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本文引用的文献

1
Mechanisms and control of pathologic bone loss in periodontitis.牙周炎中病理性骨质流失的机制与控制
Periodontol 2000. 2010 Jun;53:55-69. doi: 10.1111/j.1600-0757.2010.00347.x.
2
FoxO1 expression in osteoblasts regulates glucose homeostasis through regulation of osteocalcin in mice.成骨细胞中的 FoxO1 通过调节骨钙素来调节小鼠的葡萄糖稳态。
J Clin Invest. 2010 Jan;120(1):357-68. doi: 10.1172/JCI39901. Epub 2009 Dec 14.
3
Antitumor necrotic factor agent promotes BMP-2-induced ectopic bone formation.抑肿瘤坏死因子制剂促进 BMP-2 诱导的异位骨形成。
J Bone Miner Metab. 2010 Mar;28(2):157-64. doi: 10.1007/s00774-009-0127-x. Epub 2009 Oct 29.
4
Inhibition of osteoblastic bone formation by nuclear factor-kappaB.核因子-κB对成骨细胞骨形成的抑制作用。
Nat Med. 2009 Jun;15(6):682-9. doi: 10.1038/nm.1954.
5
Denosumab update.地诺单抗最新情况
Curr Opin Rheumatol. 2009 Jul;21(4):369-73. doi: 10.1097/BOR.0b013e32832ca41c.
6
Osteoblast function is compromised at sites of focal bone erosion in inflammatory arthritis.在炎症性关节炎中,成骨细胞功能在局灶性骨侵蚀部位受损。
J Bone Miner Res. 2009 Sep;24(9):1572-85. doi: 10.1359/jbmr.090320.
7
Resveratrol inhibits the expression of SREBP1 in cell model of steatosis via Sirt1-FOXO1 signaling pathway.白藜芦醇通过Sirt1-FOXO1信号通路抑制脂肪变性细胞模型中SREBP1的表达。
Biochem Biophys Res Commun. 2009 Mar 13;380(3):644-9. doi: 10.1016/j.bbrc.2009.01.163. Epub 2009 Jan 31.
8
AAV2/1-TNFR:Fc gene delivery prevents periodontal disease progression.AAV2/1-TNFR:Fc 基因传递可预防牙周病进展。
Gene Ther. 2009 Mar;16(3):426-36. doi: 10.1038/gt.2008.174. Epub 2008 Dec 11.
9
Activation of the acquired immune response reduces coupled bone formation in response to a periodontal pathogen.获得性免疫反应的激活会降低对牙周病原体的耦合骨形成。
J Immunol. 2008 Dec 15;181(12):8711-8. doi: 10.4049/jimmunol.181.12.8711.
10
Bone remodeling: Multiple cellular interactions required for coupling of bone formation and resorption.骨重塑:骨形成与吸收偶联所需的多种细胞相互作用。
Semin Cell Dev Biol. 2008 Oct;19(5):444-51. doi: 10.1016/j.semcdb.2008.07.016. Epub 2008 Jul 31.

炎症和去偶联作为牙周骨丢失的机制。

Inflammation and uncoupling as mechanisms of periodontal bone loss.

机构信息

Department of Periodontics, School of Dental Medicine, University of Pennsylvania, USA.

出版信息

J Dent Res. 2011 Feb;90(2):143-53. doi: 10.1177/0022034510385236. Epub 2010 Dec 6.

DOI:10.1177/0022034510385236
PMID:21135192
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3144100/
Abstract

Periodontal disease is characterized by both inflammation and bone loss. Advances in research in both these areas have led to a new appreciation of not only each field but also the intimate relationship between inflammation and bone loss. This relationship has resulted in a new field of science called osteoimmunology and provides a context for better understanding the pathogenesis of periodontal disease. In this review, we discuss several aspects of the immuno-inflammatory host response that ultimately results in loss of alveolar bone. A proposal is made that periodontal inflammation not only stimulates osteoclastogenesis but also interferes with the uncoupling of bone formation and bone resorption, consistent with a pathologic process. Furthermore, arguments based on experimental animal models suggest a critical role of the spatial and temporal aspects of inflammation in the periodontium. A review of these findings leads to a new paradigm to help explain more fully the impact of inflammation on alveolar bone in periodontal disease so that it includes the effects of inflammation on uncoupling of bone formation from resorption.

摘要

牙周病的特征是炎症和骨丧失。这两个领域的研究进展不仅使人们对每个领域有了新的认识,而且还使人们对炎症和骨丧失之间的密切关系有了新的认识。这种关系产生了一个名为骨免疫学的新科学领域,为更好地理解牙周病的发病机制提供了背景。在这篇综述中,我们讨论了最终导致牙槽骨丧失的免疫炎症宿主反应的几个方面。提出了这样一种观点,即牙周炎炎症不仅刺激破骨细胞形成,而且还干扰骨形成和骨吸收的解偶联,这与一种病理过程一致。此外,基于实验动物模型的论据表明,炎症在牙周组织中的空间和时间方面起着关键作用。对这些发现的回顾导致了一种新的范例,以帮助更充分地解释炎症对牙周病中牙槽骨的影响,从而包括炎症对骨形成与吸收解偶联的影响。