{"title":"Involvement of Impaired Angiogenesis and Myelosuppression in Antiresorptive-agent Related Osteonecrosis of the Jaw Mouse Model.","authors":"Hisao Igarashi, Satoru Nishizawa, Takeshi Miyamoto, Atsuhiko Hikita, Kazuto Hoshi","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To explore the involvement of bone marrow cells and angiogenesis in the pathogenesis of antiresorptive agent-related osteonecrosis of the jaw (ARONJ).</p><p><strong>Methods: </strong>We performed micro-computed tomography (CT) and histological analyses in an ARONJ mouse model generated using bisphosphonate (BP) and cyclophosphamide (CY).</p><p><strong>Results: </strong>Micro-CT analysis showed that BP and CY inhibited osteoneogenesis in the extraction socket. Histological analysis at 3 days after tooth extraction showed inhibition of vascular endothelial cell and mesenchymal stem cell mobilization into the extraction socket. When neovascularization of the extraction fossa was observed from as early as 1 day after extraction, it occurred predominantly in the area adjacent to the extraction fossa and close to the bone marrow cavity. In addition, the extraction fossa communicated with the adjacent bone marrow via the vasculature. Histological evaluation of the alveolar bone marrow around the extraction socket showed a decrease in bone marrow cells in the BP + CY group.</p><p><strong>Conclusion: </strong>Both inhibition of angiogenesis and suppression of bone marrow cell mobilization are involved in the pathogenesis of ARONJ.</p>","PeriodicalId":38819,"journal":{"name":"Tokai Journal of Experimental and Clinical Medicine","volume":"48 1","pages":"22-31"},"PeriodicalIF":0.0000,"publicationDate":"2023-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tokai Journal of Experimental and Clinical Medicine","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: To explore the involvement of bone marrow cells and angiogenesis in the pathogenesis of antiresorptive agent-related osteonecrosis of the jaw (ARONJ).
Methods: We performed micro-computed tomography (CT) and histological analyses in an ARONJ mouse model generated using bisphosphonate (BP) and cyclophosphamide (CY).
Results: Micro-CT analysis showed that BP and CY inhibited osteoneogenesis in the extraction socket. Histological analysis at 3 days after tooth extraction showed inhibition of vascular endothelial cell and mesenchymal stem cell mobilization into the extraction socket. When neovascularization of the extraction fossa was observed from as early as 1 day after extraction, it occurred predominantly in the area adjacent to the extraction fossa and close to the bone marrow cavity. In addition, the extraction fossa communicated with the adjacent bone marrow via the vasculature. Histological evaluation of the alveolar bone marrow around the extraction socket showed a decrease in bone marrow cells in the BP + CY group.
Conclusion: Both inhibition of angiogenesis and suppression of bone marrow cell mobilization are involved in the pathogenesis of ARONJ.
期刊介绍:
The Tokai Journal of Experimental and Clinical Medicine, also referred to as Tokai Journal, is an official quarterly publication of the Tokai Medical Association. Tokai Journal publishes original articles that deal with issues of clinical, experimental, socioeconomic, cultural and/or historical importance to medical science and related fields. Manuscripts may be submitted as full-length Original Articles or Brief Communications. Tokai Journal also publishes reviews and symposium proceedings. Articles accepted for publication in Tokai Journal cannot be reproduced elsewhere without written permission from the Tokai Medical Association. In addition, Tokai Journal will not be held responsible for the opinions of the authors expressed in the published articles.