Expression Of Voltage Gated Sodium Channel Nav1.7in Rat Pulpitis

Objective Voltage gated sodium channel Nav1.7expresses specifically in peripheral nervous system, and plays a key role in regulating the action potential. It underlies pain associated with tissue injury and inflammation. The nerve fibers in pulp tissue is nociceptor. The normal pulp seems insensitive to exteroceptive stimulate. However, in pathological states, electrical, thermal, mechanical and chemical stimulate all could produce nocieptive responses to pulp. This study aimed to determine the expression level of Nav1.7in inflamed pulps of rats, and to investigate the relationship between dental pain and Nav1.7expression level. In order to provide novel view for relieving the tooth pain efficiently.Methods48rats were randomly divided into4groups (12rats in each group):a nontreatment group (A); three inflammation groups:day1(B), day3(C) and day5(D).Inflammation was induced by creating pulp exposures to LPS in rat incisors. Histopathological changes in the induced pulpitis were evaluated0,1,3,5days after exposure. Using immunohistochemistry, ELISA(Enzyme-linked immunosorbent assay) and RT-PCR (reverse transcription polymerase chain reaction) to determine the expression of Nav1.7in normal pulps and inflamed pulps of rats.Results At day1, no inflammation was evident in the pulp tissue, whereas increased levels of inflammatory responses were identified at day3and day5. The Immunohistochemistry results revealed that Nav1.7was expressed in all rat dental pulp and increased significantly at day3and day5after treatment compared with control group (P<0.05). And ELISA showed similar results. RT-PCR results also demonstrated that Nav1.7mRNA up-regulation significantly at day3and day5after treatment compared with normal group(P<0.05).Conclusions The results showed that the expression level of Nav1.7increased significantly in painful dental pulp tissue, suggesting that Nav1.7may play a possible role in the development and transmission of dental pain. Nav1.7channels seem to be expressed significantly more under a temporal control so as to be associated with a severity of inflammation during pulpitis. As Nav1.7has been considered to play a role in pain, its expression within dental pulp may contribute to the pathophysiology of tooth pain. Thus speculated that specifically block the expression or function of Nav1.7may inhibit the pain sensitization process of pulpitis, resulting in a analgesic effect with no side effects.