The Link Between Periodontal Inflammation and Obesity.

Q2 Dentistry Current Oral Health Reports Pub Date : 2021-01-01 Epub Date: 2021-10-01 DOI:10.1007/s40496-021-00296-4
Misaki Iwashita, Masato Hayashi, Yuki Nishimura, Akiko Yamashita
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引用次数: 12

Abstract

Purpose of review: Obesity is a trigger for multiple diseases such as diabetes mellitus, hypertension, and cardiovascular diseases. Epidemiological studies have shown that obesity may be a risk factor for periodontal disease. Recently, there have been reports of presumed mechanisms of the associations between periodontitis and lipid metabolism or thermogenesis. This review aims to discuss the link between periodontal disease and energy regulatory function based on recent findings.

Recent findings: It has been demonstrated that activation of the C-C motif chemokine ligand/C-C chemokine receptor 7 pathway in adipose tissue induces inflammation and impairment of lipid metabolism and energy regulation in mice. Porphyromonas gingivalis administration has been shown to induce further weight gain and increased adipose tissue in diet-induced obese mice. Additionally, it has been reported that Porphyromonas gingivalis-induced endotoxemia potentially affect obesity by altering endocrine functions in brown adipose tissue in mice. Several cohort studies have shown that obesity is associated with tooth loss 5 years later, and periodontal conditions of obese individuals are significantly worse 2 and 6 months after the treatment compared with those of non-obese individuals. It has also been reported that body mass index is positively associated with the periodontal inflamed surface area index, a measure of periodontal inflammation. These results suggest that not only the enhancement of inflammation due to obesity but also the activation of inflammatory signaling may affect energy regulation.

Summary: Loss of adipose tissue homeostasis induces increase and activation of immune cells in adipose tissue, leading to impaired immune function in obesity. Various cytokines and chemokines are secreted from obese adipose tissue and promote inflammatory signaling. Some of these signaling pathways have been suggested to affect energy regulation. The combination of obesity and periodontitis amplifies inflammation to levels that affect the whole body through the adipose tissue. Obesity, in turn, accelerates the exacerbation of periodontitis.

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牙周炎症与肥胖之间的联系。
综述目的:肥胖是糖尿病、高血压、心血管疾病等多种疾病的诱因。流行病学研究表明,肥胖可能是牙周病的一个危险因素。最近,有报道推测牙周炎与脂质代谢或产热之间的关联机制。本文就牙周病与能量调节功能之间的关系作一综述。最近的研究发现:已经证明,在脂肪组织中激活C-C基序趋化因子配体/C-C趋化因子受体7通路可诱导小鼠炎症和脂质代谢和能量调节的损害。在饮食诱导的肥胖小鼠中,给予牙龈卟啉单胞菌已被证明可诱导进一步的体重增加和脂肪组织增加。此外,据报道,牙龈卟啉单胞菌诱导的内毒素血症可能通过改变小鼠棕色脂肪组织的内分泌功能来影响肥胖。几项队列研究表明,肥胖与5年后牙齿脱落有关,肥胖个体在治疗后2个月和6个月的牙周状况明显比非肥胖个体更糟。也有报道称,身体质量指数与牙周炎症表面指数呈正相关,这是牙周炎症的一种衡量标准。这些结果表明,肥胖不仅导致炎症的增强,而且炎症信号的激活也可能影响能量调节。摘要:脂肪组织稳态的丧失会导致脂肪组织中免疫细胞的增加和激活,导致肥胖患者的免疫功能受损。肥胖脂肪组织分泌多种细胞因子和趋化因子,促进炎症信号传导。其中一些信号通路被认为影响能量调节。肥胖和牙周炎的结合将炎症放大到通过脂肪组织影响全身的程度。肥胖反过来又加速了牙周炎的恶化。
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来源期刊
Current Oral Health Reports
Current Oral Health Reports Immunology and Microbiology-Immunology and Microbiology (miscellaneous)
CiteScore
3.00
自引率
0.00%
发文量
20
期刊介绍: Current Oral Health Reports strives to provide state-of-the-art reviews in critical areas relevant to the study and practice of dentistry. Translational breakthroughs have their roots in the application of innovative basic science. Many of the most fruitful areas for new discoveries are at the intersection of scientific disciplines and, indeed, from quite separate scientific subject areas. The purpose of this journal is to provide readers with impactful new material in a wide range of dentally relevant disciplines that are essential to the dentally related scientist, with international authorities serving as editorial board members and section editors. Timely and current reviews of the literature, written by some of the world’s leading researchers, will address a constantly updated list of subjects that will encompass host defenses, microbiology, wound healing, systemic disease interactions, risk factors, prevention, regenerative medicine, stem cells, cancer, genetics, and aging.
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