Departmental Papers (Dental)

Document Type

Journal Article

Date of this Version


Publication Source

Scientific Reports





Start Page

Article number 2759




Injury of the tooth pulp is excruciatingly painful and yet the receptors and neural circuit mechanisms that transmit this form of pain remain poorly defined in both the clinic and preclinical rodent models. Easily quantifiable behavioral assessment in the mouse orofacial area remains a major bottleneck in uncovering molecular mechanisms that govern inflammatory pain in the tooth. In this study we sought to address this problem using the Mouse Grimace Scale and a novel approach to the application of mechanical Von Frey hair stimuli. We use a dental pulp injury model that exposes the pulp to the outside environment, a procedure we have previously shown produces inflammation. Using RNAscope technology, we demonstrate an upregulation of genes that contribute to the pain state in the trigeminal ganglia of injured mice. We found that mice with dental pulp injury have greater Mouse Grimace Scores than sham within 24 hours of injury, suggestive of spontaneous pain. We developed a scoring system of mouse refusal to determine thresholds for mechanical stimulation of the face with Von Frey filaments. This method revealed that mice with a unilateral dental injury develop bilateral mechanical allodynia that is delayed relative to the onset of spontaneous pain. This work demonstrates that tooth pain can be quantified in freely behaving mice using approaches common for other types of pain assessment. Harnessing these assays in the orofacial area during gene manipulation should assist in uncovering mechanisms for tooth pulp inflammatory pain and other forms of trigeminal pain. © 2020, The Author(s).


Animals, Behavior, Animal, Dental Pulp, Disease Models, Animal, Gene Expression Profiling, Gene Expression Regulation, Humans, Hyperalgesia, Inflammation, Male, Mice, Mice, Inbred C57BL, Nerve Tissue Proteins, Pain, Pain Measurement, Severity of Illness Index, Tooth Injuries, Trigeminal Ganglion, nerve protein, animal, animal behavior, C57BL mouse, disease model, gene expression profiling, gene expression regulation, genetics, human, hyperalgesia, inflammation, injury, innervation, male, metabolism, mouse, pain, pain measurement, pathophysiology, procedures, severity of illness index, tooth injury, tooth pulp, trigeminus ganglion



Date Posted: 10 February 2023

This document has been peer reviewed.