高原低氧环境下牙周炎的发病机制

牙周炎的病理过程受全身和局部因素的综合调控,一些调查研究显示高原牙周炎患病率高于平原地区,显然高原特殊环境在牙周炎的发生和发展过程中起到一定的作用,因此本文就高原低氧环境下牙周病变组织的变化、可能的发病机制作一综述。     

缺氧条件下建立SD大鼠牙周炎动物模型的研究

目的:在模拟高原缺氧条件下建立稳定的缺氧SD大鼠牙周炎动物模型。方法:40只SD大鼠,雌雄各半,采用随机数字表法分为4组:常氧对照组(A组),常氧牙周炎组(B组),缺氧对照组(C组),缺氧牙周炎组(D组),每组10只。B、D组大鼠结扎牙颈部、高糖饮食、口腔涂菌及注射激素,A、C组不作任何处理,正常饮食。C、D组喂养的同时进入模拟海拔5000 m的低压氧舱。8 w后检测牙龈指数GI、菌斑指数PLI、牙周袋深度PD、牙槽骨吸收度ABL及组织病理学观察,对模型进行评估。结果:GI、PD及ABL指数在B组与A组,D组与C组,C组与A组,D组与B组比较均有统计学差异(P0.05)。PLI指数在B组与A组,D组与C组比较有统计学差异(P0.05),在C组与A组,D组与B组比较无统计学差异(P0.05)。HE染色见A、C组无明显改变,B、D组牙龈糜烂,结合上皮向根方增殖迁移,牙周膜间隙增宽。结论:将采用结扎牙颈部、高糖饮食、口腔涂菌及注射激素综合方法作用的SD大鼠放入模拟海拔5000 m的低压氧舱,建立模拟高原缺氧大鼠牙周炎模型具有可行性,为高原牙周病的防治奠基了实验基础。     

高原鼢鼠对戊巴比妥钠的麻醉反应

为了解高原鼢鼠Eospalax baileyi对植物次生代谢物的解毒能力,比较分析了戊巴比妥钠对高原鼢鼠和高原鼠兔Ochotona curzoniae产生的麻醉时间,及连续注射戊巴比妥钠对实验室内高原鼢鼠麻醉时间的影响过程。研究显示,在野外状态下,雌、雄高原鼢鼠的麻醉时间分别为134.23 min±27.73 min和121.14 min±35.23 min,雌、雄高原鼠兔的麻醉时间分别为90.92 min±31.10 min和116.37 min±37.13 min。统计分析表明,高原鼢鼠的麻醉时间显著长于高原鼠兔(P0.05),意味着高原鼢鼠的解毒能力弱于高原鼠兔,这可能与有毒植物在高原鼠兔食物中所占比例较大有关。在实验室条件下,雌、雄高原鼢鼠麻醉时间均有明显的波动,显示麻醉剂对高原鼢鼠的解毒能力有一定的诱导作用。此外,雌、雄高原鼢鼠之间麻醉时间的变化过程差别较大,这可能与两种性别的高原鼢鼠个体对新环境的应激行为明显不同有关。     

FcrRIIA基因多态性与牙周炎关系的研究进展

牙周炎是一种由菌斑引起的以牙周软组织和牙槽骨破坏为特征的慢性感染性疾病,其病因尚不明确,目前普遍认为是细菌 感染和宿主防御相互作用的结果,受遗传有关的宿主易感性、环境、行为因素的影响。致病菌的存在是牙周炎发生的必要条件,基 因因素影响宿主在应对细菌免疫应答过程中的强度,从而导致不同程度的牙周组织破坏。许多有关牙周炎基因方面的研究把目 光对准了在免疫调节和新陈代谢中发挥重要作用的物质的基因多态性,比如细胞因子、细胞表面受体、趋化因子、酶以及其他与 抗原识别有关的物质。FcrR 就是其中之一。FcrR 属于免疫球蛋白超家族,主要有FcrRI、FcrRII、FcrRIII 三类,大量研究表明 FcrRIIA 基因多态性与牙周炎的易感性有关。在针对不同种族的调查中,Fc酌RIIA 基因多态性与牙周炎的易感性的研究结果不尽 相同。也提示我们基因多态性的等位基因频率在各个种族之间存在差异,这种基因标识在界定牙周炎病因和预后方面的相关应 用会变得有所不同。基因诊断将会成为未来牙周病预防和治疗的新方向。本文主要对近年来FcrRIIA 基因多态性与牙周炎关系 的研究进展进行了综述。     

习服高原与脱习服

目的:研究人体进入低氧、低气压、低温的高海拔环境后机体出现生理应激反应和习服高原的过程。并探索在高原居住若干年后返回低海拔常氧地区机体呈现脱高原习服的临床征象。方法:习服高原环境采用回顾在藏工作50年资料、摘取相关数据,青藏铁路施工中调查资料、空运部队进藏公开发表资料之汇总共5万例。脱高原习服采用曾在藏工作生活过3~50年返回平原后问卷调查2 060人(分布全国各地)的综合资料。结果:①习服高原环境方面:5万例资料显示:当人进入高原低氧环境出现生理性的调节,临床上出现轻微的高原反应。也有个别人根本无任何反应。若体内缺氧状况得不到及时改善,原属生理应激反应就转变为病理生理范畴,出现重症高原反应,进一步发展可发生急性高原肺水肿、高原脑水肿,应迅速送医院治疗,贻误会造成死亡。在已习服高原人群中若干年后有10%左右的移居者出现红细胞过度增生,血红蛋白超过210mg/L,肺动脉收缩压大于50mmHg,右心增大,呈"多血貌"的慢性高原病(蒙赫氏病)。脱高原习服方面:我们采用在西藏曾已习服高原3~50年后返回平原2 060人,分布全国各地已完成脱高原习服和正在脱高原习服者问卷调查临床征象。②脱高原习服的症状轻重及持续时间的久暂与在高原环境海拔高度、年龄及习服高原时间久暂成正相关。一般情况下三年后就可完全脱高原习服,也有极少数人1‰无法脱习服,在低原无法生活而重返高原。在脱习服人群中有200人分布在黄土高原,这里平均海拔1 000m以上,这些人反应极轻微,况三个月后就完全脱高原习服。结论:习服高原最佳选择阶梯性适应训练法进入高原。脱习服如能选择阶梯性适应到低海拔地区,则可减少脱习服时间与减轻症状。     

高原鼠兔脑组织中精子特异性乳酸脱氢酶的作用

高原鼠兔对高原低氧环境有很强的适应性。研究发现,精子特异性乳酸脱氢酶(LDH-C4)基因在高原鼠兔脑组织中表达,为阐明LDH-C4在高原鼠兔脑组织中的作用,应用荧光定量PCR和Western blot方法,测定了Ldh-c基因在高原鼠兔脑组织中的表达水平;应用对精子特异性乳酸脱氢酶(LDH-C4)特异性的抑制剂(N-isopropyl oxamate),通过肌肉注射后,研究抑制剂对高原鼠兔脑组织中LDH比活力、乳酸和ATP含量的影响。结果表明,在mRNA和蛋白水平,Ldh-c基因在高原鼠兔脑组织中均有表达,相对表达水平分别为0.38±0.05和0.74±0.13;当肌肉注射1 m L 1 mol/L的抑制剂30 min后,血液中抑制剂浓度为0.08 mmol/L;与对照组相比,抑制剂组脑组织中LDH比活力、乳酸和ATP含量显著下降,抑制剂对LDH、乳酸和ATP的抑制率分别为30.78%、46.47%和21.04%。结果表明,精子特异性乳酸脱氢酶基因在高原鼠兔脑组织中表达。LDH-C4通过催化无氧糖酵解过程,为其脑组织生命活动提供至少20%的ATP,可能使高原鼠兔减小在低氧环境中对氧气的依赖,增强对低氧环境的适应能力。     

高原鼠兔的血象及其与低氧适应的关系

高原鼠兔是新开发的实验动物,能很好地适应高原低氧环境。本研究报道了驯化高原鼠兔的部分血液指标,并与野生高原鼠兔及部分其它实验动物和人的相应指标作了比较。同时对高原鼠兔能适应高原低氧环境的机理作了探讨。高原鼠兔红细胞数量高、体积小、红细胞膜表面积大,从而提高了Ｈｂ的利用率,使尽可能多的Ｈｂ参与摄氧和释氧。     

急性低氧时Wistar大鼠与高原鼠兔肺组织内皮型一氧化氮合酶基因表达的变化

目的探讨内皮型一氧化氮合酶(endothelial nitric oxide synthase, eNOS)在高原动物适应高原低氧环境中的作用.方法通过模拟4000m、6000m高原低氧,运用免疫组织化学技术,分别检测Wistar大鼠和高原鼠兔肺血管内皮和肺内气道上皮内皮型一氧化氮合酶蛋白表达水平的变化.结果无论是在肺血管内皮,还是肺内气道上皮,Wistar 大鼠eNOS蛋白表达在模拟4000m与6000m高原低氧处理2h后,均显著升高,而高原鼠兔基本保持不变,但高原鼠兔气道上皮eNOS的基础表达水平显著高于Wistar大鼠.结论相比Wistar大鼠,高原鼠兔eNOS基因表达在模拟高原低氧时增加较少甚或无明显增加,eNOS是急性高原低氧耐受过程中的一个重要机制.     

FcγRIIA基因多态性与牙周炎关系的研究进展

牙周炎是一种由菌斑引起的以牙周软组织和牙槽骨破坏为特征的慢性感染性疾病,其病因尚不明确,目前普遍认为是细菌感染和宿主防御相互作用的结果,受遗传有关的宿主易感性、环境、行为因素的影响。致病菌的存在是牙周炎发生的必要条件,基因因素影响宿主在应对细菌免疫应答过程中的强度,从而导致不同程度的牙周组织破坏。许多有关牙周炎基因方面的研究把目光对准了在免疫调节和新陈代谢中发挥重要作用的物质的基因多态性,比如细胞因子、细胞表面受体、趋化因子、酶以及其他与抗原识别有关的物质。FcγR就是其中之一。FcγR属于免疫球蛋白超家族,主要有FcγRI、FcγRII、FcγRIII三类,大量研究表明FcγRIIA基因多态性与牙周炎的易感性有关。在针对不同种族的调查中,FcγRIIA基因多态性与牙周炎的易感性的研究结果不尽相同。也提示我们基因多态性的等位基因频率在各个种族之间存在差异,这种基因标识在界定牙周炎病因和预后方面的相关应用会变得有所不同。基因诊断将会成为未来牙周病预防和治疗的新方向。本文主要对近年来FcγRIIA基因多态性与牙周炎关系的研究进展进行了综述。     

前列腺素E2在成人牙周炎诊断中的价值

利用前列腺素Ｅ_２在成人牙周炎病变过程中含量的变化,采用Ｂａｙｅｓ逐步判别回归分析方法,首次建立了成人牙周炎的计量诊断模型。     

Single nucleotide polymorphisms associated with aggressive periodontitis and severe chronic periodontitis in Japanese

Periodontitis is a common inflammatory disease causing destruction of periodontal tissues. It is a multifactor disease involving genetic factors and oral environmental factors. To determine genetic risk factors associated with aggressive periodontitis or severe chronic periodontitis, single nucleotide polymorphisms (SNPs) in multiple candidate genes were investigated in Japanese. We studied 134 patients with aggressive periodontitis, 117 patients with severe chronic periodontitis, and 125 healthy volunteers without periodontitis, under case-control setting, and 310 SNPs in 125 candidate genes were genotyped. Association evaluation by Fisher's exact test (p < 0.01) revealed statistically significant SNPs in multiple genes, not only in inflammatory mediators (IL6ST and PTGDS, associated with aggressive periodontitis; and CTSD, associated with severe chronic periodontitis), but also in structural factors of periodontal tissues (COL4A1, COL1A1, and KRT23, associated with aggressive periodontitis; and HSPG2, COL17A1, and EGF, associated with severe chronic periodontitis). These appear to be good candidates as genetic factors for future study.     

Microbiome Profiles in Periodontitis in Relation to Host and Disease Characteristics

Periodontitis is an inflammatory condition that affects the supporting tissues surrounding teeth. The occurrence of periodontitis is associated with shifts in the structure of the communities that inhabit the gingival sulcus. Although great inter-subject variability in the subgingival microbiome has been observed in subjects with periodontitis, it is unclear whether distinct community types exist and if differences in microbial signatures correlate with host characteristics or with the variable clinical presentations of periodontitis. Therefore, in this study we explored the existence of different community types in periodontitis and their relationship with host demographic, medical and disease-related clinical characteristics. Clustering analyses of microbial abundance profiles suggested two types of communities (A and B) existed in the 34 subjects with periodontitis evaluated. Type B communities harbored greater proportions of certain periodontitis-associated taxa, including species historically associated with the disease, such as Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola, and taxa recently linked to periodontitis. In contrast, subjects with type A communities had increased proportions of different periodontitis-associated species, and were also enriched for health-associated species and core taxa (those equally prevalent in health and periodontitis). Periodontitis subgingival clusters were not associated with demographic, medical or disease-specific clinical parameters other than periodontitis extent (proportion of sites affected), which positively correlated with the total proportion of cluster B signature taxa. In conclusion, two types of microbial communities were detected in subjects with periodontitis. Host demographics and underlying medical conditions did not correlate with these profiles, which instead appeared to be related to periodontitis extent, with type B communities present in more widespread disease cases. The two identified periodontitis profiles may represent distinct dysbiotic processes potentially requiring community-tailored therapeutic interventions.     

实验性牙周炎合并咬合创伤模型的研究进展

不正常的咬合接触关系或者过大的咬合力,造成咀嚼系统各部位的病理性损害或者适应性变化称为咬合创伤,而牙周炎是一种慢性炎症性疾病,是由牙菌斑生物膜引起的牙周组织的感染性疾病,导致牙周支持组织的破坏-牙周袋形成和炎症、进行性的附着丧失和牙槽骨吸收。近年来有学者对咬合创伤作为一类独立疾病进行研究,也有学者将咬合创伤作为牙周炎的一个重要的局部促进因素进行研究。牙周炎和咬合创伤的关系至今不是很明确,关于咬合创伤和牙周炎的相互关系,虽然早在20世纪初已开始研究,却直到70年代才有严格对照的动物实验研究。大鼠牙周炎合并咬合创伤的模型在牙周炎和咬合创伤关系的相关研究中起着十分重要的作用。本文从牙周炎和咬合创伤复合模型的建立方面,综述了各种建模方法的研究进展,以期为牙周炎合并咬合创伤的深入研究提供参考。     

Risk factors for bovine periodontal disease – a preliminary study

The work presented in this pilot study aimed to identify potential risk factors associated with bovine periodontitis development. Bovine periodontitis is a multifactorial polymicrobial infectious disease for which the aetiopathogenesis and risk factors are not fully understood. From cattle slaughtered in an abattoir in Scotland, 35 dental arcades with periodontal lesions and 40 periodontally healthy arcades were selected over seven visits for study. Multivariable logistic regression analysis was used to evaluate the association between periodontitis and the independent variables, gender, age and breed. For every increase in year of age, cattle were 1.5 times more likely to have periodontitis. A graphical analysis indicated that within the limits of this study, we could not detect any major influence of breed on the age-effect. Although logistic regression analysis demonstrated that periodontitis lesions are more prevalent with increasing age of cattle the underlying mechanisms remain unclear. It is likely that periodontitis is an important cause of oral pain in older cattle and can contribute to reduced productivity/performance. Further studies with a larger sample size are necessary to elucidate the associations between potential risk factors and periodontitis in cattle and to define its effects on animal welfare and productivity.     

Resveratrol improves oxidative stress and prevents the progression of periodontitis via the activation of the Sirt1/AMPK and the Nrf2/antioxidant defense pathways in a rat periodontitis model

Oxidative stress is a key factor regulating the systemic pathophysiological effects associated with periodontitis. Resveratrol is a phytochemical with antioxidant and anti-inflammatory properties that can reduce oxidative stress and inflammation. We hypothesized that resveratrol may prevent the progression of periodontitis and reduce systemic oxidative stress through the activation of the sirtuin 1 (Sirt1)/AMP-activated protein kinase (AMPK) and the nuclear factor E2-related factor 2 (Nrf2)/antioxidant defense pathways. Three groups of male Wistar rats (periodontitis treated with melinjo resveratrol, periodontitis without resveratrol, and control rats with no periodontitis or resveratrol treatment) were examined. A ligature was placed around the maxillary molars for 3 weeks to induce periodontitis, and the rats were then given drinking water with or without melinjo resveratrol. In rats with periodontitis, ligature placement induced alveolar bone resorption, quantified using three-dimensional images taken by micro-CT, and increased proinflammatory cytokine levels in gingival tissue. Melinjo resveratrol intake relieved alveolar bone resorption and activated the Sirt1/AMPK and the Nrf2/antioxidant defense pathways in inflamed gingival tissues. Further, melinjo resveratrol improved the systemic levels of 8-hydroxydeoxyguanosine, dityrosine, nitric oxide metabolism, nitrotyrosine, and proinflammatory cytokines. We conclude that oral administration of melinjo resveratrol may prevent the progression of ligature-induced periodontitis and improve systemic oxidative and nitrosative stress.     

慢性牙周炎与原发性肝硬化的相关性分析

目的:探究慢性牙周炎与原发性肝硬化之间的相关性。方法:选择2017年1月至2019年1月于我院接受治疗的60例原发性肝硬化患者为研究组,选择同期于我院接受体格检查的100例健康个体为对照组,对两组患者分别实施牙周检查,对比两组患者牙周炎发生率,分析吸烟、饮酒对牙周炎发生率影响,按照Child-改良分级法对肝硬化患者进行评分并分级,对比各级原发性肝硬化患者慢性牙周亚发生率,并就慢性牙周炎与肝硬化相关性进行分析。结果:(1)对照组慢性牙周炎发生率显著低于研究组慢性牙周炎发病率(44.00%vs. 71.67%,P0.05);(2)研究组和对照组中吸烟者的慢性牙周炎患病率显著高于不吸烟者(P0.05),研究组中吸烟者发生慢性牙周炎患病率高于对照组,对比无统计学意义(P0.05);研究组和对照组饮酒者的慢性牙周炎患病率显著高于不饮酒者(P0.05),研究组中饮酒者发生慢性牙周炎患病率显著高于对照组(P0.05);(3)随着原发性肝硬化患者评分的升高,患者牙周炎患病率也随之上升,牙周附着丧失程度也出现加剧(P0.05)。结论:原发性肝硬化患者慢性牙周炎患病率高于健康个体,随着肝硬化患者病情的加剧,患者慢性牙周炎发生率也随之上升;另外,吸烟及饮酒会增加健康个体慢性牙周炎患病率。     

Secretory leukocyte protease inhibitor reduces inflammation and alveolar bone resorption in LPS-induced periodontitis in rats and in MC3T3-E1 preosteoblasts

In periodontitis, alveolar bone resorption is induced by excessive host immune and inflammatory response against bacterial infection. Secretory leukocyte protease inhibitor (SLPI) has anti-bacterial and anti-inflammatory activity in inflammatory responses. SLPI inhibits joint inflammation and bone destruction, but the function of SLPI in periodontitis is unclear. Therefore, this study investigated whether SLPI inhibits the inflammatory response and alveolar bone resorption in LPS-induced periodontitis of rats. Micro-computed tomography and histological analysis showed that SLPI inhibited alveolar bone resorption by LPS-induced periodontitis. Immunohistochemistry revealed that SLPI decreased tumor necrosis factor-α (TNF-α) and interleukine-1β (IL-1β) expression in periodontitis tissue, and decreased mRNA and protein expression of TNF-α and IL-1β in LPS-stimulated MC3T3-E1 cells. The results indicated that SLPI reduced alveolar bone resorption in LPS-induced periodontitis and inhibited inflammatory cytokine, such as TNF-α and IL-1β, expression in LPS-stimulated MC3T3-E1 preosteoblasts. Therefore, SLPI could be a regulatory molecule by inhibiting alveolar bone resorption through the reduction of inflammatory cytokines, and inducing osteoblast activation for bone formation.     

牙周炎病人龈下韦荣球菌的实验观察

目的 探讨牙周炎病人龈下韦荣球菌的变化及牙周炎的细菌因素。方法 采用厌氧培养及活菌计数（CFU）的方法检测莲球菌（Streptococcus）、韦荣球菌（Veillonella）、乳杆菌(Lactobacillus）及类杆菌（Bacteroids)的含量。结果牙周炎病人龈下莲球菌含量显著低于正常对照组（P＜0.001）,韦荣球菌、乳杆菌及类杆菌的含量显著高于正常对照组（P＜0.001）。结论 牙周炎病人龈下菌群处于严重失调状态,韦荣球菌对牙周炎发病的作用应引起高度重视。