• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

炎症性牙周病中的破骨细胞激活

Osteoclast activation in inflammatory periodontal diseases.

作者信息

Wiebe S H, Hafezi M, Sandhu H S, Sims S M, Dixon S J

机构信息

Department of Physiology, Faculty of Dentistry, University of Western Ontario, London, Canada.

出版信息

Oral Dis. 1996 Jun;2(2):167-80. doi: 10.1111/j.1601-0825.1996.tb00218.x.

DOI:10.1111/j.1601-0825.1996.tb00218.x
PMID:8957930
Abstract

OBJECTIVE

In this paper, we review the mechanisms thought to be involved in the activation of osteoclasts in periodontitis.

SUMMARY

Osteoclasts are regulated by both microbial and host factors. Some factors act directly on cells of the osteoclast lineage, whereas others act indirectly through other cell types in the bone environment. The proinflammatory cytokines (interleukins 1 and 6, tumor necrosis factors) have been implicated in the stimulation of osteoclastic resorption. The roles of the immunoregulatory cytoknes (interleukins 2 and 4, interferon gamma) are less clear, but decreased levels of these factors may contribute to periodontitis. A number of lipid mediators may be involved in stimulation of bone resorption. These include bacterial lipopolysaccharide and host-derived platelet-activating factor and prostaglandins. More recently, reactive oxygen intermediates and extracellular nucleotides, both present at sites of inflammation, have been investigated as possible modulators of osteoclast activity. The potential use of antiresorptive therapies in periodontitis is reviewed.

CONCLUSIONS

A wide range of host and bacterial factors contribute to the loss of alveolar bone in periodontitis. However, much remains to be understood about the complex mechanisms through which these factors regulate osteoclast activity. Further studies at the cellular and molecular level will lead to a better understanding of these processes and perhaps suggest new approaches for periodontal therapy.

摘要

目的

在本文中,我们回顾了被认为与牙周炎中破骨细胞激活有关的机制。

总结

破骨细胞受微生物和宿主因素的双重调节。一些因素直接作用于破骨细胞谱系的细胞,而其他因素则通过骨环境中的其他细胞类型间接起作用。促炎细胞因子(白细胞介素1和6、肿瘤坏死因子)与破骨细胞吸收的刺激有关。免疫调节细胞因子(白细胞介素2和4、干扰素γ)的作用尚不清楚,但这些因子水平的降低可能导致牙周炎。一些脂质介质可能参与骨吸收的刺激。这些包括细菌脂多糖和宿主来源的血小板活化因子以及前列腺素。最近,炎症部位存在的活性氧中间体和细胞外核苷酸已被研究作为破骨细胞活性的可能调节因子。本文还综述了抗吸收疗法在牙周炎中的潜在应用。

结论

多种宿主和细菌因素导致牙周炎中牙槽骨的丧失。然而,关于这些因素调节破骨细胞活性的复杂机制仍有许多有待了解。在细胞和分子水平上的进一步研究将有助于更好地理解这些过程,并可能为牙周治疗提出新的方法。

相似文献

1
Osteoclast activation in inflammatory periodontal diseases.炎症性牙周病中的破骨细胞激活
Oral Dis. 1996 Jun;2(2):167-80. doi: 10.1111/j.1601-0825.1996.tb00218.x.
2
Evidence that diabetes mellitus aggravates periodontal diseases and modifies the response to an oral pathogen in animal models.在动物模型中,有证据表明糖尿病会加重牙周疾病并改变对口腔病原体的反应。
Compend Contin Educ Dent. 2004 Jul;25(7 Suppl 1):38-45.
3
The role of cytokines in the pathogenesis of periodontal disease.细胞因子在牙周病发病机制中的作用。
Curr Opin Periodontol. 1994:39-53.
4
Metabolic syndrome exacerbates inflammation and bone loss in periodontitis.代谢综合征会加重牙周炎的炎症和骨质流失。
J Dent Res. 2015 Feb;94(2):362-70. doi: 10.1177/0022034514561658. Epub 2014 Dec 11.
5
Selective blockade of voltage-gated potassium channels reduces inflammatory bone resorption in experimental periodontal disease.电压门控钾通道的选择性阻断可减少实验性牙周病中的炎性骨吸收。
J Bone Miner Res. 2004 Jan;19(1):155-64. doi: 10.1359/JBMR.0301213.
6
Pathogenesis of periodontitis: role of cytokines in host response.牙周炎的发病机制:细胞因子在宿主反应中的作用。
Dent Today. 2010 Sep;29(9):60-2, 64-6; quiz 68-9.
7
Mechanisms of Bone Resorption in Periodontitis.牙周炎中骨吸收的机制
J Immunol Res. 2015;2015:615486. doi: 10.1155/2015/615486. Epub 2015 May 3.
8
Bone cell interactions and regulation by inflammatory mediators.骨细胞与炎症介质的相互作用及调节
Curr Opin Periodontol. 1996;3:34-44.
9
Anti-inflammatory, anti-osteoclastic, and antioxidant activities of genistein protect against alveolar bone loss and periodontal tissue degradation in a mouse model of periodontitis.染料木黄酮具有抗炎、抗破骨细胞和抗氧化活性,可防止牙周炎小鼠模型中牙槽骨丢失和牙周组织降解。
J Biomed Mater Res A. 2017 Sep;105(9):2510-2521. doi: 10.1002/jbm.a.36109. Epub 2017 Jun 6.
10
Mechanisms of alveolar bone destruction in periodontitis.牙周炎中牙槽骨破坏的机制
Periodontol 2000. 1997 Jun;14:158-72. doi: 10.1111/j.1600-0757.1997.tb00196.x.

引用本文的文献

1
Surface Pre-Reacted Glass-Ionomer Eluate Suppresses Osteoclastogenesis through Downregulation of the MAPK Signaling Pathway.表面预反应玻璃离子洗脱液通过下调MAPK信号通路抑制破骨细胞生成。
Biomedicines. 2024 Aug 12;12(8):1835. doi: 10.3390/biomedicines12081835.
2
Insights and Advancements in Periodontal Tissue Engineering and Bone Regeneration.牙周组织工程与骨再生的新见解和进展。
Medicina (Kaunas). 2024 May 7;60(5):773. doi: 10.3390/medicina60050773.
3
External cervical resorption-a review of pathogenesis and potential predisposing factors.
颈外吸收——发病机制及潜在易感因素综述
Int J Oral Sci. 2021 Jun 10;13(1):19. doi: 10.1038/s41368-021-00121-9.
4
Destroy to Rebuild: The Connection Between Bone Tissue Remodeling and Matrix Metalloproteinases.破而后立:骨组织重塑与基质金属蛋白酶之间的联系
Front Physiol. 2020 Feb 5;11:47. doi: 10.3389/fphys.2020.00047. eCollection 2020.
5
All-trans retinoic-acid inhibits heterodimeric bone morphogenetic protein 2/7-stimulated osteoclastogenesis, and resorption activity.全反式维甲酸抑制异二聚体骨形态发生蛋白2/7刺激的破骨细胞生成及吸收活性。
Cell Biosci. 2018 Aug 23;8:48. doi: 10.1186/s13578-018-0246-y. eCollection 2018.
6
MicroRNAs and Periodontal Homeostasis.微小RNA与牙周稳态
J Dent Res. 2017 May;96(5):491-500. doi: 10.1177/0022034516685711. Epub 2017 Jan 9.
7
Spontaneous destructive periodontitis and skeletal bone damage in transgenic mice carrying a human shared epitope-coding allele.携带人类共享表位编码等位基因的转基因小鼠中的自发性破坏性牙周炎和骨骼损伤
RMD Open. 2016 Dec 1;2(2):e000349. doi: 10.1136/rmdopen-2016-000349. eCollection 2016.
8
Osteoprotegerin disrupts peripheral adhesive structures of osteoclasts by modulating Pyk2 and Src activities.骨保护素通过调节Pyk2和Src活性破坏破骨细胞的外周黏附结构。
Cell Adh Migr. 2016 May 3;10(3):299-309. doi: 10.1080/19336918.2015.1129480. Epub 2016 Jan 8.
9
Mechanisms of Bone Resorption in Periodontitis.牙周炎中骨吸收的机制
J Immunol Res. 2015;2015:615486. doi: 10.1155/2015/615486. Epub 2015 May 3.
10
Effects of lipopolysaccharide on osteoblast-osteoclast bidirectional EphB4-EphrinB2 signaling.脂多糖对成骨细胞-破骨细胞双向EphB4-EphrinB2信号传导的影响
Exp Ther Med. 2014 Jan;7(1):80-84. doi: 10.3892/etm.2013.1357. Epub 2013 Oct 23.