Susceptibility of normal and arthritic human articular cartilage to degradative stimuli. 1992

S Ismaiel, and R M Atkins, and M F Pearse, and P A Dieppe, and C J Elson
Department of Pathology and Microbiology, University of Bristol.

Recombinant interleukin-1 (IL-1) alpha and beta stimulated significant loss of glycosaminoglcan (GAG) content from normal (non-arthritic) articular cartilage explants but only after incubation for 14 days and only in specimens from 8/21 (38%) individuals. By contrast, all cartilage specimens but one from patients with osteoarthritis (OA) and rheumatoid arthritis (RA) were degraded (as judged by their reduced GAG content) by the recombinant cytokines but again only after 14 days' incubation. The reduction in GAG induced by IL-1 was also greater for both OA and RA cartilage than normal cartilage. Synovial fluids (SFs) from RA patients stimulated greater loss of GAG content from OA cartilage explants than normal explants although in both cases the loss was evident within 2 days. It is concluded that cartilage explants from some individuals are susceptible to the degradative effects of IL-1 whereas others are refractory and that arthritic cartilage is more susceptible to degradation by both IL-1 and RA SFs than non-arthritic cartilage.

UI MeSH Term Description Entries
D007375 Interleukin-1 A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. IL-1,Lymphocyte-Activating Factor,Epidermal Cell Derived Thymocyte-Activating Factor,Interleukin I,Macrophage Cell Factor,T Helper Factor,Epidermal Cell Derived Thymocyte Activating Factor,Interleukin 1,Lymphocyte Activating Factor
D010003 Osteoarthritis A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. Arthritis, Degenerative,Osteoarthrosis,Osteoarthrosis Deformans,Arthroses,Arthrosis,Arthritides, Degenerative,Degenerative Arthritides,Degenerative Arthritis,Osteoarthritides,Osteoarthroses
D011994 Recombinant Proteins Proteins prepared by recombinant DNA technology. Biosynthetic Protein,Biosynthetic Proteins,DNA Recombinant Proteins,Recombinant Protein,Proteins, Biosynthetic,Proteins, Recombinant DNA,DNA Proteins, Recombinant,Protein, Biosynthetic,Protein, Recombinant,Proteins, DNA Recombinant,Proteins, Recombinant,Recombinant DNA Proteins,Recombinant Proteins, DNA
D002358 Cartilage, Articular A protective layer of firm, flexible cartilage over the articulating ends of bones. It provides a smooth surface for joint movement, protecting the ends of long bones from wear at points of contact. Articular Cartilage,Articular Cartilages,Cartilages, Articular
D005270 Femur Head The hemispheric articular surface at the upper extremity of the thigh bone. (Stedman, 26th ed) Femoral Head,Femoral Heads,Femur Heads,Head, Femoral,Head, Femur
D006025 Glycosaminoglycans Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine (see ACETYLGLUCOSAMINE) or N-acetylgalactosamine (see ACETYLGALACTOSAMINE). Glycosaminoglycan,Mucopolysaccharides
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000368 Aged A person 65 years of age or older. For a person older than 79 years, AGED, 80 AND OVER is available. Elderly
D000369 Aged, 80 and over Persons 80 years of age and older. Oldest Old
D001172 Arthritis, Rheumatoid A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated. Rheumatoid Arthritis

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