Abstract
Normal human joints contain only a few milligrams of hyaluronate whereas in degenerative or in inflammatory conditions these joints may contain several hundreds of milligrams of this polysaccharide. The increase in total hyaluronate content in diseased joints reflects the higher synthesis of this polysaccharide by the synovial cell in pathology1. The intrinsic viscosity of these fluids (as a parameter of the mean hyaluronate molecular weight) however is decreased2–3. In view of the pH required for acid hydrolase activity we have some difficulties in accepting this lowering in hyaluronate molecular weight as a consequence of any extracellular acid hydrolase activity. In this way a disturbed synthesis seems more plausible and the overproduction of a less polymerized hyaluronate can be seen as a loss of quality control by the synovial cell under inflammatory stress4.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Sundblad, L. (1953). Acta Soc. Med. Ups., 58, 115
Balazs, E. A. et al. (1967). Arthritis Rheum., 10, 357
Castor, C. W. et al. (1966). Arthritis Rheum., 9, 783
Verbruggen, G. and Veys, E. M. (1980). Acta Rheum. (Belgium) (In press)
Castor, C. W. et al. (1971) Arthritis Rheum., 14, 41
Mankin, H. J. and Lipiello, L. (1970). J. Bone Jt. Surg., 52A, 424
Hardingham, T. E. etal. (1972). Biochem. J. , 129, 101
McDevitt, C. A. el al. (1973). Biochem. Soc. Trans., 1, 287
Brandt, K. et al. (1976). Arthritis Rheum., 19, 1308
McDevitt, C. A. et al. (1978). Ann. Rheum. Dis., 37, 484
Greiling, el al. (1971). In Müller, W, Harwerth, H. G. and Fehr, K. (eds). Rheumatoid Arthritis, Pathogenetic mechanism and consequences in therapeutics, p. 173. (London: Academic Press)
Fell, H. B. and Dingle, J. T. (1963). Biochem. J., 87, 403
Sapolski, A. I. et al. (1974). J. Clin. Invest., 53, 1044
Nevo, Z. et al. (1972). Dev. Biol., 28, 219
Kosher, R. A. etal. (1973). Dev. Biol., 35, 210
Wiebkin, O. W. and Muir, H. (1973). In E, Kulonen, Biology of fibroblast, J. Pikkarainen, (eds.) p. 231. (New York: Academic Press)
Schwartz, N.B. and Dorfman, A. (1975). Conn. Tiss. Res., 3, 115
Verbruggen, G. and Veys, E. M. (1977). Acta Rheum. (Belgium)., 1, 75
Verbruggen, G. and Veys, E. M. (1980). J. Rheumatol., (In press)
Verbruggen, G. and Veys, E. M. (1979). J. Rheumatol, 6, 554
Green, W. T. (1971). Clin. Orthop. Relat. Res., 75, 248
Reissig, etal. (1955). J. Biol. Chem., 217, 959
Levine, M. G. and Kling, D. M. (1956). J. Clin. Invest., 35, 1419
Enislidis, A. C. (1972). Med. Welt, 23, 733
Ueno, R. (1976). Z. Orthop. Ihre Grenzgeb., 114, 105
Muir, H. (personal communication)
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1980 MTP Press Limited
About this chapter
Cite this chapter
Verbruggen, G., Veys, E.M., Luyten, F.P., Suykens, S. (1980). Some ‘anti-arthritic’ properties of an oversulphated glycosaminoglycan in degenerative joint disease. In: Willoughby, D.A., Giroud, J.P. (eds) Inflammation: Mechanisms and Treatment. Inflammation: Mechanisms and Treatment, vol 4. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-9423-8_22
Download citation
DOI: https://doi.org/10.1007/978-94-010-9423-8_22
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-010-9425-2
Online ISBN: 978-94-010-9423-8
eBook Packages: Springer Book Archive