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牙周疾病(最常见的炎症事件)在连接营养与能量代谢的过氧化物酶体增殖物激活受体中的作用。

Influence of the Periodontal Disease, the Most Prevalent Inflammatory Event, in Peroxisome Proliferator-Activated Receptors Linking Nutrition and Energy Metabolism.

作者信息

Román-Malo Lourdes, Bullon Pedro

机构信息

Laboratorio de Investigacion, Departamento de Estomatologia, Universidad de Sevilla, c/ Avicena s/n, Sevilla 41009, Spain.

出版信息

Int J Mol Sci. 2017 Jul 5;18(7):1438. doi: 10.3390/ijms18071438.

DOI:10.3390/ijms18071438
PMID:28678155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5535929/
Abstract

Periodontal disease is considered one of the main pathologic diseases occurring in humans. Its pathologic process involves inflammatory reactions producing periodontal bone resorption and the tooth loss. But some patients do not present an evident clinical inflammation with bone resorption, and in others, the inflammation is prominent without bone resorption. A key question could be to investigate a different way of responding to aggression. Inflammation requires a complex intracellular metabolic process, starting with the harmful recognition and activation of the inflammasome, continues the energy supply with the alteration of oxidative stress conditions, and finishes with the elimination of the aggression with autophagy/apoptosis mechanisms, then concludes with recovery. Peroxisome proliferator-activated receptors (PPARs) are essential molecules produced in inflammation, and its genes and its activation have been related to periodontal disease. Also, an important aspect is the influence of PPARs in bone metabolism; the main periodontitis symptom is bone loss and PPARγ activation that can downregulate the bone resorption in experimental periodontitis, PPARγ-coated titanium dental implant surfaces could carry the antiinflammatory gene and restrain inflammation. PPARs could be one of the meeting background points with atherosclerosis/cardiovascular disease, diabetes and metabolic syndrome showing a modified proinflammatory statement such as it is described in periodontitis.

摘要

牙周病被认为是人类主要的病理疾病之一。其病理过程涉及产生牙周骨吸收和牙齿脱落的炎症反应。但有些患者没有明显的伴有骨吸收的临床炎症,而在另一些患者中,炎症很突出却没有骨吸收。一个关键问题可能是研究一种应对侵袭的不同方式。炎症需要一个复杂的细胞内代谢过程,始于炎性小体的有害识别和激活,接着随着氧化应激条件的改变进行能量供应,最后通过自噬/凋亡机制消除侵袭,然后以恢复告终。过氧化物酶体增殖物激活受体(PPARs)是炎症中产生的关键分子,其基因及其激活与牙周病有关。此外,PPARs对骨代谢的影响是一个重要方面;牙周炎的主要症状是骨质流失,PPARγ激活可下调实验性牙周炎中的骨吸收,涂有PPARγ的钛牙种植体表面可携带抗炎基因并抑制炎症。PPARs可能是与动脉粥样硬化/心血管疾病、糖尿病和代谢综合征的交汇点之一,表现出如牙周炎中所描述的改变的促炎状态。

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