Innervation Changes in Apical Periodontitis and its Correlation with Preoperative Symptoms

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.