The role of cellular interactions in joint erosions

Clin Orthop Relat Res. 1984 Jan-Feb:(182):24-30.

Abstract

Maintenance of the normal integrity of articular cartilage is due to a balance between the synthesis and degradation of the extracellular matrix. This balance is maintained as a result of the anabolic and catabolic activities of the indigenous cells, the chondrocytes. It is becoming understood that the metabolic activity of the chondrocytes can be modified by certain intercellular messengers. To date, two such intercellular messengers have been recognized and partially characterized: the interleukins and the catabolins. These messengers are probably part of a much wider family of proteins that function in the control of connective tissue structure in general. In terms of the arthritic diseases, the catabolins seem likely to play a role in the early stages of chondrocyte-mediated matrix degradation in osteoarthritis, (OA), while in rheumatoid arthritis (RA) the catabolins, probably coming from the fibroblastic cells of the synovium, and the interleukins, probably originating from the inflammatory cells of the pannus, may work in association with extrinsic proteinases secreted by a number of component cells of the inflammatory synovium. Recognition of the role of intercellular messengers in both the physiology and pathology of articular tissues provides new and exciting possibilities in pharmacodynamic systems for prevention of joint damage.

Publication types

  • Review

MeSH terms

  • Animals
  • Arthritis, Rheumatoid / metabolism*
  • Cartilage, Articular / enzymology
  • Cartilage, Articular / metabolism*
  • Cells, Cultured
  • Dinoprostone
  • Humans
  • Interleukin-1 / metabolism
  • Interleukin-1beta
  • Peptide Hydrolases / metabolism
  • Prostaglandins E / metabolism
  • Proteins / isolation & purification
  • Proteins / metabolism
  • Proteoglycans / metabolism
  • Synovial Membrane / cytology

Substances

  • Interleukin-1
  • Interleukin-1beta
  • Prostaglandins E
  • Proteins
  • Proteoglycans
  • Peptide Hydrolases
  • Dinoprostone