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Background: Masticatory muscle pain may occur following immediate occlusal alteration by dental treatment. The underlying mechanisms are poorly understood. Transient receptor potential vanilloid-1 (TRPV1) and acid-sensing ion channel-3 (ASIC3) mediate muscle hyperalgesia under various pathologic conditions. We have developed a rat model of experimental occlusal interference (EOI) that consistently induces mechanical hyperalgesia in jaw muscles. Whether TRPV1 and ASIC3 mediate this EOI-induced hyperalgesia is unknown., Methods: Rat model of EOI-induced masseter hyperalgesia was established. Real-time polymerase chain reaction, Western blot and retrograde labelling combined with immunofluorescence were performed to evaluate the modulation of TRPV1 and ASIC3 expression in trigeminal ganglia (TGs) and masseter afferents of rats after EOI. The effects of intramuscular administration of TRPV1 and ASIC3 antagonists on the EOI-induced hyperalgesia in masseter muscle were examined., Results: After EOI, gene expressions and protein levels of TRPV1 and ASIC3 in bilateral TGs were up-regulated. The percentage of ASIC3- (but not TRPV1-) positive neurons in masseter afferents increased after EOI. More small-sized and small to medium-sized masseter afferents expressed TRPV1 and ASIC3 separately following EOI. These changes peaked at day 7 and then returned to original status within 10 days after EOI. Intramuscular administration of the TRPV1 antagonist AMG-9810 partially reversed this mechanical hyperalgesia in masseter muscle. No improvement was exhibited after administration of the ASIC3 antagonist APETx2. Co-injection of AMG-9810 and APETx2 enhanced the effect of AMG-9810 administration alone., Conclusions: Peripheral TRPV1 and ASIC3 contribute to the development of the EOI-induced mechanical hyperalgesia in masseter muscle., (© 2015 European Pain Federation - EFIC®)

Background: Patients with an orofacial pain history appear to be more susceptible to occlusal interference pain in dental practice for unknown reasons. Pain memory has a critical function in subsequent pain perception. This study aims to explore whether orofacial pain memory could affect the masticatory muscle pain perception for occlusal interference., Methods: Cross-injection of 2% carrageenan into bilateral masseters in male rats was carried out to establish the inflammatory pain memory model. The effects of pain memory on masseter muscle nociception were tested by applying crowns with heights beyond the occlusal plane by 0.2 or 0.4 mm onto a maxillary molar 2 weeks after inflammation in the right masseter. The 0.4-mm crowns were removed on day 2 or day 4 after application to further confirm the effects of pain memory. Moreover, memory impairment was established using ibotenic acid (IBO) infusion into the bilateral hippocampus, followed by behaviour tests, including the Morris water maze test and the locomotor activity test. The relationship between pain memory and occlusal interference-induced masseter muscle pain perception was subsequently re-examined. The head withdrawal thresholds of masseters on both sides were measured to reflect the perception., Results: Inflammatory pain memory aggravated the 0.2-mm crown-induced mechanical hyperalgesia of the masseters, but not in the 0.4-mm crown group. However, the recovery of the 0.4-mm crown-induced mechanical hyperalgesia was postponed. The effects of pain memory were reversed in rats with impaired mnemonic function of the hippocampus., Conclusions: Inflammatory pain memory facilitated occlusal interference-induced masseter muscle pain., (© 2015 European Pain Federation - EFIC®)