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Mechanisms underlying ectopic persistent tooth-pulp pain following pulpal inflammation
Shingo Matsuura1, Kohei Shimizu, Masamichi Shinoda
1Department of Endodontics, Nihon University School of Dentistry, Tokyo, Japan.
Plos One
|January 24, 2013
Summary
Tooth pulp inflammation in one tooth can cause persistent pain in adjacent teeth. This occurs due to activated trigeminal ganglion (TG) satellite cells and shared nerve pathways, increasing pain signaling.
Area of Science:
- Neuroscience
- Pain Research
- Dental Research
Background:
- Ectopic persistent pain in tooth pulp following adjacent tooth inflammation is a clinical challenge.
- Peripheral mechanisms underlying this referred pain are not fully understood.
Purpose of the Study:
- To investigate the role of trigeminal ganglion (TG) satellite cell activation and neuronal innervation patterns in ectopic tooth pulp pain.
- To clarify the peripheral mechanisms contributing to persistent pain in non-inflamed teeth adjacent to an inflamed tooth.
Main Methods:
- Induction of molar tooth pulp inflammation (M1) in rats using Complete Freund's Adjuvant (CFA).
- Application of capsaicin to an adjacent molar tooth pulp (M2) to assess pain response.
- Immunohistochemistry for phosphorylated extracellular signal-regulated protein kinase (pERK), TRPV1, and glial fibrillary acidic protein (GFAP) in the TG.
- Neuronal tracing using Fluorogold (FG) and DiI to identify TG neuron innervation patterns.
- Administration of a satellite cell inhibitor (fluorocitrate) into the TG.
Main Results:
- CFA-induced M1 inflammation significantly increased masseter muscle activity and pERK-immunoreactive (IR) TG cells upon M2 stimulation.
- Satellite cell activation in the TG was linked to increased M2-evoked masseter activity.
- TRPV1 expression in TG cells innervating M2 was elevated following M1 inflammation and reduced by satellite cell inhibition.
- A subset of TG neurons (6%) innervated both M1 and M2, indicating shared innervation.
Conclusions:
- Satellite cell activation in the TG plays a crucial role in mediating ectopic pain signaling from inflamed to adjacent non-inflamed teeth.
- Enhanced TRPV1 expression in TG neurons and shared innervation of multiple tooth pulps by single TG neurons contribute to referred tooth pain.
- These findings elucidate peripheral mechanisms involved in persistent ectopic tooth pain, offering potential targets for pain management.
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