局部药物对口腔溃疡治疗作用的动物实验研究

目的研究3种不同制剂药物局部治疗口腔溃疡的效果,为临床应用提供实验依据。方法利用冰醋酸法建立动物口腔溃疡模型,应用3种药物局部治疗,分别于用药48小时、96小时后每组处死2只兔,切取标本进行光镜观察。结果用药96小时后,重组牛碱性成纤维细胞生长因子喷剂组有大量成纤维细胞增生、毛细血管增生,上皮基本愈合。结论重组牛碱性成纤维细胞生长因子喷剂能明显促进口腔溃疡愈合。     

复发性口腔溃疡动物模型改进

本实验应用动物的口腔粘膜、心脏、肝脏组织及提取口腔粘膜蛋白质分别作为抗原，通过免疫学技术，诱导兔产生口腔粘膜病损。其体征、组织学变化、血清中抗口腔粘膜抗体检测及免疫荧光抗体检测等观察结果，说明口腔粘膜的组织匀浆和粘膜蛋白质作为抗原，均可引起口腔粘膜溃疡病损，进一步证实这种方法可作为人类ＲＡＵ的动物模型。     

磨牙缺失对昆明小鼠空间学习记忆能力的影响

目的：观察牙齿缺失对昆明小鼠空间学习记忆能力的影响.方法：90只成年雄性昆明小鼠随机分为上颌拔牙组和假手术组、下颌拔牙组和假手术组.术后8w采用Morris水迷宫做行为学测试.结果：拔牙组小鼠4d平均逃避潜伏期（上颌组：38.6±14.6s;下颌组：39.0±14.0s）明显长于假手术组（上颌组：29.0±19.7s;下颌组 29.1±18.6s）（P＜0.01）.拔牙组小鼠的第一次穿越平台时间（上颌组：13.6±3.3s;下颌组：13.1±4.3s）明显长于假手术组（上颌组：5.8±3.9s;下颌组：5.9±2.2s）（P＜0.01）.结论：磨牙缺失8w后昆明小鼠空间学习记忆能力下降.     

多功能频谱治疗仪对金黄地鼠创伤口腔溃疡治疗作用的研究

目的：研究多功能频治疗仪（ＷＳ频谱仪）对金枘地鼠创伤性口腔疡的治疗作用。方法：６～８周龄金黄地鼠,用机械方法制造动物口腔粘膜创伤性溃疡,用ＷＳ频谱治疗仪进行治疗,观察其促进溃疡愈合的作用。结果：治疗组动物平均愈合时间明显少于对照组缩短２天,第４、７、９天溃疡面积及第４天溃疡临床观察值两个方面进行统计学分析均有显著性差异。结论：ＷＳ频谱仪对实验动物的创伤性怕有着明显的促愈合作用。     

五倍子缓释药膜治疗口腔溃疡的动物实验研究

目的：观察五倍子缓释药膜治疗口腔溃疡的效果。方法：用冰醋酸法建立动物口腔溃疡模型,分3组,五倍子缓释药膜组及锡类散组为实验组,每日用药2次。另1组为空白对照组。分别于用药2 d,4 d,6 d观察溃疡愈合情况。结果：五倍子组平均愈合天数为（4.70±1.06）d,明显优于其余两组（P〈0.01）。结论：复方五倍子缓释药膜能明显促进口腔溃疡的愈合。     

口腔溃疡动物实验模型的建立

目的为评价局部用药效果建立动物实验性口腔溃疡模型。方法利用40％冰醋酸烧灼兔上唇60秒,观察48小时形成溃疡,切取标本分别采用肉眼、光镜、扫描和透射电镜观察鉴定。结果溃疡病理特点与人类复发性口腔溃疡基本相似。结论成功制备了动物口腔溃疡模型。     

多功能频谱治疗仪对金黄地鼠创伤性口腔溃疡治疗作用的研究

目的:研究多功能频谱治疗仪(简称WS频谱仪)对金黄地鼠创伤性口腔溃疡的治疗作用.方法:6～8周龄金黄地鼠,用机械方法制造动物口腔粘膜创伤性溃疡,用WS频谱治疗仪进行治疗,观察其促进溃疡愈合的作用.结果:治疗组动物平均愈合时间明显少于对照组,特别是高能量组平均愈合时间较对照组缩短2天,第4、7、9天溃疡面积及第4天溃疡临床观察值两个方面进行统计学分析均有显著性差异.结论:WS频谱仪对实验动物的创伤性溃疡有着明显的促愈合作用.     

免疫方法建立复发性口腔溃疡动物模型

目的 :利用试验家兔口腔黏膜蛋白注射方法 ,建立复发性口腔溃疡动物模型 ,为研究人类RAU的发病机制及治疗提供理论基础。方法 :应用从试验家兔提取的口腔黏膜蛋白及沉淀物 ,分别作为抗原免疫家兔。将上述抗原注入家兔脊柱二侧皮内 ,2周注射一次 ,观察家兔口腔溃疡的发病情况及愈合情况。检测试验家兔血清中抗口腔黏膜抗体并做溃疡的组织病理学检查。结果 :以口腔黏膜蛋白作为抗原的实验家兔都发生了RAU ,血清中抗口腔黏膜抗体阳性。以口腔黏膜蛋白作为抗原组与以沉淀物作为抗原组引发实验家兔RAU有显著统计学差异(p <0 .0 1)。结论 :利用兔口腔黏膜蛋白作为抗原 ,可引起实验家兔发生RAU ,其临床表现及组织学检查均与人类RAU相似 ,表明此动物模型可作为研究人类RAU的模型。也提示了人类RAU的发生可能与自身免疫有关。     

脉冲Nd：YAG激光治疗口腔溃疡的临床与动物实验研究

目的 为了采用脉冲Ｎｄ：ＹＡＧ激光治疗口腔溃疡。方法 在５只健康大白鼠口腔内,用甲基紫精（除草剂）注射于颊粘膜下制成溃疡动物模型,再模拟临床应用脉冲Ｎｄ：ＹＡＧ激光进行治疗。对８３例口腔溃疡进行了对照观察。结果 ８３例口腔溃疡性损害,治疗组显效率为４８％,对照组为１６％,两者对比有显著性差异。经激光治疗后的溃疡模型提前３天愈合。结论 本研究为脉冲Ｎｄ：ＹＡＧ激光治疗口腔溃疡性损害提供了重要的临床观     

两种方法建立SD大鼠RAU模型的对比研究

目的:比较实验性SD大鼠口腔黏膜组织匀浆+完全弗氏佐剂的免疫注射法和乙酸灼烧法建立RAU动物模型,为研究人类RAU的发病机制及治疗提供理论基础。方法:应用免疫法和灼烧法建立大鼠RAU模型,观察大鼠口腔内RAU的形成及体重和摄食量变化情况。研究溃疡的组织学改变、流式细胞仪测定外周血T淋巴细胞变化。结果:2种方法建模的实验大鼠都发生了RAU,模型建立过程中大鼠体重和摄食量均有变化且有显著统计学差异(P<0.05)。流式细胞仪测定免疫组、乙酸组外周血T淋巴细胞发现CD3+CD4+、CD4+/CD8+均低于对照组(P<0.05)。乙酸组CD3+CD8+的细胞数高于对照组但统计学差异无显著性(P>0.05)。结论:利用免疫法和乙酸法均可引起SD大鼠发生实验性RAU,其临床表现及组织学观察均与人类RAU相似。     

口腔溃疡药膜对豚鼠实验性口腔溃疡的治疗作用

将口腔溃疡散处方的各组份,经不同方法提取,制得干浸膏.以聚乙烯醇做基质,用铺板器制成口腔溃疡药膜.用90%石碳酸烧灼法,制作豚鼠口腔溃疡模型,观察该药膜对口腔溃疡的治疗作用.结果表明,口腔溃疡药膜对豚鼠实验性口腔溃疡,有明显的促进愈合作用.     

Plasma polyunsaturated fatty acids and periodontal recovery in Taiwanese with periodontitis: A significant relationship

BackgroundPlasma levels of polyunsaturated fatty acids (PUFAs) are different before and after periodontal treatment. Asians and Westerners have significantly different baseline levels of plasma PUFAs. However, no Asian study has reported the effects of nonsurgical treatment on the correlation between periodontal condition and plasma levels of PUFAs. We analyzed whether recovery from periodontitis was correlated with the elevation of plasma fatty acids 3 months after the nonsurgical intervention and with no recommended supplements.DesignThirty-five Taiwanese patients with periodontitis were recruited. Probing pocket depths (PPDs) and clinical attachment levels (CALs) were measured at baseline and 3 months after the nonsurgical treatment. Plasma levels of fatty acids were determined using gas chromatography. Differences and correlations between plasma fatty acid composition and periodontitis severity at baseline and 3 months after treatment were determined.ResultsTwenty-six patients completed the study. At the baseline, PPDs were negatively correlated with plasma n-3 PUFAs (r = −0.52, p < 0.01), but at 3 months post intervention, periodontitis severity had declined and the weight percentages of n-3 PUFAs, DPA, and DHA were significantly (p = 0.019, 0.005, and 0.037, respectively) higher. The recovery percentages of CALs were positively and significantly correlated with plasma ΔPUFAs and the percentage of Δn-3 PUFAs in ΔPUFAs (r = 0.42 and 0.45, respectively; p < 0.05 for both).ConclusionsWe conclude that a higher weight percentage of n-3 PUFAs in total PUFAs was related to the recovery of CALs 3 months after the nonsurgical periodontal treatment. However, no such relationship was found for PPDs.     

The inhibitory action of fatty acids on oral bacteria

Saturated and unsaturated fatty acids and fatty acid derivatives were examined for their growth-inhibitory effects towards three selected oral bacteria: Porphyromonas gingivalis, Selenomonas artemidis , and Streptococcus sobrinus. Of the 45 compounds surveyed, only one, myristoleic acid, was inhibitory towards S. artemidis at a concentration <100 μg/ml. cis -Hexadecenoic and cis -octadecenoic acids were generally inhibitory towards P. gingivalis and S. sobrinus , but there was no correlation between the position of the double bond and the minimum inhibitory concentration. Supra-minimum inhibitory concentrations of palmitoleic acid did not promote leakage of intracellular materials from either P. gingivalis or S. sobrinus , nor was l - iso -leucine uptake by S. sobrinus inhibited. Fatty acids and derivatives were also examined for prospective synergistic or antagonistic interactions with thymol vis-à-vis growth inhibition of the test strains. Laurie acid and myristic acid each behaved synergistically with thymol to inhibit the growth of at least one test strain, whereas cis -10-heptadecenoic acid and thymol were noticeably antagonistic towards the growth of S. sobrinus.     

非肥胖型糖尿病小鼠自发性涎腺炎的发生与发展

目的 观察雌性非肥胖型糖尿病（NOD）小鼠自发性涎腺炎的发生发展过程。方法 选择5、10、15、20周龄雌性NOD小鼠各6只。测定刺激全唾液流率（STFR）、施墨试验、唾液总蛋白、常规HE切片及电镜超微结构观察涎腺组织的改变。以BALB／c小鼠作对照。结果 10、15、20周NOD小鼠STFR、唾液总蛋白均明显低于对照组（P〈0．05），相应的下颌下腺分泌颗粒减少。10周雌性NOD小鼠涎腺炎发病率为4／6，15、20周均为6／6。淋巴细胞浸润主要见于下颌下腺，舌下腺极少，腮腺未见。10周时NOD小鼠已有淋巴细胞浸润灶形成。15周显著增多而且面积增加。STFR与淋巴细胞浸润灶数呈负相关。结论 雌性NOD小鼠5～10周淋巴细胞开始浸润下颌下腺，刺激唾液和蛋白分泌降低。不同腺体受累情况不同。     

Effect of dietary omega-3 polyunsaturated fatty acids on experimental periodontitis in the mouse

Background and Objective:  Periodontitis is an infective disease caused predominantly by gram-negative anerobes. The host inflammatory response to these bacteria causes alveolar bone loss, which characterizes periodontitis. Omega-3 polyunsaturated fatty acids have recognized anti-inflammatory effects; their oxygenated derivatives are key mediators in reducing inflammation. In this study we tested the hypothesis that dietary supplementation with tuna fish oil rich in the n-3 polyunsaturated fatty acid, docosahexaenoic acid, would reduce alveolar bone loss in mice inoculated with periodontopathic bacteria.
Material and Methods:  Adult mice were fed experimental diets containing either 10% tuna oil or Sunola oil for 57 d. After 14 d, 35 mice on each diet were inoculated orally with Porphyromonas gingivalis , with a mixture of P. gingivalis and Fusobacterium nucleatum , with carboxymethylcellulose or remained untreated. The mice were killed, and soft tissue biopsies from the oral cavity of treated mice were used to determine the polyunsaturated fatty acid concentrations. The maxilla was removed, stained and digitally imaged to assess bone loss around the upper molars.
Results:  n-3 polyunsaturated fatty acid levels were significantly higher in oral soft tissues of mice fed tuna oil compared with the control group. Mice fed tuna oil and inoculated with P. gingivalis or with the combination of F. nucleatum and P. gingivalis exhibited 72% and 54% less alveolar bone loss respectively, compared with the treatment control group.
Conclusion:  Alveolar bone loss was inversely related to n-3 polyunsaturated fatty acid tissue levels. In conclusion, fish oil dietary supplementation may have potential benefits as a host modulatory agent in the prevention and/or adjunctive management of periodontitis.     

The effects of medium chain fatty acids and fluoride on fissure caries in Wistar rats

This work was to compare the degree of caries protection provided by fatty acids with chain lengths of 9-12 carbons and to assess the anti-caries potential of a fluoride-fatty acid mixture. Male Wistar rats were weaned at 21 days, maintained on a standard laboratory diet for 7 days and then provided with a cariogenic, 45% sucrose diet for 34 days. This regimen produced a very reproducible degree of fissure caries and the inclusion of 1% powdered potassium nonanoate or decanoate in the diet gave large and significant reductions in total and advanced lesions. Decanoate was significantly more inhibitory towards advanced lesions than was nonanoate. In contrast, 1% potassium laurate was considerably less effective under these conditions. Caries protection with a mixture of 0.25% decanoate and 76 parts/10(6) fluoride was found to be cumulative rather than synergistic. It is suggested that the optimal effect obtained with decanoate was due to a favourable combination of the surfactant and wetting properties of this molecule at the low pH values found in fissure dental plaque. It is also suggested that fluoride and decanoate acted in an independent manner to enhance remineralization of early lesions and to inhibit the acidogenic flora, respectively.     

口腔疣状癌伴灶性鳞癌颈淋巴结转移灶裸鼠移植瘤模型的建立

目的:建立口腔疣状癌伴灶性鳞癌颈淋巴结转移灶移植瘤原代模型,探讨建立模型的方法.方法:将口腔疣状癌伴灶性鳞癌颈淋巴结转移组织,通过组织块皮下接种法建立颈部淋巴结转移灶模型.观察其生长状况,对移植瘤、裸鼠肝、肾、肺及淋巴结行系列检查并与来源肿瘤组织进行比较.结果:成瘤率87.5%(7/8),移植瘤具有来源肿瘤组织类似的形态学特征,肝、肾、肺未见转移,腋下及腹股沟淋巴结反应性增生.结论:通过组织块皮下接种法,成功建立了口腔疣状癌伴灶性鳞癌颈淋巴结转移灶移植瘤原代模型.     

Pilot study on n-3 polyunsaturated fatty acids in the treatment of human experimental gingivitis

Abstract The anti-inflammatory effect of n-3 PUFA on the gingivae has already been demonstrated in animal models. The aim of this double-blind, randomized pilot study versus placebo is to evaluate this action in human experimentally-induced gingivitis. For 14 days (D0-D14), 37 healthy volunteers practised intensive oral hygiene, then abstained from brushing their teeth for 21 days (D14 to D35). On D28, the patients were randomized into 2 groups: 18 received the drug (fish oil: 30%n-3 PUFA) and 19 received the placebo (olive oil containing only 1% of n-3 PUFA) at a daily dosage of 6 g (i.e., 1.8 g of n-3 PUFA) 3× for 8 days (D28-D35). The plaque (PI), gingival (GI) and papillary bleeding (PBI) indices were measured on D14, D28 and D35. On D28 and D35, 10 volunteers underwent removal of an inter-dental vestibular papilla, between the 1st and the 2nd superior premolars, to measure out arachidonic acid (AA), eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and docosapentaenoic acid (DPA). A gingival biopsy was also taken in another 11 patients, to assay prostaglandin E₂ (PGE₂) and leukotriene B₄ (LTB₄). The clinical results of the trial demonstrated, in particular, a significant reduction of GI in the treated group (p)<0.05, Student t-test), but no significant difference between the groups. The biochemical results showed that EPA, DHA and DPA were found in the cells sampled, at higher levels in the subjects taking the drug, with a significant difference for EPA between the 2 groups (p<0.05, Student t-test). The levels of AA, PGE₂ and LTB₄ are reduced in the experimental group and increased in the control group, with no significant difference. The LTB₄ levels decreased but this difference just failed to reach significance (p= 0.09. Student t-test). This human experimental gingivitis study demonstrated that n-3 PUFA induced a tendency towards reduced inflammation but it was not possible to conclude significant efficacy.     

Effects of short‐chain fatty acids on Actinomyces naeslundii biofilm formation

Actinomyces naeslundii is an early colonizer and has important roles in the development of the oral biofilm. Short‐chain fatty acids (SCFA) are secreted extracellularly as a product of metabolism by gram‐negative anaerobes, e.g. Porphyromonas gingivalis and Fusobacterium nucleatum; and the SCFA may affect biofilm development with interaction between A. naeslundii and gram‐negative bacteria. Our aim was to investigate the effects of SCFA on biofilm formation by A. naeslundii and to determine the mechanism. We used the biofilm formation assay in 96‐well microtiter plates in tryptic soy broth without dextrose and with 0.25% sucrose using safranin stain of the biofilm monitoring 492 nm absorbance. To determine the mechanism by SCFA, the production of chaperones and stress‐response proteins (GrpE and GroEL) in biofilm formation was examined using Western blot fluorescence activity with GrpE and GroEL antibodies. Adding butyric acid (6.25 mm ) 0, 6 and 10 h after beginning culture significantly increased biofilm formation by A. naeslundii, and upregulation was observed at 16 h. Upregulation was also observed using appropriate concentrations of other SCFA. In the upregulated biofilm, production of GrpE and GroEL was higher where membrane‐damaged or dead cells were also observed. The upregulated biofilm was significantly reduced by addition of anti‐GroEL antibody. The data suggest biofilm formation by A. naeslundii was upregulated dependent on the production of stress proteins, and addition of SCFA increased membrane‐damaged or dead cells. Production of GroEL may physically play an important role in biofilm development.