Pulpitis pain relief by modulating sodium channels in trigeminal ganglia
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Objectives: The pulp is the center of the tooth containing nerves and blood vessels. The condition in which the pulp becomes inflamed due to caries or periodontitis is called pulpitis. Pulpitis is a difficult-to-treat disease and causes peripheral nerve tissue changes and severe pain; however, the relationship between neuronal activity and voltage-gated sodium channel 1.7 (Nav1.7) expression in the trigeminal ganglion (TG) during pulpitis has not been well studied. In this study, we found that experimentally induced pulpitis activates Nav1.7 expression in the periphery, leading to neuronal overexpression in the TG. Thus, we sought to identify ways to regulate this process. Methods: Acute pulpitis was induced in rat maxillary molars by treating the pulp with allyl isothiocyanate (AITC). Three days later, in vivo optical imaging was used to record and compare neural activities in the TG. Western blotting was used to identify molecular changes in terms of the expression of extracellular signal-regulated kinase (ERK), c-Fos, transient receptor potential ankyrin 1 (TRPA1), and collapsin response mediator protein-2 (CRMP2) in the brain stem. Results: The results confirmed the neurological changes in the TGs of the pulpitis model, and histological and molecular biological evidence confirmed that increased Nav1.7 expression induced by pulpitis leads to pain. Furthermore, selective inhibition of Nav1.7 resulted in changes in neural activity, suggesting that pulpitis induces increased Nav1.7 expression, and that effective control of Nav1.7 could potentially reduce pain. Conclusions: The inhibition of overexpressed Nav1.7 channels may modulate nociceptive signal processing in the brain and effectively control pain associated with pulpitis.
Abstract
Objectives: The pulp is the center of the tooth containing nerves and blood vessels. The condition in which the pulp becomes inflamed due to caries or periodontitis is called pulpitis. Pulpitis is a difficult-to-treat disease and causes peripheral nerve tissue changes and severe pain; however, the relationship between neuronal activity and voltage-gated sodium channel 1.7 (Nav1.7) expression in the trigeminal ganglion (TG) during pulpitis has not been well studied. In this study, we found that experimentally induced pulpitis activates Nav1.7 expression in the periphery, leading to neuronal overexpression in the TG. Thus, we sought to identify ways to regulate this process. Methods: Acute pulpitis was induced in rat maxillary molars by treating the pulp with allyl isothiocyanate (AITC). Three days later, in vivo optical imaging was used to record and compare neural activities in the TG. Western blotting was used to identify molecular changes in terms of the expression of extracellular signal-regulated kinase (ERK), c-Fos, transient receptor potential ankyrin 1 (TRPA1), and collapsin response mediator protein-2 (CRMP2) in the brain stem. Results: The results confirmed the neurological changes in the TGs of the pulpitis model, and histological and molecular biological evidence confirmed that increased Nav1.7 expression induced by pulpitis leads to pain. Furthermore, selective inhibition of Nav1.7 resulted in changes in neural activity, suggesting that pulpitis induces increased Nav1.7 expression, and that effective control of Nav1.7 could potentially reduce pain. Conclusions: The inhibition of overexpressed Nav1.7 channels may modulate nociceptive signal processing in the brain and effectively control pain associated with pulpitis.
참고문헌 (26)
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