IL-1 alpha and TNF-alpha expression in rat periapical lesions and dental pulp after unilateral sympathectomy

Neuroimmunomodulation. 2004;11(6):376-84. doi: 10.1159/000080148.

Abstract

Objectives: Apical periodontitis is an inflammatory disease characterized by bone resorption, and sympathetic nerves are known to modulate bone resorption and bone remodeling. Higher numbers of osteoclasts and larger periapical lesions have been observed after sympathectomy in rats, but the mechanisms underlying the inhibitory effect of sympathetic nerves on osteoclasts are unknown. This study aimed to test the hypothesis that sympathetic nerves inhibit the production of the bone-resorbing pro-inflammatory cytokines IL-1 alpha and TNF-alpha in rat periapical lesions.

Methods: Rats were unilaterally sympathectomized and apical lesions were induced by exposing the dental pulp of molar teeth to the oral microflora. We quantified the cytokines IL-1 alpha and TNF-alpha by enzyme-linked immunosorbent assay, and immunohistochemical analysis was done for qualitative localization. Pulp from intact incisor teeth was tested as a control.

Results: We showed that IL-1 alpha was increased, but not TNF-alpha, in the periapical lesions on the sympathectomized side. Both IL-1 alpha and TNF-alpha were expressed in unexposed pulp. TNF-alpha was significantly decreased in the denervated incisor pulp, whereas the level of IL-1 alpha remained unchanged.

Conclusions: This study suggests that sympathetic nerves have an inhibitory effect on IL-1 alpha in periapical lesions and a stimulatory effect on TNF-alpha in the intact rat pulp.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone Resorption / immunology
  • Bone Resorption / physiopathology
  • Cytokines / metabolism*
  • Denervation
  • Dental Pulp / immunology*
  • Dental Pulp / innervation*
  • Dental Pulp / physiopathology
  • Disease Models, Animal
  • Down-Regulation / immunology
  • Immunohistochemistry
  • Interleukin-1 / metabolism
  • Male
  • Neural Inhibition / immunology
  • Neuroimmunomodulation / physiology*
  • Neuropeptides / metabolism
  • Osteoclasts / immunology
  • Periapical Periodontitis / immunology*
  • Periapical Periodontitis / physiopathology
  • Rats
  • Rats, Sprague-Dawley
  • Sympathetic Fibers, Postganglionic / injuries
  • Sympathetic Fibers, Postganglionic / physiology*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • Interleukin-1
  • Neuropeptides
  • Tumor Necrosis Factor-alpha