OR20 - Quantification and Characterization of Mechanosensitive Innervation in Apical Periodontitis

Mechanical allodynia, a hallmark of apical periodontitis (AP), is thought to be caused by peripheral and central sensitization. However, the mechanisms of peripheral mechanical transduction in AP are poorly understood. Recently, the ionotropic channel Piezo2 has been found to be the main mechanotransducer in proprioceptive and nociceptive nerve fibers. We hypothesized that Piezo2 expression in periradicular innervation increases in AP. To test this hypothesis, we employed an AP model in transgenic mice with the expression of the fluorescent molecule TdTomato under the Piezo2 promoter control. Mice had pulp exposures in their first mandibular molar or sham procedures on the contralateral tooth (five serial sections/mouse; n=3 mice). After 21 days Piezo2 expression was visualized by scanning laser confocal microscopy. Expression was quantified using a subtractive threshold in Image J by blinded observers. The percent of Piezo2 positive expression within the total apical lesion area was compared to contralateral control using a student’s T-test (p < 0.05). There was an approximately 60% increase (p=0.04) in Piezo2 expression in apical lesions compared to contralateral control. This expression was primarily found in nociceptive fibers surrounding the apical lesion sites. These novel findings suggest that neurophysiological changes in AP include an increased receptor field with enrichment of mechanosensitive transduction. Thus, AP leads to remarkable neurophysiological changes and the results of this study have strong clinical translation to better understand biological changes that under lie symptoms during disease progression and resolution.