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Three-dimensional Inflammatory Human Tissue Equivalents of Gingiva
Published on: April 3, 2018
2-Hydroxyethyl methacrylate inflammatory effects in human gingival fibroblasts
C Di Nisio1, S Zara, A Cataldi
1Dipartimento di Farmacia, Università G. d'Annunzio, Chieti-Pescara, Italy.
International Endodontic Journal
|November 10, 2012
Summary
Low concentrations of 2-hydroxyethyl methacrylate (HEMA) induce inflammation in human gingival fibroblasts (HGFs). This involves increased reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), cyclooxygenase-2 (COX-2) gene expression, and prostaglandin E2 (PGE₂) release.
Area of Science:
- Oral biology
- Dental materials science
- Inflammation research
Background:
- 2-Hydroxyethyl methacrylate (HEMA) is a common monomer in dental materials.
- Understanding HEMA's inflammatory potential in oral cells is crucial for material safety.
- Human gingival fibroblasts (HGFs) are key cells involved in the oral inflammatory response.
Purpose of the Study:
- To investigate the inflammatory response of HGFs to low-concentration HEMA.
- To assess the role of reactive oxygen species (ROS) in HEMA-induced inflammation.
- To quantify changes in key inflammatory markers: COX-2, TNF-α, and PGE₂.
Main Methods:
- HGFs were treated with 3 mmol L⁻¹ HEMA for 0, 24, or 96 hours.
- ROS production was measured using flow cytometry.
- Gene expression (COX-2, TNF-α) was analyzed by RT-PCR, and PGE₂ release was quantified via enzyme immunoassay.
Main Results:
- HEMA significantly increased ROS levels (8-11 fold) after 24 and 96 hours.
- COX-2 gene expression elevated (2-4 fold) with HEMA exposure.
- TNF-α mRNA levels increased (66% at 24h, 5-fold at 96h), and PGE₂ release rose by 17% after 96h.
Conclusions:
- Low-dose HEMA (3 mmol L⁻¹) triggers an inflammatory response in HGFs.
- This response is mediated by ROS production.
- Increased TNF-α and COX-2 gene expression, along with PGE₂ release, contribute to HEMA-induced inflammation.

