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Paradoxical surrogate markers of dental injury-induced pain in the mouse

Gibbs, Jennifer L.a,*,1; Urban, Rochelleb,1; Basbaum, Allan I.b

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doi: 10.1016/j.pain.2013.04.018
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In a chronic dental injury model, mice lose weight relative to controls despite maintaining food consumption, and increase consumption of a palliative sucrose solution.

Dental pain, including toothache, is one of the most prevalent types of orofacial pain, causing severe, persistent pain that has a significant negative effect on quality of life, including eating disturbances, mood changes, and sleep disruption. As the primary cause of toothache pain is injury to the uniquely innervated dental pulp, rodent models of this injury provide the opportunity to study neurobiological mechanisms of tissue injury-induced persistent pain. Here we evaluated behavioral changes in mice with a dental pulp injury (DPI) produced by mechanically exposing the pulp to the oral environment. We monitored the daily life behaviors of mice with DPI, including measures of eating, drinking, and movement. During the first 48 hours, the only parameter affected by DPI was locomotion, which was reduced. There was also a significant short-term decrease in the amount of weight gained by DPI animals that was not related to food consumption. As cold allodynia is frequently observed in individuals experiencing toothache pain, we tested whether mice with DPI demonstrate an aversion to drinking cold liquids using a cold-sucrose consumption test. Surprisingly, mice with DPI increased their consumption of sucrose solution, to over 150% of baseline, regardless of temperature. Both the weight loss and increased sucrose intake in the first 2 days of injury were reversed by administration of indomethacin. These findings indicate that enhanced sucrose consumption may be a reliable measure of orofacial pain in rodents, and suggest that alterations in energy expenditure and motivational behaviors are under-recognized outcomes of tooth injury.

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

aDepartment of Preventive and Restorative Dental Sciences, Division of Endodontics, UCSF School of Dentistry, San Francisco, CA, USA

bDepartment of Anatomy, University of California San Francisco, San Francisco, CA, USA

*Corresponding author. Present address: Department of Endodontics, Endodontics Clinic 7W, New York University College of Dentistry, 345 East 24th St. New York, NY 10010-4020, USA. Tel.: +1 212 998 9438; fax: +1 212 995 4834.

1These authors contributed equally to this work.

E-mail address: jlg15@nyu.edu

Submitted November 6, 2012; revised April 1, 2013; accepted April 9, 2013.

© 2013 Lippincott Williams & Wilkins, Inc.
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