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Endoplasmic reticulum stress and mineralization inhibition mechanism by the resinous monomer HEMA

E Diamanti1, S Mathieu, C Jeanneau

  • 1Departments of Endodontics and Basic Sciences, Dental School, University of Athens, Athens, Greece. ediamanti@dent.uoa.gr

International Endodontic Journal
|August 15, 2012
PubMed
Abstract

Insights

Resinous monomers like HEMA increase ERdj5 and BiP chaperone proteins, indicating ER stress. This may inhibit dentine mineralization by disrupting DSP and OSN secretion.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Dental Materials Science

Background:

  • Resinous monomers are used in dental restorative materials.
  • Some monomers, like 2-hydroxyethyl methacrylate (HEMA), can inhibit biomineralization.
  • The cellular mechanisms underlying HEMA-induced mineralization inhibition are not fully understood.

Purpose of the Study:

  • To investigate the expression of ERdj5 and BiP chaperone proteins in human pulp cells exposed to HEMA.
  • To explore the relationship between ERdj5 and BiP expression and HEMA-induced inhibition of mineralization.
  • To examine the effect of HEMA on the expression and localization of odontoblast markers (DSP and OSN).

Main Methods:

  • In vitro study using primary human pulp cell cultures.
  • Treatment with three different concentrations of HEMA over various time periods.
  • Analysis of ERdj5, BiP, dentine sialoprotein (DSP), and osteonectin (OSN) expression and localization.

Main Results:

  • ERdj5 and BiP expression were upregulated in pulp cells following HEMA exposure.
  • DSP and OSN, normally dispersed in the cytoplasm, accumulated in a perinuclear area after HEMA treatment.
  • Expression levels of DSP and OSN were not significantly affected by HEMA.

Conclusions:

  • Increased ERdj5 and BiP expression suggests activation of endoplasmic reticulum (ER) stress in response to HEMA.
  • Accumulation of DSP and OSN within cells may cause secretion arrest, inhibiting dentine matrix formation.
  • These findings elucidate a potential mechanism for HEMA-induced inhibition of mineralization.

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