Effects of interleukin-1 beta on human pulpal fibroblast proliferation and collagen synthesis

J Endod. 1998 Jun;24(6):409-13. doi: 10.1016/S0099-2399(98)80022-8.

Abstract

The aim of this study was to investigate the effect of interleukin-1 beta (IL-1 beta) on pulpal fibroblast proliferation and collagen synthesis in vitro. Cell proliferation was assessed by [3H]thymidine uptake at 24, 48, and 72 h. These cells were compared with dermal fibroblasts under a range of conditions. IL-1 beta inhibited pulp cell proliferation, but this effect was decreased by the presence of indomethacin. In contrast, IL-1 beta stimulated dermal fibroblast proliferation in the absence and presence of indomethacin. Collagen synthesis was analyzed by incorporation of 5-[3H]proline into polypeptide chains. IL-1 beta stimulated synthesis of type I collagen both in the absence and presence of indomethacin. Results suggest that the inhibitory effect on pulp cell proliferation is dependent upon IL-1 beta-induced prostaglandin E2 synthesis and that IL-1 beta is a potent mediator of prostaglandin E2 synthesis in dental pulp. These observations imply a role of IL-1 beta in collagen synthesis, but not in the fibroblast proliferation phase of the healing process.

MeSH terms

  • Analysis of Variance
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Cell Division / drug effects
  • Collagen / biosynthesis*
  • Dental Pulp / cytology
  • Dental Pulp / drug effects*
  • Dental Pulp / metabolism
  • Dose-Response Relationship, Drug
  • Fibroblasts / cytology
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Humans
  • Indomethacin / pharmacology
  • Inflammation Mediators / pharmacology*
  • Interleukin-1 / pharmacology*

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Inflammation Mediators
  • Interleukin-1
  • Collagen
  • Indomethacin