牙周炎患者自身组织核酸刺激小鼠巨噬细胞后对破骨相关因子mRNA表达的影响

目的 检测牙周炎患者自身组织核酸刺激巨噬细胞后破骨相关因子白细胞介素-6（IL-6）、白细胞介素-12（IL-12）p35、IL-12p40、基质金属蛋白酶-9（MMP-9）、活化T细胞核因子 1（NFATc1）、核激活因子κB受体（RANK）、肿瘤坏死因子-α（TNF-α）mRNA的表达,观察牙周炎患者自身组织核酸对巨噬细胞向破骨细胞分化的影响作用。方法 采集翻瓣术中慢性牙周炎患者炎症牙周组织及正畸患者健康牙拔除术获取的健康牙周组织,提取组织总RNA逆转录cDNA。培养小鼠巨噬细胞系RAW264.7,加入质量浓度1 μg•mL-1的特定序列寡核苷酸MT01共孵育3 h后（以1 μg•mL-1的PBS作为对照）,加入已提取的炎症牙周组织及健康牙周组织cDNA（质量浓度为1 μg•mL-1）。实验分4组：健康组织cDNA,炎症组织cDNA,MT01+健康组织cDNA,MT01+炎症组织cDNA。4组细胞分别孵育3、6、12、24 h,采用实时定量聚合酶链反应法检测破骨相关因子IL-6、IL-12p35、IL-12p40、MMP-9、NFATc1、RANK及TNF-α mRNA的表达,进行两两组间比较。结果 牙周炎患者自身组织核酸可上调RAW264.7破骨相关因子IL-6、IL-12p35、IL-12p40、MMP-9、NFATc1、RANK及TNF-α mRNA的表达;在免疫抑制剂MT01的作用下,牙周炎患者自身组织核酸上调RAW264.7内破骨相关因子mRNA的表达状况受到抑制。结论 牙周炎患者自身组织核酸可以影响小鼠巨噬细胞向破骨细胞的分化。     

慢性牙周炎患者唾液蛋白酶谱分析

目的 比较慢性牙周炎患者和牙周健康者的唾液蛋白谱差异,以期为慢性牙周炎的诊断和治疗监测提供依据。方法 收集慢性牙周炎患者和牙周健康者刺激性唾液,采用蛋白芯片技术,对慢性牙周炎患者和正常人的唾液蛋白酶谱进行分析。结果 慢性牙周炎患者和牙周健康者唾液蛋白酶的表达具有统计学差异。其中,慢性牙周炎患者唾液中去整合素金属蛋白酶（ADAM）8,基质金属蛋白酶（MMP）-8、-12,脑啡肽酶/CD10,尿激酶纤维蛋白溶酶原激活剂/尿激酶的表达高于牙周健康者（P<0.01）;ADAM9,含凝血酶敏感素基序的去整合素金属蛋白酶（ADAMTS）1、13,组织蛋白酶B、E、L、V、X/Z/P,激肽释放酶6、7、11、13,MMP-9,蛋白酶3、早老素1和前蛋白转化酶9的表达低于牙周健康者（P<0.05）。结论 慢性牙周炎患者的唾液蛋白酶谱与牙周健康者具有显著差异,唾液蛋白酶谱分析将有望成为慢性牙周炎临床诊断和治疗监测的实验检查手段。     

鼻咽癌患者放射治疗前后龋活性及唾液中钙、磷质量浓度的变化

目的 探讨鼻咽癌患者放射治疗前后龋活性的变化,定量分析鼻咽癌患者放射治疗前后唾液中的钙、磷质量浓度的变化。方法 选择鼻咽癌患者28例为试验组,健康志愿者20例为对照组。采用刃天青纸片法检测试验 组放射治疗前、放射治疗（放射剂量为70 Gy）后龋活性的变化;采用火焰原子吸收光谱法和钼锑抗分光光度法测定试验组放射治疗前、放射治疗（放射剂量为70 Gy）后及对照组非刺激性唾液中钙、磷的质量浓度。结果 试验组放射治疗后龋活性增加,与治疗前的差异有统计学意义（P＜0.01）。试验组放射治疗前唾液中钙质量浓度为（63.19± 3.27）mg·L-1,治疗后为（33.38±0.32）mg·L-1;放射治疗前磷质量浓度为（132.96±5.13）mg·L-1,治疗后为（49.18±2.66）mg·L-1。放射治疗前后唾液中钙、磷质量浓度的差异均有统计学意义（P＜0.01）,放射治疗后低于治疗前。结论 鼻咽癌患者放射治疗后的龋活性增加,唾液中钙、磷质量浓度降低。     

中、重度慢性牙周炎与冠心病相关性的研究

目的探讨中、重度慢性牙周炎与冠心病的相关性以及急性期蛋白成分纤维蛋白原（Fg）在其中的作用。方法选择不同牙周和心血管健康状态者共95人,分为健康对照（HC）组、牙周炎（MSP）组、冠心病（CHD）组和MSP+CHD组,检测牙周临床指数、血浆Fg质量浓度和冠心病常规血清学指标,采用单因素方差分析和协方差分析法分析3种指标间的关系。结果4组研究对象的Fg质量浓度分别为（2.36±0.37）、（3.63±0.73）、（4.08±0.84）和（4.14±0.96）g/L,中、重度慢性牙周炎患者（MSP组和MSP+CHD组）血浆Fg质量浓度明显高于HC组（P<0.01）;排除血压和体重指数的影响后,中、重度慢性牙周炎患者发生CHD的可能性高于牙周健康者（OR=2.527,P=0.047）。结论中、重度慢性牙周炎可能是冠心病的危险因素,而Fg则可能是联系二者的生物学基础之一。     

慢性牙周炎牙周基础治疗前后血清超敏C反应蛋白与单核细胞趋化蛋白-1变化研究

目的    研究慢性牙周炎对血清超敏C反应蛋白（hs-CRP）和单核细胞趋化蛋白-1（MCP-1）浓度的影响。方法    选取2015—2016年于中国人民解放军陆军总医院口腔科门诊就诊的80例牙周炎患者（牙周病组）和40名无牙周炎症状的志愿者（对照组）。初诊记录探诊出血（BOP）、牙周探诊深度（PD）和临床附着丧失（CAL）情况,收集空腹静脉血,检测血清超敏C反应蛋白（hs-CRP）和单核细胞趋化蛋白-1（MCP-1）。对牙周病组进行为期3个月的牙周基础治疗,治疗结束3个月后,再次收集空腹静脉血,检测血清hs-CRP和MCP-1。结果    牙周病组与对照组基线条件无明显差异。对照组hs-CRP和MCP-1浓度为（1.48 ± 1.1）mg/L和（42.3 ± 4.9）mg/L,牙周病组分别为（3.89 ± 2.8）mg/L和（88.7 ± 5.8）mg/L,两组差异有统计学意义（P＜0.05）。牙周治疗结束3个月后,牙周病组hs-CRP和MCP-1浓度为（2.04 ± 1.5）mg/L和（64.2 ± 5.1）mg/L,与治疗前比较差异有统计学意义（P＜0.05）。结论    　慢性牙周炎可引起低滴度菌血症,造成血清炎症标志物hs-CRP和MCP-1浓度增高,有效的牙周基础治疗可降低血清hs-CRP和MCP-1。     

左下颌角部婴儿型肌纤维瘤病1例

目的探讨中、重度慢性牙周炎与冠心病的相关性以及急性期蛋白成分纤维蛋白原（Fg）在其中的作用。方法选择不同牙周和心血管健康状态者共95人，分为健康对照（HC）组、牙周炎（MSP）组、冠心病（CHD）组和MSP+CHD组，检测牙周临床指数、血浆Fg质量浓度和冠心病常规血清学指标，采用单因素方差分析和协方差分析法分析3种指标间的关系。结果4组研究对象的Fg质量浓度分别为（2.36±0.37）、（3.63±0.73）、（4.08±0.84）和（4.14±0.96）g/L，中、重度慢性牙周炎患者（MSP组和MSP+CHD组）血浆Fg质量浓度明显高于HC组（P<0.01）；排除血压和体重指数的影响后，中、重度慢性牙周炎患者发生CHD的可能性高于牙周健康者（OR=2.527，P=0.047）。结论中、重度慢性牙周炎可能是冠心病的危险因素，而Fg则可能是联系二者的生物学基础之一。     

牙龈沟液中骨膜蛋白含量与牙周炎的关系

目的探讨骨膜蛋白与牙周炎的关系,检测和对比牙周炎患者与健康对照组龈沟液中骨膜蛋白的含量。 方法从2016年9月至2018年6月于深圳市人民医院口腔内科的初诊患者中直接抽选法随机选取48例慢性牙周炎患者作为试验组,17名牙周健康者作为对照组。在入选病例选取观察牙,记录观察牙的出血指数（BI）、牙周袋探诊深度（PD）、附着丧失（AL）。依据观察牙PD和AL分为轻度牙周炎组15例、中度牙周炎组22例及重度牙周炎组11例。采集观察牙的龈沟液,酶联免疫吸附实验（ELISA）法检测样本中骨膜蛋白的含量。采用SPSS 25.0统计软件对实验数据进行分析。 结果牙周病患者龈沟液中均可检测出较低浓度的骨膜蛋白[（0.45 ± 0.13）pg/μL],而牙周健康人群的龈沟液中均检测出较高浓度的骨膜蛋白[（0.56 ± 0.23）pg/μL],两者差异具有统计学意义（t = 2.40,P = 0.019）;牙周炎轻度、中度、重度各组骨膜蛋白的浓度值分别为（0.57 ± 0.09）、（0.43 ± 0.09）和（0.34 ± 0.11）pg/μL,骨膜蛋白浓度值随炎症程度加重而逐渐降低;经相关分析,龈沟液中骨膜蛋白与BI呈负相关关系（r = -0.529,P<0.001）,与PD、AL均分别呈负相关关系（r = -0.806/-0.772,P<0.001）。 结论牙周炎患者龈沟液中骨膜蛋白的含量显著低于牙周健康人群;骨膜蛋白可能与牙周炎的病变严重程度之间具有密切关系。     

口腔内毒素监测牙周病初探

25名全身健康的中一重度牙周炎初诊病人为研究对象,20名全身健康的牙周健康者作对照研究,用鲎试验的合成基质偶氮显色法定量检测口腔中唾液和龈沟液的内毒素。 结果表明唾液内毒素量与唾液厌氧菌总数及G厌氧菌的百分比呈正相关。牙周炎组唾液内素素的均数为1.089μg/ml,牙周健康组为0.121μg/m1,牙周炎部位龈沟液内毒素的均数为3.616μg/ml,牙周健康部位为0.445μg/ml,二者间均有非常显著差别(P<0.01)。唾液龈沟液的内毒素变动和牙周炎临床症状紧密联系,其测定方法简便,正确性重要性也大于细菌研究,为监测牙周病带来广阔的前景。     

牙周炎患者唾液一氧化氮的含量及其与牙周病指标相关性的研究

目的：研究牙周炎患者唾液一氧化氮（ＮＯ）的含量,及其与牙周病各临床指标的相关性。方法：选择成人牙周炎患者２３例为实验组,健康人２７例为对照组。记录牙周炎患者的牙龈出血指数（ＧＢＩ）、牙周袋深度（ＰＤ）和附着丧失量（ＡＬ）。ＮＯ的含量由检测唾液亚硝酸盐的含量来代表。测定实验组和对照组所有病例的唾液ＮＯ的含量。结果：对照组唾液ＮＯ的含量为２８．８０６±６．６０４μｍ／Ｌ,男女间无显著性差异。实验组唾液ＮＯ的含量为５５．３６１±１３．３１９μｍｏｌ／Ｌ,明显高于对照组。牙周炎患者唾液ＮＯ的含量与ＰＤ、ＡＬ间存在明显的正相关。结论：牙周炎患者唾液ＮＯ的含量显著高于健康人,并与牙周炎的严重程度有关。     

应激中述情障碍对唾液SlgA及Cor的影响

目的：探讨应激过程中述情障碍对唾液分泌型免疫球蛋白A（SIgA）及皮质醇（Cor）的影响。方法：60例高中男生为研究对象,应用多伦多述情障碍量表（TAS）评分（高分组A与低分组B）,评定其心理状况;应用放免法测定应激前后唾液SIgA和Cor浓度的变化。所得数据用t检验和单因素相关分析进行评价。结果：（1）考试前1个月和考试当天,A组学生唾液SIgA浓度均低于B组（P均〈0．05）;2组学生考试当天SIgA值和考试前1个月类似（P均〉0．05）。（2）考试前1个月和考试当天,A组学生唾液Cor浓度均显著高于B组（P均〈0．05）;2组学生考试当天Cor浓度均高于考试前1个月（其中A组P〈0．01;B组P〈0．05）;（3）2组学生应激前后SIgA、Cor变化率差异显著（其中SIgA变化率P〈0．05;Cor变化率P〈0．01）;（4）TAS总分、因子Ⅰ、因子Ⅱ与考试前1个月SIgA值、Cor变化率均显著相关（P〈0．05）;因子Ⅲ和Cor变化率呈负相关（P〈0．05）;因子Ⅳ和各测量指标无显著相关（P〉0．05）。结论：应激和应激中述情障碍均可导致唾液SIgA及唾液Cor的改变。     

Collagenase activity and tissue inhibitor of metalloproteinases-1 (TIMP-1) content in human whole saliva from clinically healthy and periodontally diseased subjects

Total TIMP-1 concentration in whole saliva of periodontally diseased subjects, 137 ± 67 ng/ml (mean ± SD), was clearly lower (p < 0.001) than that of clinically healthy subjects, 273±145, and that of edentulous subjects, 332±121. On the contrary, both active [1.58±0.35 units/ml (mean ± SD)] and total (2.08 ± 0.25) collagenase activities inTIMP-1-free whole saliva of diseased subjects were significantly higher than the activities (0.14 ± 0.14 and 0.50 ± 0.27, respectively) in TIMP-1-free whole saliva of healthy subjects. Most of the total collagenase in whole saliva of healthy subjects consisted of procollagenase, while mainly active collagenase was present in whole saliva from patients with periodontal diseases. Significant reciprocal changes of TIMP-1 and collagenase levels, that is, increase in TIMP-1 concentration and decrease in collagenase activity, were observed after the initial therapy of periodontitis patients.     

Studies on immunologic and inflammatory factors in saliva in patients with asthma and in patients with periodontitis

Abstract To study the salivary response in asthma and periodontitis, calcium and phosphorus concentrations were determined from parotid and whole saliva. The IgE and histamine concentrations and the activities of lysozyme and arginine aminopeptidases were assayed from whole saliva. The values were compared with those obtained from matched healthy controls (n = 20 in each group). In whole saliva the phosphorus concentrations were elevated in the asthma group and the calcium concentrations in the periodontitis group. Regarding parotid saliva no significant differences between the group? were observed. The results indicate that in patients with asthma the IgE concentrations in whole saliva were elevated, while in patients with periodontitis and in healthy controls no detectable values were obtained. Both histamine and lysozyme concentrations seemed to increase in the asthma and periodontitis groups. A slight increase was also observed in the arginine aminopeptidase activities in the saliva of patients with asthma and patients with periodontitis.     

PAF levels in saliva are regulated by inflammatory cells

Platelet activating factor (PAF), a powerful inflammatory phospholipid mediator, has been detected in normal human saliva and found to be increased in periodontitis. The cellular source of PAF in saliva is controversial although several data suggest an origin related to the presence of inflammatory cells. PAF levels in biological fluids are regulated by PAF-producing cells and by the PAF-degrading acetylhydrolase. Although in normal human saliva acetylhydrolase activity is very low, no information is available on the levels of this enzyme in inflammatory conditions of the mouth. The aim of our study was to assess the contribution of inflammatory cells to the levels of PAF in saliva in normal subjects and in patients with periodontitis. PAF was measured by radioimmunoassay (RIA) in mixed uncentrifuged saliva and in cell-free saliva from healthy subjects, before and after tooth brushing, and in patients with periodontitis. In healthy subjects PAF levels were significantly higher in whole saliva than in centifuged saliva (1.51 ± 0.22 vs. 0.92 ± 0.04 ng/ml, p<0.0039). A significant increase in the amount of PAF was detected in whole saliva, but not in centifuged saliva, 2 h after tooth brushing. In patients with periodontitis PAF levels were not different from those of healthy individuals when using centrifuged saliva but were significantly higher when using whole, uncentrifuged saliva. Exogenous radiolabelled PAF was degraded much more rapidly by the saliva of periodontitis patients than by that of normal subjects. In conclusion, our study shows that inflammatory cells regulate the levels of PAF in saliva contributing to its production and degradation. The differential degradation of PAF in normal and inflammatory saliva highlights the absolute need of a series of methodological precautions when performing studies on salivary PAF.     

Salivary IgA subclasses and bacteria-reactive IgA in patients with aggressive periodontitis

The local salivary immunoglobulin A (IgA) response in patients with aggressive periodontitis to oral microorganisms and its role for the pathogenesis has not been determined. This study investigated the hypothesis that aggressive periodontitis patients have impaired oral secretory immunity. Our test group was made-up of 19 aggressive periodontitis patients and 19 age- and gender-matched periodontally healthy controls. Total IgA, IgA subclass 1, IgA subclass 2 and IgA reactive to Actinobacillus actinomycetemcomitans Y4, Treponema denticola ATCC 35404 and Candida albicans DSM 3454 were determined by enzyme-linked immunosorbent assay in whole unstimulated and stimulated saliva. A statistically significantly lower concentration and secretion rate of total salivary IgA (P < 0.01) and IgA1 (P < 0.001) was found in the aggressive periodontitis group in resting and stimulated saliva. A decrease of IgA2 (P < 0.05) was seen in resting saliva. Although only minor differences were detected in the concentration and secretion of bacteria-reactive IgA in both groups, the proportion of bacteria-reactive IgA from the total IgA was significantly higher (P < 0.01) in the aggressive periodontitis group in all three microorganisms tested. Our results indicate an inhibition of total secretory IgA. In particular an IgA subclass 1-specific decrease in aggressive periodontitis was noted, while the bacteria-reactive humoral immune system in saliva was activated. The role of the decrease of IgA1 immunoglobulins in aggressive periodontitis with respect to susceptibility for periodontal diseases has to be elucidated.     

Associations between salivary calcium and oral health

Abstract. Recently, we have shown positive correlations between high salivary calcium content and periodontitis, and between high salivary calcium level and the number of intact teeth in selected groups of subjects. The aim of our present study was to determine whether these correlations could be seen in a randomized group of healthy adults, A thorough oral examination including orthopantomograms was carried out for a total of 137 healthy subjects, 63 men (35.4±5.6 years) and 74 women (33.2±4.7 years). Paraffin-stimulated saliva was collected from the subjects and salivary flow (ml min). buffering capacity, calcium (mMol/l) and microbial variables including lactobacilli, yeasts, mutans streptococci. total streptococci, total number of aerobes, and anaerobes were determined. The calcium level of whole saliva had a median of 1.23 mMol/l. Subjects with calcium level below the median were categorized as 'low', while those with higher values formed the'high'salivary calcium group. There were more men than women in the'High'salivary calcium group ( p =0.025), Subjects in the'high'calcium group showed more bleeding on probing ( p = 0.026). had more intact teeth ( p =0.045) and lower DMF-scores ( p = 0.025) than their counterparts. No other differences were found between the two groups.
We found clear assosiations between the level of salivary calcium and factors reflecting gingival health on one hand, and dental health on the other in a randomly selected group of healthy subjects, and conclude that salivary calcium may be important with regard to both dental and gingival health.     

Protein composition of whole and parotid saliva in healthy and periodontitis subjects

Cystatins are physiological inhibitors of cysteine proteinases and they are widely distributed in human tissues and body fluids including saliva. We previously reported an increased cystatin activity in whole saliva of gingivitis and periodontitis subjects. Based on this result we decided to investigate the type and origin of cystatins involved in this increased cystatin activity by collecting both whole and parotid saliva of 25 healthy and 30 periodontitis subjects. Saliva samples were quantified for cystatins S and C by enzyme-linked immunosorbent assay and cystatin activities were measured toward papain. Besides, three other salivary proteins were determined: the plasma protein albumin, the typical parotid derived amylase and the salivary immunoglobulin IgA. The present investigation shows that levels of total protein and cystatin activity as well as the levels of glandular derived proteins amylase and cystatin C were significantly higher in whole and parotid saliva of subjects with periodontitis than in healthy controls. Cystatin S, the major salivary cystatin. however was higher in the whole saliva of the healthy group. Whole saliva concentrations of albumin and IgA, originating from sources other than the glandular cells, were not different between healthy and periodontitis subjects and were also not correlated with the typical salivary gland proteins. In conclusion, this study provides additional evidence that the human salivary glands may respond to an inflammatory disease of the oral cavity, periodontitis, by enhanced synthesis of some acinar proteins.     

Acute myocardial infarction elevates serine protease activity in saliva of patients with periodontitis

Mäntylä P, Buduneli E, Emingil G, Tervahartiala T, Pussinen PJ, Bar?? N, Ak?ll? A, Atilla G, Sorsa T. Acute myocardial infarction elevates serine protease activity in saliva of patients with periodontitis. J Periodont Res 2012; 47: 345–353. © 2011 John Wiley & Sons A/S Background and Objective: There are indications that acute myocardial infarction (AMI) may have an effect on the oral environment, which is reflected in the expression of salivary and gingival proteinases. According to our knowledge, no studies have been carried out to investigate the effect of AMI on the activities of two major tissue‐destructive serine protease and microbial effectors, elastase and cathepsin G, produced by oral fluid polymorphonuclear granulocytes (PMN). Therefore, we compared the activities of elastase and cathepsin G in saliva from patients with AMI and from systemically healthy subjects (non‐AMI) with similar periodontal conditions. Material and Methods: A total of 92 patients (47 AMI and 28 non‐AMI patients with gingivitis or periodontitis, and 17 systemically and periodontally healthy subjects as a control group) were recruited. Clinical periodontal measurements were recorded, and stimulated whole‐saliva samples were collected. The patients with AMI were clinically examined within 3–4 d after admission to the coronary care unit. The activities of saliva neutrophil elastase and cathepsin G were measured after collection, at specific time‐points during incubation (from baseline to 23 h) by specific synthetic peptide substrate assays. Results: The saliva of patients with AMI and periodontitis had a significant trend for the highest elastase activities among the study groups. Elastase and cathepsin G activities correlated significantly with each other in the AMI periodontitis group (r = 0.8, p < 0.01). In a logistic regression analysis, the level of salivary elastase activity associated significantly with periodontitis. Conclusion: AMI may be reflected in PMN serine protease elastase activity in saliva, despite its strong association with periodontitis.     

Salivary albumin of edentulous patients

In order to evaluate the contribution of the periodontal sulcus or pocket to the presence of albumin in the mouth, this protein was analysed in whole saliva of 20 completely dentate adults, aged between 63 and 83 years, and in 23 edentulous patients of similar age (51–88 years). In spite of the considerable intra- and interindividual variations revealed by a preliminary trial, the concentration of salivary albumin was significantly higher (range 60–1080 mg/l) in the dentate that in edentulous individuals (range 2–690 mg/l). The low albumin content in saliva of old edentulous people was similar to that in a group of younger individuals with a healthy periodontium.     

Correlation between salivary IL-1beta levels and periodontal clinical status

OBJECTIVE: To assess the concentration of the proinflammatory cytokine IL-1beta in saliva of periodontally diseased and healthy patients and their relationship with the periodontal status. DESIGN: Unstimulated whole saliva samples from patients with chronic periodontitis (n=30), aggressive periodontitis (n=18) and healthy controls (n=18) were obtained for the study. The periodontal status of each subject was assessed by criteria based on probing depth, clinical attachment loss and the extent/severity of periodontal breakdown. The levels of IL-1beta were measured in saliva samples with a high sensitivity enzyme-linked immunosorbent assay (ELISA). RESULTS: Although no significant difference (P=0.624) was found for salivary IL-1beta levels between periodontitis groups, they were significantly greater (P<0.01) than those detected for healthy controls. Furthermore, Spearman correlation analysis showed statistically significant correlations (P<0.01) between data from salivary IL-1beta levels and clinical measurements. CONCLUSION: The findings of the present study reemphasize the importance of whole saliva as sampling method in terms of immunological purposes in periodontal disease and suggest that the elevated IL-1beta concentration may be one of the host-response components associated to the clinical manifestations of periodontal disease.