著者

Tatsuki Oto Kentaro Urata Yoshinori Hayashi Suzuro Hitomi Ikuko Shibuta Koichi Iwata Toshimitsu Iinuma Masamichi Shinoda

出版者

Tohoku University Medical Press

雑誌

The Tohoku Journal of Experimental Medicine (ISSN:00408727)

巻号頁・発行日

pp.2022.J004, (Released:2022-03-17)

被引用文献数

1

著者

Naoki Murakami Kenji Yoshikawa Kohei Tsukada Noriaki Kamio Yoshinori Hayashi Suzuro Hitomi Yuki Kimura Ikuko Shibuta Ayaka Osada Shuichi Sato Koichi Iwata Masamichi Shinoda

出版者

Nihon University School of Dentistry

雑誌

Journal of Oral Science (ISSN:13434934)

巻号頁・発行日

pp.21-0483, (Released:2021-12-29)

参考文献数

29

被引用文献数

1

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Purpose: Periodontitis progresses with chronic inflammation, without periodontal pain. However, the underlying mechanisms are not well known. Here, the involvement of butyric acid (BA) in periodontal pain sensitivity in Porphyromonas gingivalis (P. gingivalis)-induced periodontitis was examined.Methods: P. gingivalis was inoculated into the ligature which was tied around the molar (P. gingivalis-L) and the gingival mechanical head withdrawal threshold (MHWT) was measured. Following P. gingivalis-L, the expressions of orphan G protein-coupled receptor 41 (GPR41) in trigeminal ganglion (TG) neurons were examined. The amount of gingival BA was analyzed following the P. gingivalis-L and the changes in the MHWT in complete Freund’s adjuvant (CFA)-injected gingival tissue by gingival BA were examined. The changes in the MHWT following P. gingivalis-L by gingival GPR41 antagonist (HA) were examined.Results: No change in the MHWT was observed, GPR41-immunoreactive TG neurons were increased following P. gingivalis-L. The gingival BA amount increased following P. gingivalis-L, and the gingival BA suppressed the decrease in MHWT following CFA. HA decreased MHWT following P. gingivalis-L.Conclusion: Gingival BA modulates periodontal mechanical nociception via GPR41 signaling in P. gingivalis-L-induced periodontitis.

著者

Masamichi Shinoda Yoshinori Hayashi Asako Kubo Koichi Iwata

出版者

Nihon University School of Dentistry

雑誌

Journal of Oral Science (ISSN:13434934)

巻号頁・発行日

pp.19-0373, (Released:2020-03-04)

参考文献数

86

被引用文献数

16

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Nociceptive stimuli to the orofacial region are typically received by the peripheral terminal of trigeminal ganglion (TG) neurons, and noxious orofacial information is subsequently conveyed to the trigeminal spinal subnucleus caudalis and the upper cervical spinal cord (C1-C2). This information is further transmitted to the cortical somatosensory regions and limbic system via the thalamus, which then leads to the perception of pain. It is a well-established fact that the presence of abnormal pain in the orofacial region is etiologically associated with neuroplastic changes that may occur at any point in the pain transmission pathway from the peripheral to the central nervous system (CNS). Recently, several studies have reported that functional plastic changes in a large number of cells, including TG neurons, glial cells (satellite cells, microglia, and astrocytes), and immune cells (macrophages and neutrophils), contribute to the sensitization and disinhibition of neurons in the peripheral and CNS, which results in orofacial pain hypersensitivity.