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Related Concept Videos

Local Anesthetics: Differential Sensitivity of Nerve Fibers01:24

Local Anesthetics: Differential Sensitivity of Nerve Fibers

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Local anesthetics (LAs) block the sodium channels of nerve trunks, sensory nerve endings, and neuromuscular junctions. Although LAs can block all kinds of nerves, the sensitivity of nerve fibers differs according to nerve types and structures. LAs are known to block myelinated fibers faster than unmyelinated ones. Also, they block pain or sensory neurons at low concentrations without affecting the motor neurons involved in muscle contractions. This helps relieve labor pain without affecting the...
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Assessment of apical radial pulse01:25

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Apical-Radial (A-R) Pulse Assessment
The A-R pulse assessment involves simultaneous evaluation of the apical and radial pulses. When the apical and radial pulse rates vary, this assessment helps identify a pulse deficit.
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Related Experiment Video

Updated: Sep 12, 2025

Inducing Apical Periodontitis in Mice
10:26

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Innervation Changes in Apical Periodontitis and its Correlation with Preoperative Symptoms.

Austah Obadah1, Johnathan Fu2, David Wong2

  • 1Department of Endodontics, University of Texas Health Science Center at San Antonio, San Antonio, Texas; Faculty of Dentistry, Department of Endodontics, King Abdulaziz University, Jeddah, Saudi Arabia.

Journal of Endodontics
|August 7, 2025
PubMed
Summary

Symptomatic apical periodontitis (AP) shows significantly increased sensory nerve density and expression of pain-related sodium channels Nav1.8 and Nav1.9. These neural changes likely contribute to AP pain and anesthesia resistance.

Keywords:
Apical periodontitisNav1.8biopsyinnervationpain

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Area of Science:

  • Neuroscience
  • Oral Biology
  • Pain Research

Background:

  • Apical periodontitis (AP) lesion cellularity is known, but neural innervation remains understudied.
  • Periapical innervation influences AP cellular responses and pain.
  • Nav1.8 and Nav1.9 sodium channels are implicated in pain signaling.

Purpose of the Study:

  • To quantify sensory innervation in AP lesions.
  • To evaluate Nav1.8 and Nav1.9 expression in symptomatic versus asymptomatic AP.
  • To understand the role of neural changes in AP pain.

Main Methods:

  • Soft tissue biopsies from endodontic microsurgery (n=20).
  • Protein extraction and immunohistochemistry for neural markers (β-tubulin III, CGRP, NF-H, PGP9.5) and sodium channels (Nav1.8, Nav1.9).
  • Quantification via ELISA and confocal microscopy; statistical analysis using Mann-Whitney U test.

Main Results:

  • Symptomatic AP lesions had ~6-fold higher innervation density compared to asymptomatic lesions.
  • Significantly increased Nav1.8 and Nav1.9 expression in symptomatic AP.
  • Predominance of Nav1.8-expressing (nociceptive) nerve fibers in symptomatic lesions.

Conclusions:

  • Symptomatic AP exhibits heightened sensory innervation and elevated Nav1.8/Nav1.9 expression.
  • These neural alterations may drive AP pain mechanisms.
  • Increased innervation could explain challenges with local anesthesia in symptomatic AP.