Biorheology - Volume 37, issue 1-2

Article Type: Other

Citation: Biorheology, vol. 37, no. 1-2, pp. 1-2, 2000

Authors: Stoltz, J.F. | Dumas, D. | Wang, X. | Payan, E. | Mainard, D. | Paulus, F. | Maurice, G. | Netter, P. | Muller, S.

Article Type: Research Article

Citation: Biorheology, vol. 37, no. 1-2, pp. 3-14, 2000

Article Type: Research Article

Citation: Biorheology, vol. 37, no. 1-2, pp. 15-15, 2000

Authors: Oddou, C. | Wendling, S. | Petite, H. | Meunier, A.

Article Type: Research Article

Abstract: The biomechanical mechanisms involved in the processes of tissue remodeling and adaptation are reviewed with emphasis on mechanotransduction at the cellular level. New theoretical models associated with experimental rheological techniques are briefly commented.

Keywords: Tissue remodeling, cell mechanotransduction

Citation: Biorheology, vol. 37, no. 1-2, pp. 17-25, 2000

Authors: Guilak, Farshid

Article Type: Research Article

Abstract: Chondrocytes in articular cartilage utilize mechanical signals in conjunction with other environmental factors to regulate their metabolic activity. However, the sequence of biomechanical and biochemical events involved in the process of mechanical signal transduction has not been fully deciphered. A fundamental step in determining the role of various factors in regulating chondrocyte activity is to characterize accurately the biophysical environment within the tissue under physiological conditions of mechanical loading. Microscopic imaging studies have revealed that chondrocytes as well as their nuclei undergo shape and volume changes in a coordinated manner with deformation of the tissue matrix. Through micromechanical experiments, it …has been shown that the chondrocyte behaves as a viscoelastic solid material with a mechanical stiffness that is several orders of magnitude lower than that of the cartilage extracellular matrix. These properties seem to be due to the structure of the chondrocyte cytoskeleton, and in part, the viscoelastic properties of the cell nucleus. The mechanical properties of the pericellular matrix that immediately surrounds the chondrocyte significantly differ from those of the chondrocyte and the extracellular matrix, suggesting that the pericellular matrix plays an important role in defining the mechanical environment of the chondrocyte. These experimentally measured values for chondrocyte and cartilage mechanical properties have been used in combination with theoretical constitutive modeling of the chondrocyte within articular cartilage to predict the non‐uniform and time‐varying stress‐strain and fluid flow environment of the cell. The ultimate goal of these studies has been to elucidate the sequence of biomechanical and biochemical events through which mechanical stress influences chondrocyte activity in both health and in disease. Show more

Citation: Biorheology, vol. 37, no. 1-2, pp. 27-44, 2000

Authors: van de Lest, C.H.A. | van den Hoogen, B.M. | van Weeren, P.R.

Article Type: Research Article

Abstract: The object of this study was to determine whether changes in the synovial fluid (SF) induced by in vivo loading can alter the metabolic activity of chondrocytes in vitro, and, if so, whether insulin‐like growth factor‐I (IGF‐I) is responsible for this effect. Therefore, SF was collected from ponies after a period of box rest and after they had been exercised for a week. Normal, unloaded articular cartilage explants were cultured in 20% solutions of these SFs for 4 days and chondrocyte bioactivity was determined by glycosaminoglycan (GAG) turnover (i.e., the incorporation of {}^{35} SO_4 into GAG and …the release of GAG into the medium). Furthermore, the extent to which the bioactivity is IGF‐I‐dependent was determined in a cartilage explant culture in 20% SF, in the presence and absence of anti‐IGF‐I antibodies. In explants cultured in post‐exercise SF, GAG synthesis was enhanced and GAG release was diminished when compared to cultures in pre‐exercise SF. SF analysis showed that IGF‐I and IGFBP‐3 levels were increased in post‐exercise SF. There was a positive correlation between IGF‐I levels and proteoglycan synthesis, but no correlation between IGF‐I levels and proteoglycan release. Addition of anti‐IGF‐I antibodies significantly inhibited stimulation of proteoglycan synthesis in explants cultured in SF with 40%. However, there was no difference in inhibition of proteoglycan synthesis between pre‐ and post‐exercise SF which indicated that the relative contribution of IGF‐I in the stimulating effect of SF did not change. Proteoglycan release was not influenced by the presence of anti‐IGF‐I antibodies. It is concluded that chondrocyte metabolic activity is at least partially regulated by changes in the SF induced by in vivo loading. Exercise altered the SF in a way that it had a favourable effect on cartilage PG content by enhancing the PG synthesis and reducing the PG breakdown. IGF‐I is an important contributor to the overall stimulating effect of SF on cartilage metabolism. It is, however, unlikely that IGF‐I is the only mediator in the exercise‐induced increase in this stimulating effect. Show more

Citation: Biorheology, vol. 37, no. 1-2, pp. 45-55, 2000

Authors: Jin, Z.M. | Pickard, J.E. | Forster, H. | Ingham, E. | Fisher, J.

Article Type: Research Article

Abstract: The experimentally measured indentation displacement and friction of normal and degraded (treated with chondroitinase AC) bovine articular cartilage plugs against a smooth steel plate were compared with the predictions based on the biphasic theory using the finite element method. It was found that the measured indentation displacement of both cartilage specimens could be predicted from the biphasic theory and the permeability for the degraded cartilage specimen was increased approximately three times. However, the measured friction coefficient was much lower for short period of loading, and the difference in the finite element prediction of friction coefficient between the normal and degraded …cartilage specimens was not observed in the experiment. Therefore, it was concluded that both biphasic and other mechanisms were important in controlling the frictional and lubricating characteristics of articular cartilage in mixed and boundary lubrication regimes. Show more

Citation: Biorheology, vol. 37, no. 1-2, pp. 57-63, 2000

Article Type: Research Article

Citation: Biorheology, vol. 37, no. 1-2, pp. 65-65, 2000

Authors: Wilkins, Robert J. | Browning, Joseph A. | Urban, Jill P.G.

Article Type: Research Article

Abstract: The effects of load on articular cartilage are complex. Dynamic loading of cartilage is associated with slight cell and tissue deformation as well as cyclical fluctuations in the hydrostatic pressure of cartilage and in fluid movement. Static loading results in expression of fluid from the tissue, concentrating extracellular matrix macromolecules and consequently increasing the concentrations of cations, reducing extracellular pH and increasing extracellular osmolarity. Each of these alterations is implicated in regulating the synthetic response of chondrocytes to load. However, the mechanisms by which these changes affect matrix turnover are poorly understood. In this review we consider how load may …affect chondrocyte behaviour through its influence on membrane transport processes and thus on the intracellular environment. Show more

Citation: Biorheology, vol. 37, no. 1-2, pp. 67-74, 2000

Authors: D’Andrea, Paola | Calabrese, Alessandra | Capozzi, Ilaria | Grandolfo, Micaela | Tonon, Rossana | Vittur, Franco

Article Type: Research Article

Abstract: Articular cartilage is a tissue designed to withstand compression during joint movement and, in vivo, is subjected to a wide range of mechanical loading forces. Mechanosensitivity has been demonstrated to influence chondrocyte metabolism and cartilage homeostasis, but the mechanisms underlying mechanotransduction in these cells are poorly understood. In many cell types mechanical stimulation induces increases of the cytosolic Ca^{2+} concentration that propagates from cell to cell as an intercellular Ca^{2+} wave. Cell‐to‐cell communication through gap junctions underlies tissue co‐ordination of metabolism and sensitivity to extracellular stimuli: gap junctional permeability to intracellular second messengers allows signal transduction …pathways to be shared among several cells, ultimately resulting in co‐ordinated tissue responses. Mechanically‐induced Ca^{2+} signalling was investigated with digital fluorescence video imaging in primary cultures of rabbit articular chondrocytes. Mechanical stimulation of a single cell, obtained by briefly distorting the plasmamembrane with a micropipette, induced a wave of increased Ca^{2+} that was communicated to surrounding cells. Intercellular Ca^{2+} spreading was inhibited by 18α‐glycyrrhetinic acid, suggesting the involvement of gap junctions in signal propagation. The functional expression of gap junctions was assessed, in confluent chondrocyte cultures, by the intercellular transfer of Lucifer yellow dye in microinjection experiments while the expression of connexin 43 could be detected in Western blots. A series of pharmacological tools known to interfere with the cell calcium handling capacity were employed to investigate the mechanism of mechanically‐induced Ca^{2+} signalling. In the absence of extracellular Ca^{2+} mechanical stimulation induced communicated Ca^{2+} waves similar to controls. Mechanical stress induced Ca^{2+} influx both in the stimulated chondrocyte but not in the adjacent cells, as assessed by the Mn^{2+} quenching technique. Cells treatment with thapsigargin and with the phospholipase C inhibitor U73122 blocked mechanically‐induced signal propagation. These results provide evidence that in chondrocytes mechanical stimulation activates phospholipase C, thus leading to an increase of intracellular inositol 1,4,5‐trisphosphate. The second messenger, by permeating gap junctions, stimulates intracellular Ca^{2+} release in neighbouring cells. Intercellular Ca^{2+} waves may provide a mechanism to co‐ordinate tissue responses in cartilage physiology. Show more

Citation: Biorheology, vol. 37, no. 1-2, pp. 75-83, 2000