著者

Yuwa Takahashi Norihisa Watanabe Noriaki Kamio Ryutaro Kobayashi Toshimitsu Iinuma Kenichi Imai

出版者

Nihon University School of Dentistry

雑誌

Journal of Oral Science (ISSN:13434934)

巻号頁・発行日

vol.63, no.1, pp.1-3, 2021 (Released:2020-12-23)

参考文献数

40

被引用文献数

14 82

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Coronavirus infectious disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was declared a pandemic in March 2020 by the World Health Organization. Periodontitis, one of the most prevalent diseases worldwide, leads to alveolar bone destruction and subsequent tooth loss, and develops due to pro-inflammatory cytokine production induced by periodontopathic bacteria. Periodontopathic bacteria are involved in respiratory diseases, including aspiration pneumonia and chronic obstructive pulmonary disease (COPD), and other systemic diseases, such as diabetes and cardiovascular disease. Patients with these diseases have an increased COVID-19 aggravation rate and mortality. Because aspiration of periodontopathic bacteria induces the expression of angiotensin-converting enzyme 2, a receptor for SARS-CoV-2, and production of inflammatory cytokines in the lower respiratory tract, poor oral hygiene can lead to COVID-19 aggravation. Conversely, oral care, including periodontal treatment, prevents the onset of pneumonia and influenza and the exacerbation of COPD. The reduced chance of receiving professional oral care owing to long-term hospitalization of patients with COVID-19 may increase the aggravation risk of infection in the lower respiratory tract. It can be hypothesized that periodontopathic bacteria are involved in the COVID-19 aggravation and therefore, the management of good oral hygiene potentially contributes to its prevention.

著者

Yuwa Takahashi Norihisa Watanabe Noriaki Kamio Ryutaro Kobayashi Toshimitsu Iinuma Kenichi Imai

出版者

Nihon University School of Dentistry

雑誌

Journal of Oral Science (ISSN:13434934)

巻号頁・発行日

pp.20-0388, (Released:2020-11-12)

参考文献数

40

被引用文献数

82

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Coronavirus infectious disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was declared a pandemic in March 2020 by the World Health Organization. Periodontitis, one of the most prevalent diseases worldwide, leads to alveolar bone destruction and subsequent tooth loss, and develops due to pro-inflammatory cytokine production induced by periodontopathic bacteria. Periodontopathic bacteria are involved in respiratory diseases, including aspiration pneumonia and chronic obstructive pulmonary disease (COPD), and other systemic diseases, such as diabetes and cardiovascular disease. Patients with these diseases have an increased COVID-19 aggravation rate and mortality. Because aspiration of periodontopathic bacteria induces the expression of angiotensin-converting enzyme 2, a receptor for SARS-CoV-2, and production of inflammatory cytokines in the lower respiratory tract, poor oral hygiene can lead to COVID-19 aggravation. Conversely, oral care, including periodontal treatment, prevents the onset of pneumonia and influenza and the exacerbation of COPD. The reduced chance of receiving professional oral care owing to long-term hospitalization of patients with COVID-19 may increase the aggravation risk of infection in the lower respiratory tract. It can be hypothesized that periodontopathic bacteria are involved in the COVID-19 aggravation and therefore, the management of good oral hygiene potentially contributes to its prevention.

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

Hidekazu Nagashima Masamichi Shinoda Kuniya Honda Noriaki Kamio Akira Hasuike Naoyuki Sugano Yoshinori Arai Shuichi Sato Koichi Iwata

出版者

日本大学歯学部

雑誌

Journal of Oral Science (ISSN:13434934)

巻号頁・発行日

pp.16-0830, (Released:2017-10-31)

参考文献数

45

被引用文献数

13

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Periodontitis caused by bacterial infection gradually progresses accompanied by periodontal tissue destruction. As a result, teeth lose their supporting structures, and this leads to tooth exfoliation. CXC-chemokine receptor 4 (CXCR4) is known to be expressed in lymphocytes, fibroblasts and osteoclasts in periodontal tissues, suggesting that periodontal CXCR4 signaling contributes to alveolar bone resorption in the milieu of periodontitis. However, the role of CXCR4 signaling in the pathogenesis of periodontitis has remained unknown. We established a mouse model of periodontitis by inoculation of Porphyromonas gingivalis (P.g.) into a silk ligature placed around the maxillary molar. Although there was no significant difference in the mechanical sensitivity in the periodontal tissue between P.g. treatment and sham treatment during the experimental period, mechanical allodynia in the periodontal tissue was induced after gingival injection of complete Freund’s adjuvant compared with that resulting from sham and P.g. treatment alone. Moreover, CXCR4 neutralization in the periodontal tissue following P.g. treatment enhanced periodontal inflammatory cell infiltration and depressed alveolar bone resorption. These findings suggest that periodontal CXCR4 signaling in several cell types in P.g.-induced periodontal inflammation depresses alveolar bone resorption in periodontitis. CXCR4 signaling might be a target for therapeutic intervention to prevent alveolar bone resorption in periodontitis.