Skip to main content
Sign inSign up

ADSA Society

IssuesFor AuthorsAdvertisingNewsHelp

ADSA Society

Article Contents

Download PDF

The local anesthetics lidocaine and articaine are among the most widely used drugs in the dentist's arsenal, relieving pain by blocking voltage-dependent Na+ channels and thus preventing transmission of the pain signal. Given reports of infrequent but prolonged paresthesias with 4% articaine, we compared its neurotoxicity and functional impairment by screening cultured neural SH-SY5Y cells with formulations used in patients (2% lidocaine + 1:100,000 epinephrine or 4% articaine + 1:100,000 epinephrine) and with pure formulations of the drugs. Voltage-dependent sodium channels Na(v)1.2 and Na(v)1.7 were expressed in SH-SY5Y cells. To test the effects on viability, cells were exposed to drugs for 5 minutes, and after washing, cells were treated with the ratiometric Live/Dead assay. Articaine had no effect on the survival of SH-SY5Y cells, while lidocaine produced a significant reduction only when used as pure powder. To determine reversibility of blockage, wells were exposed to drugs for 5 minutes and returned for medium for 30 minutes, and the calcium elevation induced by depolarizing cells with a high-potassium solution was measured using the calcium indicator Fura-2. High potassium raised calcium in control SH-SY5Y cells and those treated with articaine, but lidocaine treatment significantly reduced the response. In conclusion, articaine does not damage neural cells more than lidocaine in this in vitro model. While this does not question the safety of lidocaine used clinically, it does suggest that articaine is no more neurotoxic, at least in the in vitro setting.

Keywords: Lidocaine; Articaine; Paresthesia; Sodium channel; Neurotoxicity; Delayed responsiveness; Calcium; Neurons
  • Download PDF
Copyright: © 2018 by the American Dental Society of Anesthesiology

Get Email Alerts

Article Contents
ANPR logo
AboutIssuesAuthor InformationSubscriptions

ADSA Society

eISSN: 1878-7177

ISSN: 0003-3006

Powered by PubFactory