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Effects of Lidocaine and Articaine on Neuronal Survival and Recovery.

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 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.

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  • Authors+Show Affiliations

    ,

    Department of Anatomy and Cell Biology, University of Pennsylvania School of Dental Medicine, Philadelphia, Pennsylvania. Department of Orthodontics, University of Pennsylvania School of Dental Medicine, Philadelphia, Pennsylvania.

    ,

    Department of Anatomy and Cell Biology, University of Pennsylvania School of Dental Medicine, Philadelphia, Pennsylvania.

    ,

    Department of Anatomy and Cell Biology, University of Pennsylvania School of Dental Medicine, Philadelphia, Pennsylvania.

    ,

    Department of Oral & Maxillofacial Surgery/Pharmacology, University of Pennsylvania School of Dental Medicine, Philadelphia, Pennsylvania.

    Department of Anatomy and Cell Biology, University of Pennsylvania School of Dental Medicine, Philadelphia, Pennsylvania. Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, and. Department of Ophthalmology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.

    Source

    Anesthesia progress 65:2 2018 pg 82-88

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    29952644

    Citation

    TY - JOUR T1 - Effects of Lidocaine and Articaine on Neuronal Survival and Recovery. AU - Albalawi,Farraj, AU - Lim,Jason C, AU - DiRenzo,Kyle V, AU - Hersh,Elliot V, AU - Mitchell,Claire H, PY - 2018/6/29/entrez PY - 2018/6/29/pubmed PY - 2018/6/29/medline KW - Articaine KW - Calcium KW - Delayed responsiveness KW - Lidocaine KW - Neurons KW - Neurotoxicity KW - Paresthesia KW - Sodium channel SP - 82 EP - 88 JF - Anesthesia progress JO - Anesth Prog VL - 65 IS - 2 N2 - 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. SN - 1878-7177 UR - https://www.unboundmedicine.com/medline/citation/29952644/Effects_of_Lidocaine_and_Articaine_on_Neuronal_Survival_and_Recovery L2 - http://www.anesthesiaprogress.org/doi/10.2344/anpr-65-02-02?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed ER -