Effects of Lidocaine and Articaine on Neuronal Survival and Recovery
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Degree type
Discipline
Subject
Calcium
Delayed responsiveness
Lidocaine
Neurons
Neurotoxicity
Paresthesia
Sodium channel
Anesthetics
Local
Calcium Signaling
Carticaine
Cell Line
Tumor
Cell Survival
Humans
Lidocaine
NAV1.2 Voltage-Gated Sodium Channel
NAV1.7 Voltage-Gated Sodium Channel
Neurons
Neurotoxicity Syndromes
Risk Assessment
Time Factors
Voltage-Gated Sodium Channel Blockers
articaine
lidocaine
local anesthetic agent
SCN2A protein
human
SCN9A protein
human
sodium channel Nav1.2
sodium channel Nav1.7
voltage gated sodium channel blocking agent
calcium signaling
cell survival
comparative study
drug effect
human
metabolism
nerve cell
pathology
risk assessment
time factor
toxicity and intoxication
tumor cell line
Dental Materials
Dentistry
Endodontics and Endodontology
Oral and Maxillofacial Surgery
Oral Biology and Oral Pathology
Orthodontics and Orthodontology
Periodontics and Periodontology
Prosthodontics and Prosthodontology
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Abstract
The local anesthetics lidocaine and articaine are among the most widely used drugs in the dentist’s arsenal, relieving pain by blocking voltage-dependent Naþ 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. © 2018 by the American Dental Society of Anesthesiology.