牙周炎与肠道菌群相关性研究进展

越来越多的研究表明牙周炎和肠道菌群之间关系密切。牙周炎的患者能够通过吞咽将口腔细菌转移到肠道定植,肠道原生菌群被改变,进而引发一系列肠道黏膜的免疫反应。肠道菌群失调又会导致一系列全身系统疾病,其中代表性的疾病就是炎症性肠病炎症性肠病(inflammatory bowel disease,IBD)。本文以IBD为切入点就牙周炎影响肠道菌群的可能途径以及炎症进展时、炎症得到控制后肠道菌群的变化进行综述。     

实验性牙周炎对小鼠焦虑样行为及肠道菌群的影响

目的 观察实验性牙周炎对小鼠焦虑样行为的影响,初步探讨肠道菌群在其中发挥的作用。方法 16只雄性C57BL/6小鼠随机分为两组：对照组和牙周炎组,牙周炎组采用丝线诱导实验性牙周炎。8周后采用旷场实验和高架十字迷宫实验检测小鼠焦虑样行为;使用16S rRNA测序检测两组小鼠粪便肠道菌群变化。结果 与对照组相比,牙周炎组小鼠牙槽骨吸收,在旷场实验中进入中心区域时间减少,高架十字迷宫实验中进入开臂时间减少。16S rRNA测序发现两组小鼠肠道菌群β多样性存在统计学差异,牙周炎组厚壁菌门/拟杆菌门比值显著下降。LEfSe分析结果显示,对照组差异菌为Acetatifactor,Oscillospirales,Coriobacteriia,Butyricicoccaceae,Coriobacteriales,牙周炎组差异菌为Peptococcus,Bacteroidia,Bacteroidota,Muribaculaceae,Bacteroidales。相关性分析结果显示,norank＿f＿＿Muribaculaceae与高架开臂时间呈负相关,Akkermansia与高架开臂时间呈正相关。功能预测...     

牙周炎与口腔菌群及肠道菌群的相关研究进展

肠道菌群为人体最大的微生物群落,近来研究显示,肠道菌群与全身健康息息相关,肠道菌群失调在肥胖症、心脏病、孤独症、糖尿病等疾病中扮演重要角色。牙周炎是最常见的口腔疾病之一,表现为牙槽骨丧失、牙齿松动等。近来研究显示,牙周炎会影响肠道菌群。本文就牙周炎对肠道菌群的影响、作用路径及可能因素做一综述,以期为探究牙周炎与肠道菌群相关性提供参考。     

牙龈卟啉单胞菌对小鼠肠道炎症的影响研究

目的:研究牙龈卟啉单胞菌(Porphyromonas gingivalis,P.g)对小鼠肠道炎症的诱导作用及机制探究。方法:将12只BALB/C小鼠随机均分为2组,P.g组灌饲0.2 mL OD₆₀₀=0.5的P.g菌液,对照组灌饲等量无菌BHI液体培养基。每只小鼠每日灌饲1次,起始和每次灌饲1周时小鼠称重,7周后采用颈椎脱臼法处死小鼠,采取小肠组织并收取粪便。粪便进行16S rRNA测序分析肠道菌群多样性;小肠组织行HE染色分析肠道炎症进展。免疫组化分析炎症因子IL-17的表达及铁死亡指标(ACSL4,SLC7A11,GPX4)的水平变化。结果:对照组和P.g灌饲组小鼠体重第7周时存在差异(P<0.05)。HE染色显示P.g组小鼠小肠黏膜下炎症细胞浸润增加,绒毛间质轻微水肿,提示肠道炎症浸润。免疫组化结果显示,P.g灌饲组小鼠小肠组织IL-17明显升高。小肠组织中ACSL4水平显著增高,SLC7A11和GPX4水平降低,小鼠小肠组织在P.g作用下发生了铁死亡。16S rRNA结果显示P.g组与对照组间肠道菌群差异明显(P<0.05)。结论:P.g可...     

牙周炎与高脂血症交互作用及致肠道菌群失调的研究进展

牙周炎和高脂血症都是较常见的慢性疾病,严重影响人类身心健康,且两种疾病可能会互相影响,加重病情,然而其具体的生物学机制尚未明确.肠道微生态为机体最大最复杂的微生态系统,牙周炎和高脂血症均可导致肠道菌群组成改变.近年来研究证实,肠道菌群可通过自身代谢产物、影响宿主代谢及免疫反应来调节宿主血脂和骨代谢.本文就牙周炎和高脂血症之间,通过导致肠道菌群紊乱而产生交互作用的病理生理机制进行综述,以期为牙周炎和高脂血症之间潜在的关系提供新思路和理论依据.     

牙周炎与高脂血症交互作用及致肠道菌群失调的研究进展

牙周炎和高脂血症都是较常见的慢性疾病,严重影响人类身心健康,且两种疾病可能会互相影响,加重病情,然而其具体的生物学机制尚未明确.肠道微生态为机体最大最复杂的微生态系统,牙周炎和高脂血症均可导致肠道菌群组成改变.近年来研究证实,肠道菌群可通过自身代谢产物、影响宿主代谢及免疫反应来调节宿主血脂和骨代谢.本文就牙周炎和高脂血症之间,通过导致肠道菌群紊乱而产生交互作用的病理生理机制进行综述,以期为牙周炎和高脂血症之间潜在的关系提供新思路和理论依据.     

牙周炎对高脂饮食小鼠血浆氧化三甲胺的影响

目的:评估牙周炎对高脂饮食小鼠血浆氧化三甲胺(trimethylamine N-oxide, TMAO)生成的影响并探索肠道菌群在其中的作用。方法:选取10只雄性C57BL/6J小鼠随机分为高脂饮食组(HFD)和高脂饮食+牙周炎组(HFD＿PD)。实验8周后安乐处死小鼠,检测牙槽骨丢失量,血浆TMAO代谢组浓度,肝脏和肠道相关基因表达,盲肠内容物微生物组成。结果:与HFD组相比,HFD＿PD组小鼠血浆TMAO浓度增加(P<0.01);门水平上,HFD＿PD组小鼠Firmicutes和Desulfobacterota的丰度降低,Bacteroidota和Campilobacterota的丰度升高;Pearson相关性分析显示,Eubacterium＿coprostanoligenes, Lachnospiraceae＿NK4A136与TMAO呈正相关,Muribaculaceae与TMAO呈负相关(P<0.05);肠道组织IL-6的基因表达量升高(P<0.01),ZO-1的表达量下降(P<0.01);肝脏IL-6和TNF-α基因表达量升高(P<0.01,P&...     

高脂饮食加重牙周炎对肠道菌群及糖代谢影响的实验研究

目的:研究高脂饮食是否加剧牙周炎对肠道菌群及糖代谢的影响。方法:将24只雄性SD大鼠通过随机数字表法随机分为4组（每组6只）：对照组,给予常规饮食;牙周炎组,用5-0号丝线结扎大鼠双侧上颌第二磨牙诱导牙周炎;高脂饮食组,给予高脂饮食;高脂饮食+牙周炎组,给予高脂饮食,并在实验开始后8周诱导牙周炎。12周后检测空腹血糖及...     

牙周炎对雌激素缺乏小鼠骨组织及肠道色氨酸代谢影响的研究

目的研究雌激素缺乏背景下, 牙周炎对骨组织和肠道色氨酸代谢的影响。方法将32只雌性C57BL6/J小鼠根据随机数字表法随机分为4组(每组8只):假手术组(Sham组);假手术牙周炎组(Sham_Lig组);去卵巢组(Ovx组);去卵巢牙周炎组(Ovx_Lig组)。Sham_Lig组与Ovx_Lig组小鼠术后4周, 以5-0号丝线结扎双侧上颌第二磨牙诱导牙周炎。丝线结扎8周后对4组小鼠实施安乐死, 取材小鼠股骨、胫骨、下颌骨及颅骨样本行显微CT(micro-CT)扫描, 并检测样本骨密度、骨体积分数(BV/TV)、骨小梁数量(Tb.N)、骨小梁厚度(Tb.Th)和骨小梁分离度(Tb.Sp)。收集4组小鼠盲肠内容物, 利用16S rRNA基因测序检测肠道菌群的组成, 通过液相色谱-质谱法检测肠道中的色氨酸及其代谢物的含量, 并对肠道菌群相对丰度水平与色氨酸代谢物含量行相关性分析。结果 Ovx_Lig组小鼠股骨骨密度[(82.23±3.97)mg/cm3]、BV/TV[(9.25±1.37)%...     

高脂饮食加重牙周炎对肠道菌群及糖代谢影响的实验研究

目的研究高脂饮食是否加剧牙周炎对肠道菌群及糖代谢的影响。方法将24只雄性SD大鼠通过随机数字表法随机分为4组(每组6只):对照组,给予常规饮食;牙周炎组,用5-0号丝线结扎大鼠双侧上颌第二磨牙诱导牙周炎;高脂饮食组,给予高脂饮食;高脂饮食+牙周炎组,给予高脂饮食,并在实验开始后8周诱导牙周炎。12周后检测空腹血糖及葡萄糖耐量。安乐处死大鼠,收集盲肠内容物,通过Illumina MiSeq平台对样本中16S rRNA基因进行测序,用RDP Classifier和SILVA(SSU123)16S rRNA数据库对测序结果进行分析。通过相关性分析研究高脂饮食和牙周炎诱导的肠道菌群变化与血糖水平的相关性。结果结扎诱导牙周炎4周后,牙周炎组大鼠和高脂饮食组大鼠的空腹血糖水平[分别为(4.93±0.28)、(5.25±0.24) mmol/L]均显著高于对照组大鼠的空腹血糖水平[(4.56±0.20) mmol/L](P<0.05),且牙周炎组大鼠和高脂饮食组大鼠均存在葡萄糖耐量受损。高脂饮食+牙周炎组的空腹血糖水平[(5.53±0.14) mmol/L]显著高于牙周炎组和高脂饮食组(P&l...     

Occurrence of Spontaneous Periodontal Disease in the SAMP1/YitFc Murine Model of Crohn Disease

Background: Oral involvement is often associated with inflammatory bowel disease (IBD). Recent evidence suggests a high incidence of periodontal disease in patients with Crohn disease (CD). To the best of the authors’ knowledge, no animal model of IBD that displays associated periodontal disease was reported previously. The aim of this study is to investigate the occurrence and progression of periodontal disease in SAMP1/YitFc (SAMP) mice that spontaneously develop a CD‐like ileitis. In addition, the temporal correlation between the onset and progression of periodontal disease and the onset of ileitis in SAMP mice was studied. Methods: At different time points, SAMP and parental AKR/J (AKR) control mice were sacrificed, and mandibles were prepared for stereomicroscopy and histology. Terminal ilea were collected for histologic assessment of inflammation score. Periodontal status, i.e., alveolar bone loss (ABL) and alveolar bone crest, was examined by stereomicroscopy and histomorphometry, respectively. Results: ABL increased in both strains with age. SAMP mice showed greater ABL compared with AKR mice by 12 weeks of age, with maximal differences observed at 27 weeks of age. AKR control mice did not show the same severity of periodontal disease. Interestingly, a strong positive correlation was found between ileitis severity and ABL in SAMP mice, independent of age. Conclusions: The present results demonstrate the occurrence of periodontal disease in a mouse model of progressive CD‐like ileitis. In addition, the severity of periodontitis strongly correlated with the severity of ileitis, independent of age, suggesting that common pathogenic mechanisms, such as abnormal immune response and dysbiosis, may be shared between these two phenotypes.     

Periodontal manifestations of inflammatory bowel disease: emerging epidemiologic and biologic evidence

Inflammatory bowel disease and periodontitis are both described as a disproportionate mucosal inflammatory response to a microbial environment in susceptible patients. Moreover, these two conditions share major environmental and lifestyle‐related risk factors. Despite this intriguing pathogenic parallel, large‐scale studies and basic research have only recently considered periodontal outcomes as relevant data. There are mounting and consistent arguments, from recent epidemiologic studies and animal models, that these two conditions might be related. This article is a comprehensive and critical up‐to‐date review of the current evidence and future prospects in understanding the biologic and epidemiologic relationships between periodontal status and inflammatory bowel disease.     

Periodontal inflammation and bone loss in aged mice

Liang S, Hosur KB, Domon H, Hajishengallis G. Periodontal inflammation and bone loss in aged mice. J Periodont Res 2010; 45: 574–578. © 2010 The Authors. Journal compilation © 2010 Blackwell Munksgaard Background and Objective: Young mice do not develop measurable periodontal bone loss, unless heavily infected with human periodontal pathogens. However, mice with a genetically altered immune system are unable to control their own oral flora and develop periodontitis early in life. Based on the potential of the indigenous oral microbiota to cause periodontitis, we hypothesized that normal mice may ultimately develop inflammatory periodontal bone loss, i.e. as a function of age. If confirmed, this could serve as an aging model of chronic periodontitis. Material and Methods: Periodontal bone levels were measured as the distance from the cementoenamel junction to the alveolar bone crest in young mice (8–10 wk of age), old mice (≥ 18 mo of age) and mice of intermediate ages. Differential expression of inflammatory mediators in the gingivae of young and old mice was determined by quantitative real‐time PCR. Results: In comparison with young mice, old mice displayed significantly (p < 0.05) increased periodontal bone loss, accompanied by elevated expression of proinflammatory cytokines (interleukin‐1β, tumor necrosis factor α and interleukin‐17A) and innate immune receptors involved in the induction or amplification of inflammation (Toll‐like receptor 2, CD14, CD11b, CD18, complement C5a receptor and triggering receptor expressed on myeloid cells 3). Conclusion: Mice develop naturally induced periodontal bone loss as a function of age. This aging model of periodontitis represents a genuinely chronic model to study mechanisms of periodontal tissue destruction.     

Periodontal inflammation and attachment loss: a critical problem for biological studies

BACKGROUND: In biological studies of periodontitis, there has been long-standing confusion between the ubiquitous phenomena of inflammation and the essential criterion of attachment loss. This is partly attributable to inadequate methods of clinical measurement, but seems also to be a consequence of an unproven and usually unstated assumption that the same biological processes underlie both inflammation and attachment loss. Developments in unidimensional clinical probing methods have helped in studies of periodontal treatment. However, such methods are intrinsically unsuitable in studies of periodontal diseases, and may have given them a false sense of security. The confusion has been compounded by inappropriate use of statistical techniques in an attempt to solve problems which do not arise from mathematical models but are intrinsic to measurement methods.
OBJECTIVE: This paper is a clinician's attempt to state the current difficulties and suggest some ways forward, including the development of three-dimensional measurement, non-invasive probing, and several objectives for biochemical, microbiological and immunolog-ical research.     

牙周炎症微环境对牙龈上皮屏障影响研究进展

牙周病是一种常见的慢性炎症性疾病,与牙周致病菌、黏膜和免疫宿主细胞之间复杂的相互作用有关.牙龈卟啉单胞菌(Porphyromonas gingivalis,P.gingivalis)在牙周病中被认为是重要的致病菌之一,与黏膜和免疫细胞相互作用,导致炎症细胞因子的产生.牙龈上皮是口腔微生物群的物理和免疫屏障,在牙周组织感...     

Chronic Periodontal Disease,Periodontal Pathogen Colonization,and Increased Risk of Precancerous Gastric Lesions

Background: This study assesses the association between periodontal pathogen colonization and the potential risk of developing precancerous lesions of gastric cancer (PLGC) in a clinical setting. Methods: Included were 35 newly diagnosed patients with PLGC and 70 age‐matched individuals without PLGC. A full‐mouth intraoral examination was performed to assess periodontal conditions. Stimulated whole saliva and pooled plaque samples were collected to evaluate colonization by Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans and to characterize oral microbial diversity in saliva and dental plaque. Results: Compared with the control group, patients with PLGC experienced higher prevalence of bleeding on probing (31.5% versus 22.4%; P <0.05), higher levels of T. denticola (P <0.01) and A. actinomycetemcomitans (P <0.01), and less bacterial diversity in their saliva (P <0.01). The final multivariate logistic regression model consisting of all key sociodemographic characteristics, oral health behavioral factors, and periodontal assessments revealed that elevated colonization with periodontal pathogens, specifically T. forsythia, T. denticola, and A. actinomycetemcomitans, decreased bacterial diversity in dental plaque, and not flossing teeth regularly was a significant predictor of increased risk of PLGC (P = 0.022). Conclusion: Findings of the present study provide new evidence suggesting that periodontal pathogen burdens and bacterial diversity in the oral cavity are important factors contributing to a potentially increased risk of developing precancerous gastric lesions.