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  <Article>
    <Journal>
      <PublisherName>MDPI</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2075-4418</Issn>
      <Volume>11</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Expression of Neurokinin B Receptor in the Gingival Squamous Cell Carcinoma Bone Microenvironment</ArticleTitle>
    <FirstPage LZero="delete">1044</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shoko</FirstName>
        <LastName>Yoshida</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tsuyoshi</FirstName>
        <LastName>Shimo</LastName>
        <Affiliation>Division of Reconstructive Surgery for Oral and Maxillofacial Region, Department of Human Biology and Pathophysiology, School of Dentistry, Health Sciences University of Hokkaido</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyofumi</FirstName>
        <LastName>Takabatake</LastName>
        <Affiliation>Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yurika</FirstName>
        <LastName>Murase</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kyoichi</FirstName>
        <LastName>Obata</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tatsuo</FirstName>
        <LastName>Okui</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Shimane University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuki</FirstName>
        <LastName>Kunisada</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Soichiro</FirstName>
        <LastName>Ibaragi</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Nagatsuka</LastName>
        <Affiliation>Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akira</FirstName>
        <LastName>Sasaki</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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    </ArticleIdList>
    <Abstract>Gingival squamous cell carcinoma (SCC) frequently invades the maxillary or mandibular bone, and bone destruction is known as a key prognostic factor in gingival SCCs. Recently, Neurokinin 3 receptor (NK-3R), the receptor ligand for NK-3, which is a member of the tachykinin family expressed in the central nervous system, was identified through pathway analysis as a molecule expressed in osteoclasts induced by the hedgehog signal. Although the expression of NK-3R has been detected in osteoclast and SCC cells at the bone invasion front, the relationship between NK-3R expression and the prognosis of gingival SCC patients remains unclear. In the present study, we retrospectively reviewed 27 patients with gingival SCC who had undergone surgery with curative intent. Significantly higher NK-3R expression in tumor cells was found in a case of jawbone invasion than in a case of exophytic poor jawbone invasion. On the other hand, no significant association was observed between NK-3R tumor-positive cases and tumor size, TNM stage, or tumor differentiation. The survival rate tended to be lower in NK-3R tumor-positive cases, but not significantly. However, the disease-specific survival rate was significantly lower in patients with a large number of NK-3R-positive osteoclasts than in those with a small number of them at the tumor bone invasion front. Our results suggest that NK-3R signaling in the gingival SCC bone microenvironment plays an important role in tumor bone destruction and should be considered a potential therapeutic target in advanced gingival SCC with bone destruction.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">gingival squamous cell carcinoma</Param>
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      <Object Type="keyword">
        <Param Name="value">osteoclast</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1462-5814</Issn>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Roles of Porphyromonas gulae proteases in bacterial and host cell biology</ArticleTitle>
    <FirstPage LZero="delete">e13312</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Alam Saki</FirstName>
        <LastName>Urmi</LastName>
        <Affiliation>Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences </Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroaki</FirstName>
        <LastName>Inaba</LastName>
        <Affiliation>Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ryota</FirstName>
        <LastName>Nomura</LastName>
        <Affiliation>Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shoko</FirstName>
        <LastName>Yoshida</LastName>
        <Affiliation>Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoya</FirstName>
        <LastName>Ohara</LastName>
        <Affiliation>Department of Oral Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and the Advanced Research Center for Oral and Craniofacial Sciences, Dental School, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumitoshi</FirstName>
        <LastName>Asai</LastName>
        <Affiliation>Department of Pharmacology, School of Veterinary Medicine Azabu University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuhiko</FirstName>
        <LastName>Nakano</LastName>
        <Affiliation>Department of Pediatric Dentistry, Osaka University Graduate School of Dentistry</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Michiyo</FirstName>
        <LastName>Matsumoto]Nakano</LastName>
        <Affiliation>Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Porphyromonas gulae, an animal-derived periodontal pathogen, expresses several virulence factors, including fimbria, lipopolysaccharide (LPS) and proteases. We previously reported that its invasive efficiency was dependent on fimbriae types. In addition, P. gulae LPS increased inflammatory responses via toll-like receptors. The present study was conducted to investigate the involvement of P. gulae proteases in bacterial and host cell biology. Porphyromonas gulae strains showed an ability to agglutinate mouse erythrocytes and also demonstrated co-aggregation with Actinomyces viscosus, while the protease inhibitors antipain, PMSF, TLCK and leupeptin diminished P. gulae proteolytic activity, resulting in inhibition of haemagglutination and co-aggregation with A. viscosus. In addition, specific proteinase inhibitors were found to reduce bacterial cell growth. Porphyromonas gulae inhibited Ca9-22 cell proliferation in a multiplicity of infection- and time-dependent manner. Additionally, P. gulae-induced decreases in cell contact and adhesion-related proteins were accompanied by a marked change in cell morphology from well spread to rounded. In contrast, inhibition of protease activity prevented degradation of proteins, such as E-cadherin, beta-catenin and focal adhesion kinase, and also blocked inhibition of cell proliferation. Together, these results indicate suppression of the amount of human proteins, such as gamma-globulin, fibrinogen and fibronectin, by P. gulae proteases, suggesting that a novel protease complex contributes to bacterial virulence.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">coaggregation</Param>
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      <Object Type="keyword">
        <Param Name="value">haemagglutination</Param>
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      <Object Type="keyword">
        <Param Name="value">P. gulae</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">protease</Param>
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      <Object Type="keyword">
        <Param Name="value">protein degradation</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Oxford University Press</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2042-8812</Issn>
      <Volume/>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Surgical resection for advanced bisphosphonate-related osteonecrosis of the jaw associated with fibrous dysplasia: a case report</ArticleTitle>
    <FirstPage LZero="delete">rjaa061</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yurika</FirstName>
        <LastName>Murase</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine,Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Kishimoto</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine,Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shoko</FirstName>
        <LastName>Yoshida</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine,Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuki</FirstName>
        <LastName>Kunisada</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine,Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichi</FirstName>
        <LastName>Kadoya</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine,Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Soichiro</FirstName>
        <LastName>Ibaragi</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine,Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akira</FirstName>
        <LastName>Sasaki</LastName>
        <Affiliation>Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine,Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
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      <ArticleId IdType="doi"/>
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    <Abstract>Bisphosphonate-related osteonecrosis of the jaw (BRONJ) is an adverse drug reaction represented by destruction and/or death of bone. Fibrous dysplasia (FD) is a rare bony disorder characterised by abnormal fibro-osseous tissue that has lowered resistance to infection. Effective treatments for BRONJ that follows FD are unclear. Here, we report that advanced BRONJ associated with FD was successfully treated by surgical resection. A 69-year-old woman, whose left maxillary bone showed a ground glass appearance on computed tomography (CT) images, was taking alendronate. At 1 year after teeth within the abnormal bone were extracted, exposed bone was observed in the extraction sites and CT images revealed separated sequestrums. Under the clinical diagnosis of Stage 2 BRONJ with FD, we performed not only sequestrectomy but also a partial resection of the FD. Thereafter, the healing was uneventful without recurrence. In conclusion, our case suggests that surgical resection is useful for advanced BRONJ associated with FD.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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