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Epithelial Cell Apoptosis in Recurrent Aphthous Ulcers.

A Al-Samadi1, A Drozd2, A Salem3

  • 1Department of Medicine, Institute of Clinical Medicine, University of Helsinki, Helsinki, Finland Department of Anatomy, Institute of Biomedicine, University of Helsinki, Helsinki, Finland ahmed.al-samadi@helsinki.fi.

Journal of Dental Research
|April 12, 2015
PubMed
Summary
This summary is machine-generated.

Recurrent aphthous ulcers (RAUs) involve top-to-bottom epithelial cell apoptosis, unlike healthy mucosa. This process, potentially leading to secondary necrosis and inflammation, contributes to ulcer formation and the surrounding inflammatory halo.

Keywords:
HMGB1IFN-γTLRTNF-αcaspase-3oral mucosa

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Area of Science:

  • Oral pathology
  • Immunology
  • Cell biology

Background:

  • Recurrent aphthous ulcer (RAU) is a common oral mucosal lesion.
  • The cellular mechanisms driving RAU pathogenesis, particularly epithelial cell apoptosis and inflammation, require further elucidation.

Purpose of the Study:

  • To investigate the role of apoptosis and inflammation in RAU development.
  • To examine the expression of caspase-3, high-mobility group box 1 (HMGB1), and DNA damage markers in RAU lesions.
  • To explore the effects of specific inflammatory mediators and cellular components on oral keratinocytes.

Main Methods:

  • Immunohistochemistry for caspase-3 and HMGB1 on RAU and healthy mucosa samples.
  • TUNEL staining to detect DNA fragmentation.
  • In vitro studies on SCC-25 keratinocytes stimulated with tumor necrosis factor α (TNFα), interferon γ (IFNγ), self-DNA, and HMGB1 variants.

Main Results:

  • RAU lesions exhibited widespread epithelial cell apoptosis (caspase-3+, TUNEL+, HMGB1+) with widened intercellular spaces, contrasting with healthy mucosa.
  • Self-DNA induced TNFα mRNA in SCC-25 cells, and both TNFα and IFNγ upregulated toll-like receptor 2 (TLR2).
  • Disulfide-HMGB1 did not stimulate proinflammatory cytokines, unlike lipopolysaccharide.

Conclusions:

  • RAU is characterized by extensive, top-to-bottom epithelial apoptosis, leading to ulceration.
  • Secondary necrosis of apoptotic cells may release proinflammatory signals, contributing to the inflammatory halo, potentially due to insufficient anti-inflammatory macrophage activity.
  • HMGB1's role in RAU appears complex and distinct from its pro-inflammatory cytokine-inducing capacity in other contexts.