Related Experiment Video
Updated: Jul 5, 2026
05:16
Establishment of a Murine Pulp Exposure Model with a Novel Mouth-Gag for Pulpitis Research
Published on: October 27, 2023
Nav1.7 expression is increased in painful human dental pulp
Songjiang Luo1, Griffin M Perry, S Rock Levinson
1Department of Endodontics, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. luos@uthscsa.edu
Molecular Pain
|April 23, 2008
Summary
Increased sodium channel (NaCh) Nav1.7 expression in dental pulp nerves, particularly at nodes of Ranvier, contributes to toothache pain. This study reveals NaCh remodeling in demyelinating axons as a key factor in pulpal pain mechanisms.
Area of Science:
- Neuroscience
- Pain Research
- Dental Research
Background:
- Sodium channels (NaCh) are implicated in pain generation.
- Nav1.7 NaCh isoform expression changes in inflammatory lesions.
- Extracted human teeth serve as a model for peripheral pain mechanisms.
Purpose of the Study:
- Examine Nav1.7 NaCh isoform expression in normal versus painful human dental pulp.
- Investigate the role of Nav1.7 in pulpal pain.
Main Methods:
- Utilized pulpal sections labeled with antibodies for Nav1.7, N52, PGP9.5, caspr, and myelin basic protein (MBP).
- Employed confocal microscopy for z-series imaging.
- Quantified Nav1.7 immunofluorescence and evaluated nodal expression using NIH ImageJ software.
Main Results:
- Observed significant increases in nerve area with Nav1.7 expression in painful dental pulp.
- Found elevated Nav1.7 expression at both typical and atypical nodes of Ranvier.
- Identified Nav1.7 augmentation in demyelinating axons, suggesting NaCh remodeling.
Conclusions:
- Increased axonal Nav1.7 expression and augmentation at intact and remodeling nodes contribute to toothache pain.
- Changes in Nav1.7 at nodes of Ranvier may underlie constant, increased evoked, and spontaneous pain responses.
- NaCh remodeling in demyelinating axons is identified as a potential pulpal pain mechanism.
