Immunohistologic study of the ruptured intervertebral disc of the lumbar spine

M Doita1, T Kanatani, T Harada

  • 1Department of Orthopedic Surgery, Kobe University School of Medicine, Japan.

Spine
|January 15, 1996
PubMed

Insights

Inflammatory cells in extruded discs express mediators that may cause new blood vessel growth and chronic inflammation. This study clarifies the pathogenesis of neovascularization in herniated lumbar discs.

Area of Science:

  • Spine surgery
  • Immunohistology
  • Cell biology

Background:

  • Herniated discs can trigger autoimmune responses and chronic inflammation.
  • The exact mechanisms of inflammatory cell infiltration and neovascularization in herniated discs are not fully understood.

Purpose of the Study:

  • To characterize the histological features of extruded/sequestrated discs and infiltrating inflammatory cells.
  • To clarify the pathogenesis of neovascularization at the disc tissue edge.

Main Methods:

  • Immunohistological analysis of herniated lumbar discs using specific antibody stains.
  • Culture of herniated disc cells and measurement of basic fibroblast growth factor (bFGF).
  • Coculture of disc cells with human endothelial cells to assess proliferation.

Main Results:

  • Vascularized granulation tissue was observed at the edge of extruded and sequestrated discs.
  • Infiltrating mononuclear cells expressed interleukin-1, intercellular adhesion molecule-1, lymphocyte function-associated antigen, and bFGF.
  • Herniated disc cells showed higher bFGF levels and enhanced endothelial cell proliferation.

Conclusions:

  • Mononuclear cells in extruded discs express inflammatory mediators.
  • These mediators may induce neovascularization and sustain inflammation in herniated discs.
Abstract

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