furthermore, proteoglycan synthesis suppression during experimental arthritis was similar in both normal and IL-6 deficient mice. We concluded that IL-6 is not a necessary cofactor in IL-1 and LIF induced suppression of proteoglycan synthesis. Furthermore, only the IL-1 induced suppression was mediated by NO, suggesting that inhibition of proteoglycan synthesis may occur through different pathways.

Animals↗
PubMed1999

In vivo triple quantum filtered twisted projection sodium MRI of human articular cartilage.

In this work, we present the first triple quantum filtered (TQF) sodium MR images of the human knee joint in vivo. A 3D TQF data set of 16 slices was obtained in 20 min using a TQF pulse sequence preencoded to a twisted projection imaging readout. Images clearly demarcate patellar cartilage and also demonstrate fluid signal suppressed by the triple quantum filter. Biexponential transverse relaxation times were calculated by fitting the TQF free induction decay to a theoretical signal expression. The average values from three healthy volunteers were T(2fall)(*) = 9.59 +/- 0.35 ms and T(2rise)(*) = 0.84 +/- 0.06 ms. Application of TQF imaging in biological tissues is discussed.

Cartilage, Articular↗
PubMed1993

Effects of long-term running exercise on canine femoral head articular cartilage.

After long-term running program (40 km/day) anterior and posterior tissue samples from canine femoral head were labeled ex vivo in the presence of 35S-SO4. Sulfate incorporation rates did not differ between runner and control groups. The statistically significant changes in runners included a decreased uronic acid concentration (p < or = 0.02) and proportion of extractable proteoglycans (p < or = 0.05) as well as increased concentration of tissue uronic acid after 4 M GuCl extraction (p < or = 0.05) in the posterior area. These results support an idea of strengthened cartilage tissue after this kind of motion and load.

Animals↗
PubMed1993

Proteolytic degradation in human articular cartilage: its relationship to stromelysin.

Proteolytic degradation of cartilage can in principle occur via the action of proteinases or free radicals, though current evidence favours the enzymic pathway. Link protein can be used as an in situ monitor to identify endogenous proteolytic agents, and its pattern of modification suggests that stromelysin may play a major role in the young, but that additional agents are active in the adult. In cartilage remaining on late-stage osteoarthritic joints, there is less evidence for the action of stromelysin than in normal cartilage, and the tissue appears to be undergoing repair rather than degeneration.

Animals↗
PubMed2003

Corresponding articular cartilage thickness measurements in the knee joint by modelling the underlying bone (commercial in confidence).

We present a method for corresponding and combining cartilage thickness readings from a population of patients using the underlying bone structure as a reference. Knee joint femoral bone and cartilage surfaces are constructed from a set of parallel slice segmentations of MR scans. Correspondence points across a population of bone surfaces are defined and refined by minimising an objective function based on the Minimum Description Length of the resulting statistical shape model. The optimised bone model defines a set of corresponding locations from which 3D measurements of the cartilage thickness can be taken and combined for a population of patients. Results are presented for a small group of patients demonstrating the feasibility and potential of the approach as a means of detecting sub-millimetre cartilage thickness changes due to disease progression.

Algorithms↗
PubMed1992

Synovial, articular cartilage and bone changes in rapidly destructive arthropathy (osteoarthritis) of the hip.

We studied ten femoral heads from eight patients suffering from rapidly destructive arthropathy (RDA) of the hip. At surgery, 1-3.5 ml of synovial fluid, ranging from citrous to hemorrhagic, was aspirated from six joints. This fluid was viscous, pauci-cellular and did not contain calcium pyrophosphate dihydrate (CaPPD) crystals, although significant amounts of alizarin S-positive material was found in three joints. Significant synovial hyperplasia was found in four joints and moderate hyperplasia in two. Synovium was hypertrophic, hypercellular and slightly to moderately fibrotic. It lacked evidence of perivascular inflammatory infiltrates. Synovium often contained amyloid micro-deposits and alizarin S-positive osteocartilagenous debris surrounded by macrophages. Synovial hyperplasia had a good correlation with osteocartilagenous debris and a poor correlation with amyloid infiltration. Femoral heads were usually flattened and exhibited large areas of exposed bone spotted by plugs of fibro-cartilagenous tissue. Subchondral bone contained large ischemic and necrotic areas, bone marrow atrophy and fibrosis, and intense bone remodeling. Subchondral bone necrosis and ischemia were the most significant findings of this study and their role in the development of RDA is discussed.

Aged↗
PubMed1988

Electrical charge of a protein determines penetration and localization in hyaline articular cartilage. Quantitative and autoradiographic studies on cartilage of different species, including man.

Sufficient antigen retention in joint structures is a prerequisite for sustained antigen-induced arthritis. In this in vitro study we investigated the retention of native and charge-modified bovine serum albumin (BSA) with patellar cartilage of different species (mouse, rat, rabbit, and man). Association of BSA with cartilage due to charge of the protein with that due to immune complex formation was compared. Using radiolabeled proteins we showed quantitatively that the retention of highly positively charged BSA is considerably higher (200-500 times) than retention of the anionic BSA in all cartilage species examined. Mouse, rat, and human cartilage bind more protein per mg dry weight, compared to rabbit cartilage. No clear-cut relation was found with the glycosaminoglycans (GAG) contents. Retention of native BSA by anti-BSA antibodies was low in the dense hyaline patellar cartilage in all species. Enhanced immune-complex formation was found in marginal regions of rabbit patellar cartilage, consisting of fibrous-like cartilage. Localization studies by autoradiography showed that cationic BSA penetrates deeply into the cartilage matrix. Even in a thick cartilage specimen, such as rabbit cartilage, very deep penetration into the calcified zone was demonstrated. This study indicates that binding and deep penetration of cationized protein in cartilage is not restricted to mouse specimen, as had been found previously, but is a general phenomenon.

Animals↗
PubMed1993

Leukaemia inhibitory factor stimulates proteoglycan resorption in porcine articular cartilage.

Leukaemia inhibitory factor (LIF) is a secretory glycoprotein produced by tumour, mesenchymal and haemopoietic cells. LIF has been found to have pleiotropic actions that include the capacity to regulate cell differentiation, promote acute-phase protein synthesis and stimulate calcium release in bone explants. In view of its similarity to other cytokines that affect cartilage metabolism, the effects of LIF on proteoglycan resorption were examined in pig cartilage explants. Endotoxin-free recombinant mouse LIF was found to produce a dose-dependent increase in sulphated glycosaminoglycan (S-GAG) release (ED50 = 123 U/ml, approx. 25-50 pM). Statistically significant stimulation was observed with doses of 100 U/ml or greater. When pig cartilage was stimulated with maximum concentrations of LIF and either interleukin 1 alpha (IL-1 alpha), interleukin 1 beta (IL-1 beta) or tumour necrosis factor alpha (TNF alpha), in each case a significantly greater release of S-GAGs was observed than with the respective cytokines alone (P < 0.05). Comparison of the areas under the curves showed that the action of LIF was additive, and not synergistic with other catabolic cytokines. Dose-response studies showed that transforming growth factor beta (TGF beta) produced a partial inhibition of LIF-stimulated release of S-GAGs (ED50 = 4.5 U/ml). Statistically significant inhibition was observed with doses of 2 U/ml or greater. These results showed that LIF stimulated proteoglycan resorption in vitro and that this effect was modulated by other cytokines. Whether LIF contributes to the progressive destruction of cartilage in septic or chronic inflammatory arthritis remains to be determined.

Absorption↗