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Participation of IL-1β in temporomandibular nociception in rats with CFA-induced inflammation

  • Ju, Jin-Sook (Department of Oral Physiology, School of Dentistry, Kyungpook National University) ;
  • Choi, Seung-Ho (Department of Oral Physiology, School of Dentistry, Kyungpook National University) ;
  • Kim, Hye-Jin (Department of Oral Physiology, School of Dentistry, Kyungpook National University) ;
  • Son, Jo-Young (Department of Oral Physiology, School of Dentistry, Kyungpook National University) ;
  • Ahn, Dong-Kuk (Department of Oral Physiology, School of Dentistry, Kyungpook National University)
  • Received : 2016.07.28
  • Accepted : 2016.08.17
  • Published : 2016.09.30

Abstract

The aim of the present study was to develop an animal model for evaluation of temporomandibular (TMJ) nociception under TMJ inflammation. We also investigated the participation of $IL-1{\beta}$ in inflammation-induced TMJ nociception. Experiments were carried out using male Sprague-Dawley rats. Intra-articular injection of 3% formalin was administered to evaluate hyperalgesia 3 days after CFA injection. Intra-articular injection of 3% formalin did not produce nociceptive behavior in normal rats. Although intra-articular injection of 3 doses of CFA produced TMJ inflammation, only 1:3 diluted CFA produced hyperalgesia when formalin was injected intra-articularly 3 days after CFA injection. Co-administration of IL-1 receptor inhibitor with formalin into the TMJ cavity 3 days after CFA injection was performed. Co-administration of IL-1 receptor inhibitor significantly inhibited formalin-induced hyperalgesia in rats with CFA-induced TMJ inflammation. These results suggested that intra-articular injection of formalin produced hyperalgesia under chronic TMJ inflammation. Moreover, $IL-1{\beta}$ plays an important role in TMJ hyperalgesia under chronic inflammation and blockade of $IL-1{\beta}$ is a potential therapeutic target for inflammatory TMJ pain.

Keywords

References

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