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维持牙周骨组织的内稳态控制。

Maintaining homeostatic control of periodontal bone tissue.

机构信息

Department of Oral Health Sciences, College of Dental Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.

出版信息

Periodontol 2000. 2021 Jun;86(1):157-187. doi: 10.1111/prd.12368. Epub 2021 Mar 10.

DOI:10.1111/prd.12368
PMID:33690918
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8294452/
Abstract

Alveolar bone is a unique osseous tissue due to the proximity of dental plaque biofilms. Periodontal health and homeostasis are mediated by a balanced host immune response to these polymicrobial biofilms. Dysbiotic shifts within dental plaque biofilms can drive a proinflammatory immune response state in the periodontal epithelial and gingival connective tissues, which leads to paracrine signaling to subjacent bone cells. Sustained chronic periodontal inflammation disrupts "coupled" osteoclast-osteoblast actions, which ultimately result in alveolar bone destruction. This chapter will provide an overview of alveolar bone physiology and will highlight why the oral microbiota is a critical regulator of alveolar bone remodeling. The ecology of dental plaque biofilms will be discussed in the context that periodontitis is a polymicrobial disruption of host homeostasis. The pathogenesis of periodontal bone loss will be explained from both a historical and current perspective, providing the opportunity to revisit the role of fibrosis in alveolar bone destruction. Periodontal immune cell interactions with bone cells will be reviewed based on our current understanding of osteoimmunological mechanisms influencing alveolar bone remodeling. Lastly, probiotic and prebiotic interventions in the oral microbiota will be evaluated as potential noninvasive therapies to support alveolar bone homeostasis and prevent periodontal bone loss.

摘要

牙槽骨是一种独特的骨组织,因为它靠近牙菌斑生物膜。牙周健康和动态平衡是由宿主对这些多微生物生物膜的平衡免疫反应来介导的。牙菌斑生物膜中的生态失调变化会导致牙周上皮和牙龈结缔组织中的促炎免疫反应状态,从而导致旁分泌信号传递到下方的骨细胞。持续的慢性牙周炎炎症会破坏“偶联”的破骨细胞-成骨细胞作用,最终导致牙槽骨破坏。本章将概述牙槽骨生理学,并强调口腔微生物群为何是牙槽骨重塑的关键调节剂。将在牙周炎是宿主动态平衡的多微生物破坏的背景下讨论牙菌斑生物膜的生态学。将从历史和当前的角度来解释牙周骨丢失的发病机制,有机会重新审视纤维化在牙槽骨破坏中的作用。将根据我们目前对影响牙槽骨重塑的骨免疫学机制的理解,回顾牙周免疫细胞与骨细胞的相互作用。最后,将评估口腔微生物群中的益生菌和益生元干预措施作为支持牙槽骨动态平衡和预防牙周骨丢失的潜在非侵入性治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/714c/8294452/df4944eb0875/nihms-1710903-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/714c/8294452/2fab382a7cbb/nihms-1710903-f0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/714c/8294452/dca59f2f8a87/nihms-1710903-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/714c/8294452/df4944eb0875/nihms-1710903-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/714c/8294452/2fab382a7cbb/nihms-1710903-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/714c/8294452/18c92265f2cf/nihms-1710903-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/714c/8294452/db7b20ecdfdd/nihms-1710903-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/714c/8294452/dca59f2f8a87/nihms-1710903-f0004.jpg
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本文引用的文献

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Probiotic Lactobacillus Rhamnosus GG Protects Against P. Gingivalis And F. Nucleatum Gut Dysbiosis.益生菌鼠李糖乳杆菌GG可预防牙龈卟啉单胞菌和具核梭杆菌引起的肠道菌群失调。
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Interleukin-35 inhibits alveolar bone resorption by modulating the Th17/Treg imbalance during periodontitis.白细胞介素-35 通过调节牙周炎期间的 Th17/Treg 失衡抑制肺泡骨吸收。
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Effect of Weissella cibaria on the reduction of periodontal tissue destruction in mice.韦荣球菌对减少牙周组织破坏的作用。
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The relationship between T-helper cell polarization and the RANKL/OPG ratio in gingival tissues from chronic periodontitis patients.慢性牙周炎患者牙龈组织中辅助性T细胞极化与RANKL/OPG比值的关系。
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IL-37- and IL-35/IL-37-Producing Plasma Cells in Chronic Periodontitis.慢性牙周炎中产生 IL-37 和 IL-35/IL-37 的浆细胞。
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