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Accessing the Cytotoxicity and Cell Response to Biomaterials
Published on: July 8, 2021
Dentin matrix protein-1 activates dental pulp fibroblasts
Ashraf Abd-Elmeguid1, Donald C Yu, Loren W Kline
1Department of Dentistry, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Journal of Endodontics
|December 14, 2011
Summary
Dentin matrix protein-1 (DMP-1) is found in inflamed dental pulps and stimulates inflammatory responses in pulp fibroblasts. Inhibiting DMP-1 may offer a new therapeutic strategy for dental pulp inflammation and calcification.
Area of Science:
- Dental research
- Biomedical science
- Cell biology
Background:
- Dentin matrix protein-1 (DMP-1) plays a role in hard dental tissue mineralization.
- The function of DMP-1 in soft tissues, including the dental pulp, is not well understood.
Purpose of the Study:
- To investigate the role of DMP-1 in dental pulp inflammation and pathologic calcification.
- To determine the effect of DMP-1 on inflammatory mediator production by dental pulp cells.
Main Methods:
- Immunohistochemistry was used to localize DMP-1 in human inflamed and normal dental pulps.
- Primary human pulp fibroblasts were cultured and treated with DMP-1.
- Enzyme-linked immunosorbent assay (ELISA) measured the production of interleukin-6 (IL-6) and IL-8.
- Flow cytometry and immunofluorescence identified fibroblast markers.
- The effect of p38 mitogen-activated protein kinase pathway inhibition was assessed.
Main Results:
- DMP-1 was detected in inflamed dental pulps and associated with areas of calcification.
- DMP-1 significantly stimulated the production of IL-6 and IL-8 by pulp fibroblasts.
- DMP-1 exhibited an additive effect with lipopolysaccharide (LPS) on cytokine production.
- Inhibition of the p38 MAPK pathway abrogated the pro-inflammatory effects of DMP-1.
Conclusions:
- DMP-1 appears to contribute to inflammatory processes and pathologic calcification in the dental pulp.
- Targeting DMP-1 could be a potential therapeutic approach for managing dental pulp inflammation and calcification.
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