{"title":"口腔细菌产生的短链脂肪酸在牙槽骨炎发展过程中的可能作用。","authors":"Takayuki Asayama, Ayaka Takada, Yoshikazu Mikami, Hirofumi Yamaguchi, Muneaki Tamura, Kunihito Matsumoto, Kiwa Miyake, Yoshiyuki Yonehara, Hiromasa Tsuda","doi":"10.2334/josnusd.23-0410","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Alveolar osteitis (dry sockets) is a painful condition characterized by a limited immune response. It is typically caused by the removal of blood clots from extracted tooth sockets, which leads to the fermentation of trapped food remnants by oral bacteria in the cavities, producing high concentrations of short-chain fatty acids (SCFAs). This study examined the effects of SCFAs on immunity and bone metabolism.</p><p><strong>Methods: </strong>Mouse macrophage Raw264.7 cells were treated with oral bacteria supernatants or SCFA mixtures, and inducible nitric oxide synthase (iNOS) levels were determined by western blot. The same cells were treated with SCFA mixtures in the presence of receptor activator of nuclear factor-kappa B ligand (RANKL), and osteoclast-like cells were counted. MC3T3-E1 cells were treated with SCFA mixtures and stained with alizarin red S.</p><p><strong>Results: </strong>Raw264.7 cells treated with oral bacterial culture supernatants of Porphyromonas gingivalis and Fusobacterium nucleatum inhibited lipopolysaccharide (LPS)-induced iNOS production, likely due to SCFA content. SCFA mixtures mimicking these supernatants inhibited the number of RANKL-induced tartrate-resistant acid phosphatase (TRAP)-positive cells and MC3T3-E1 cell mineralization.</p><p><strong>Conclusion: </strong>These data suggest that SCFAs produced by P. gingivalis and F. nucleatum may reduce the inflammatory response and mildly induce mineralization of the alveolar walls. These results may contribute to the understanding of alveolar osteitis.</p>","PeriodicalId":16646,"journal":{"name":"Journal of oral science","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Possible roles of short-chain fatty acids produced by oral bacteria in the development of alveolar osteitis.\",\"authors\":\"Takayuki Asayama, Ayaka Takada, Yoshikazu Mikami, Hirofumi Yamaguchi, Muneaki Tamura, Kunihito Matsumoto, Kiwa Miyake, Yoshiyuki Yonehara, Hiromasa Tsuda\",\"doi\":\"10.2334/josnusd.23-0410\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>Alveolar osteitis (dry sockets) is a painful condition characterized by a limited immune response. It is typically caused by the removal of blood clots from extracted tooth sockets, which leads to the fermentation of trapped food remnants by oral bacteria in the cavities, producing high concentrations of short-chain fatty acids (SCFAs). This study examined the effects of SCFAs on immunity and bone metabolism.</p><p><strong>Methods: </strong>Mouse macrophage Raw264.7 cells were treated with oral bacteria supernatants or SCFA mixtures, and inducible nitric oxide synthase (iNOS) levels were determined by western blot. The same cells were treated with SCFA mixtures in the presence of receptor activator of nuclear factor-kappa B ligand (RANKL), and osteoclast-like cells were counted. MC3T3-E1 cells were treated with SCFA mixtures and stained with alizarin red S.</p><p><strong>Results: </strong>Raw264.7 cells treated with oral bacterial culture supernatants of Porphyromonas gingivalis and Fusobacterium nucleatum inhibited lipopolysaccharide (LPS)-induced iNOS production, likely due to SCFA content. SCFA mixtures mimicking these supernatants inhibited the number of RANKL-induced tartrate-resistant acid phosphatase (TRAP)-positive cells and MC3T3-E1 cell mineralization.</p><p><strong>Conclusion: </strong>These data suggest that SCFAs produced by P. gingivalis and F. nucleatum may reduce the inflammatory response and mildly induce mineralization of the alveolar walls. These results may contribute to the understanding of alveolar osteitis.</p>\",\"PeriodicalId\":16646,\"journal\":{\"name\":\"Journal of oral science\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.9000,\"publicationDate\":\"2024-04-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of oral science\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.2334/josnusd.23-0410\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/2/29 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"DENTISTRY, ORAL SURGERY & MEDICINE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of oral science","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.2334/josnusd.23-0410","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/2/29 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}
引用次数: 0
摘要
目的:牙槽骨炎(干性牙槽炎)是一种以免疫反应受限为特征的疼痛性疾病。它通常是由拔牙后清除牙槽窝中的血块引起的,血块导致龋洞中的口腔细菌对残留的食物残渣进行发酵,产生高浓度的短链脂肪酸(SCFAs)。本研究探讨了 SCFAs 对免疫力和骨代谢的影响:方法:用口腔细菌上清液或 SCFA 混合物处理小鼠巨噬细胞 Raw264.7 细胞,并通过 Western 印迹法测定诱导型一氧化氮合酶(iNOS)的水平。在核因子-kappa B 受体激活剂配体(RANKL)存在的情况下,用 SCFA 混合物处理相同的细胞,并对破骨细胞样细胞进行计数。用 SCFA 混合物处理 MC3T3-E1 细胞并用茜素红 S 染色:结果:用牙龈卟啉菌和核酸镰刀菌的口腔细菌培养上清液处理 264.7 原始细胞可抑制脂多糖(LPS)诱导的 iNOS 生成,这可能与 SCFA 含量有关。模拟这些上清液的SCFA混合物抑制了RANKL诱导的抗酒石酸磷酸酶(TRAP)阳性细胞数量和MC3T3-E1细胞矿化:这些数据表明,牙龈脓杆菌和核酸酵母菌产生的 SCFAs 可减轻炎症反应并轻度诱导牙槽壁矿化。这些结果可能有助于理解牙槽骨炎。
Possible roles of short-chain fatty acids produced by oral bacteria in the development of alveolar osteitis.
Purpose: Alveolar osteitis (dry sockets) is a painful condition characterized by a limited immune response. It is typically caused by the removal of blood clots from extracted tooth sockets, which leads to the fermentation of trapped food remnants by oral bacteria in the cavities, producing high concentrations of short-chain fatty acids (SCFAs). This study examined the effects of SCFAs on immunity and bone metabolism.
Methods: Mouse macrophage Raw264.7 cells were treated with oral bacteria supernatants or SCFA mixtures, and inducible nitric oxide synthase (iNOS) levels were determined by western blot. The same cells were treated with SCFA mixtures in the presence of receptor activator of nuclear factor-kappa B ligand (RANKL), and osteoclast-like cells were counted. MC3T3-E1 cells were treated with SCFA mixtures and stained with alizarin red S.
Results: Raw264.7 cells treated with oral bacterial culture supernatants of Porphyromonas gingivalis and Fusobacterium nucleatum inhibited lipopolysaccharide (LPS)-induced iNOS production, likely due to SCFA content. SCFA mixtures mimicking these supernatants inhibited the number of RANKL-induced tartrate-resistant acid phosphatase (TRAP)-positive cells and MC3T3-E1 cell mineralization.
Conclusion: These data suggest that SCFAs produced by P. gingivalis and F. nucleatum may reduce the inflammatory response and mildly induce mineralization of the alveolar walls. These results may contribute to the understanding of alveolar osteitis.