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Establishment of a Murine Pulp Exposure Model with a Novel Mouth-Gag for Pulpitis Research
Published on: October 27, 2023
Angiogenic signaling triggered by cariogenic bacteria in pulp cells
R I Soden1, T M Botero, C T Hanks
1Department of Cariology, Restorative Sciences, and Endodontics, University of Michigan School of Dentistry, 1011 N. University, Rm. 2309, Ann Arbor, MI 48103-1078, USA.
Journal of Dental Research
|September 22, 2009
Summary
Lipoteichoic acid (LTA) from bacteria triggers vascular endothelial growth factor (VEGF) in dental pulp cells via TLR2 and PI3K/Akt signaling. This pathway is crucial for pulpitis inflammation and may offer new therapeutic targets.
Area of Science:
- Oral Biology
- Immunology
- Cell Signaling
Background:
- Deep caries lesions cause dental pulp inflammation with increased blood vessel density.
- Gram-positive cariogenic bacteria-derived lipoteichoic acid (LTA) is known to induce vascular endothelial growth factor (VEGF) in dental pulp cells.
Purpose of the Study:
- To investigate the signaling pathways, specifically Toll-like receptor 2 (TLR2) and PI3K/Akt, involved in LTA-induced VEGF expression in dental pulp cells.
- To determine if IKK signaling plays a role in this process.
Main Methods:
- Exposed odontoblast-like (MDPC-23) and undifferentiated pulp cells (OD-21) to LTA from Streptococcus sanguis.
- Evaluated the role of TLR2, PI3K/Akt, and IKK signaling pathways using specific inhibitors.
Main Results:
- TLR2 signaling via the PI3K-Akt pathway was found to be essential for LTA-induced VEGF expression in pulp cells.
- Inhibition of IKK signaling did not affect VEGF up-regulation in response to LTA.
Conclusions:
- TLR2 and PI3K-Akt signaling are necessary for lipoteichoic acid-induced VEGF expression in dental pulp cells.
- Understanding these pathways can identify novel therapeutic targets for managing pulpitis.
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