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目的通过观察分析中重度牙周炎患者血清中对氧磷酶-1（PON1）活性及白细胞介素-6（IL-6）在牙周基础治疗前后的变化,探讨PON1和IL-6与牙周病之间的相关性以及两者在牙周病病情变化中的作用。方法2012年5月至2013年2月在辽宁省人民医院体检中心体检的牙周健康人群30名（牙周健康组）及口腔科就诊的中重度牙周炎患者39例（牙周炎组）,对所有受试者进行基础治疗,检查治疗前后PON1、IL-6以及临床牙周检查指标。结果牙周健康组与牙周炎组在基础治疗前比较：牙周炎症指标[出血指数（BI）、牙周探诊深度（PD）]及血清IL-6差异均有统计学意义（P〈0．05）,血清中PON1活性差异无统计学意义（P〈0．05）。牙周健康组在牙周基础治疗前后各项指标差异均无统计学意义（P〉0．05）。牙周炎组在牙周基础治疗前后比较：牙周炎症指标BI、PD、血清PON1及IL-6与治疗前比较差异均有统计学意义（均P〈0．05）。结论牙周健康人群和中重度牙周炎患者血清PON1活性无差异;牙周基础治疗可改善中重度牙周病患者牙周健康状况,提高血清中PON1活性,降低IL-6水平;中重度牙周炎患者在牙周基础治疗前后血清中PON1活性和IL-6水平的变化存在负相关性。     

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高迁移率族蛋白B1（high mobility group box 1 protein,HMGB1）作为高迁移率族蛋白（high mobility group protein,HMG）家族成员,是一种含量极为丰富的细胞核内非组蛋白。研究发现,其作为一种晚期炎性介质,在牙周病及糖尿病伴牙周病的发生发展过程起到重要作用。本文就HMGB1的生物学特性及其与牙周病、糖尿病伴牙周病等的关系研究进展做一综述。     

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提要：发展一种新的方法用来提高口腔癌的诊断和治疗效果,建立能够模拟人类口腔鳞癌自然发生的动物模型是必需的,应用4-硝基喹啉-1-氧化物（4-nitroquinoline-1-oxide, 4NQO）诱导SD大鼠舌黏膜鳞癌是一种可靠的方法。水溶性喹啉衍生物4NQO可以形成DNA加成物,引起碱基的改变（G→A）或丢失突变。但4NQO要发挥这种诱变剂作用,需要在4NQO还原酶作用下将4NQO转化成4-羟氨基喹啉-1-氧化物及4-乙酰基喹啉-1-氧化物（4-AAQO）,4-AAQO能够以共价键的方式结合到核酸上并破坏染色体的结构,进一步影响抑癌基因和癌基因表达。动物舌根黏膜该酶含量较高,所以可以靶向性在舌根形成癌。饮水中很低剂量的4NQO便可特异性在舌根形成癌,其形成过程和形态学变化都和人的口腔鳞癌发生过程十分相似,该模型是研究口腔癌发生和癌变机制的理想模型。     

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肿瘤样钙盐沉着症(tumoral calcinosis,TC)是一种非肿瘤性的无定形钙盐沉积,好发于大关节附近,偶位于手、足或膝部,位于头颈部罕见。中山大学光华口腔医学院.附     

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??IL-22??interleukin-22??IL-22??is a member of the IL-10 cytokine family??which is mainly produced by T-helper??Th??-17 cells??γδ T cells??NKT cells and newly described innate lymphoid cells??ILCs??. Research of IL-22 has rapidly evolved since its discovery in 2000. The studies have found that IL-22 is related to a variety of diseases′ occurrence and development??including autoimmume diseases??inflammatoty diseases and tumor. The research of IL-22 in various oral diseases has become a hot spot recently. In this review??we will explain the research status of IL-22 in oral diseases.     

4-硝基喹啉-1-氧化物诱导大鼠舌癌过程中Notch1的表达特点

目的：研究 Notch1在大鼠舌癌模型发生发展过程中的表达变化。方法：将40只 SD 大鼠随机分为对照组（A 组10只）和实验组（B、C、D组各10只）,使用质量百分比浓度为0．004％的4-硝基喹啉-1-氧化物（4-nitroquinoline-1-oxide,4NQO）饮用水喂养实验组 SD大鼠,用蒸馏水喂养对照组 SD大鼠。B、C、D组分别于8、16、24周取大鼠舌体组织;A 组在8、16、24周同时各取3只、3只、4只作为正常对照。行常规组织学观察,并使用免疫组织化学法检测 Notch1在病变不同阶段的舌粘膜内的表达。结果：4NQO可以有效诱导大鼠舌黏膜鳞状细胞癌的发生。在不同的给药时间点,可以诱导大鼠舌黏膜产生不同程度的癌前病变。Notch1在正常舌黏膜、癌前病变、舌鳞癌中的表达逐渐增高（P＜0．01）。随着异常增生程度的增加,阳性表达部位逐渐由基底层向表层扩展,且 Notch1的膜型表达逐渐增多。结论：Notch1的高表达及其在细胞膜上的集中表达可能与舌癌的发生、发展过程相关。     

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髓样细胞触发受体-1（triggering receptor expressed on myeloid cells-1,TREM-1）是新近发现的免疫球蛋白超家族的一种跨膜受体,表达于单核（巨噬）细胞等骨髓分化细胞,在疾病作用中研究现仍处于起步阶段。多项研究显示,TREM-1在感染性疾病的炎症触发和级联放大过程中扮演重要角色,而牙周炎是由牙茵斑生物膜引起的感染性疾病,TREM-1在其引起的免疫炎症反应中可能发挥重要作用。本文就TREM-1最新研究进展及其与牙周炎的关系进行综述。     

程序性细胞死亡-1／程序性细胞死亡配体-1信号途径及其对口腔慢性疾病的作用

程序性细胞死亡-1（PD-1）／程序性细胞死亡配体-1（PD—L1）作为B7-CD28家族的重要负性共刺激信号途径,已证实能够通过抑制T细胞的活化增殖及细胞因子的产生来负调控免疫应答,参与免疫耐受及自身免疫性疾病、慢性感染、肿瘤等慢性疾病。本文综述了PD-1／PD—L1信号途径的生物学特点和功能及其在口腔扁平苔藓、慢性牙周炎、口腔恶性肿瘤等口腔慢性疾病中的研究,著探讨了调节该通路为口腔慢性疾病提供治疗的可能性。     

程序性细胞死亡-1/程序性细胞死亡配体-1信号途径及其对口腔慢性疾病的作用

程序性细胞死亡-1 (PD-1)/程序性细胞死亡配体-1 (PD-L1)作为B7-CD28家族的重要负性共刺激信号途径,已证实能够通过抑制T细胞的活化增殖及细胞因子的产生来负调控免疫应答,参与免疫耐受及自身免疫性疾病、慢性感染、肿瘤等慢性疾病.本文综述了PD-1/PD-L1信号途径的生物学特点和功能及其在口腔扁平苔藓、慢性牙周炎、口腔恶性肿瘤等口腔慢性疾病中的研究,并探讨了调节该通路为口腔慢性疾病提供治疗的可能性.     

内皮素-1对牙周膜细胞肿瘤坏死因子及白介素-1β表达的影响

目的:研究内皮素-1(endothelin-1,ET-1)对牙周膜细胞(periodontal ligament cells,PDLCs)肿瘤坏死因子(Tumor Necrosis Factor,TNF-α)和白介素-1β(Interleukin-1β,IL-1β)表达的影响。方法:不同浓度(1,10,100 n M)的ET-1处理牙周膜细胞12,24,48h后提取细胞培养上清液和细胞裂解物,采用ELISA及实时定量PCR检测ET-1作用下牙周膜细胞TNF-α和IL-1β基因及蛋白表达的改变。结果:ET-1剂量依赖性及时间依赖性促进牙周膜细胞TNF-α和IL-1βm RNA表达及蛋白分泌。但内皮素受体拮抗剂抑制了该促进效应。结论:内皮素-1可以诱导牙周膜细胞分泌TNF-α和IL-1β,而且这种促进作用呈浓度依赖性及时间依赖性。但内皮素受体拮抗剂抑制了该促进效应。     

超氧化物歧化酶与牙周病的关系

目的探讨超氧化物歧化酶（SOD）、脂质过氧化物（LPO）和谷胱甘肽过氧化物酶（GPX）与牙周组织疾病的关系。方法选择了8例单纯性龈炎、8例青少年牙周炎、8例快速进展性牙周炎、14例成人．牙周炎、50例健康对照者。分别采用放射免疫测定法（双抗体法），硫代巴比妥酸（TBA）比色法和比色法检测血清中SOD、LPO和GPx含量。结果血清中SOD活性及LPO含量牙周病各组均明显高于对照组（P＜0．01），血清中GPx活性牙周病各组与对照组之间比较均无显著性差异（P＞0．05）。结论血清中SOD活性与牙周病密切相关。     

The interleukin-1 genotype as a severity factor in adult periodontal disease

Abstract Although specific bacteria, dental plaque, and age are associated with periodontal disease, there are currently no reliable predictors of periodontitis severity. Studies in twins have suggested a genetic contribution to the pathogenesis of periodontitis, but previous attempts to identify genetic markers have been unsuccessful. The pro-inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFα) are key regulators of the host responses to microbial infection. IL-1 is also a major modulator of extracellular matrix catabolism and bone resorption. We report a specific genotype of the polymorphic IL-1 gene cluster that was associated with severity of periodontitis in non-smokers, and distinguished individuals with severe periodontitis from those with mild disease (odds ratio 18.9 for ages 40–60 years). Functionally, the specific periodontitis-associated IL-1 genotype comprises a variant in the IL-1B gene that is associated with high levels of IL-1 production. In smokers severe disease was not correlated with genotype. In this study, 86.0% of the severe periodontitis patients were accounted for by either smoking or the IL-1 genotype. This study demonstrates that specific genetic markers, that have been associated with increased IL-1 production, are a strong indicator of susceptibility to severe periodontitis in adults.     

Smoking modulates interleukin-6:interleukin-10 and RANKL:osteoprotegerin ratios in the periodontal tissues

BACKGROUND AND OBJECTIVE: This study evaluated the effect of smoking on the gene expression of interleukin-1alpha, -1ra, -6, -8 and -10, tumor necrosis factor-alpha, matrix metalloproteinase (MMP)-2 and -8, receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin, in sites with periodontitis. MATERIAL AND METHODS: Gingival biopsies were divided into three groups: the healthy group (periodontally healthy subjects; n=10); the periodontitis group [subjects with severe chronic periodontitis who never smoked (probing depth>or=7 mm) (n=25)]; and the smoking group (subjects diagnosed with severe chronic periodontitis who smoked>or=1 pack per day for at least 10 years; n=25). Gene and protein expressions were analyzed by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. RESULTS: Data analysis demonstrated that, except for MMP-8 and osteoprotegerin, the levels of all factors were increased by inflammation (p<0.001). The levels of interleukin-1alpha, -1ra, -6 and -8, and RANKL, were higher in smokers with periodontitis compared with controls, whereas the levels of interleukin-10, MMP-8 and osteoprotegerin were lower (p<0.001). Smoking lowered the levels of interleukin-1alpha, -8, -10, tumor necrosis factor-alpha, MMP-8 and osteoprotegerin, and increased the levels of interleukin-6 and -1ra in sites with a comparable type of periodontitis (p<0.001). CONCLUSION: In conclusion, smoking modulates gene expression in the periodontium, and the influence of smoking on periodontal disease may involve effects of interleukin-6:interleukin-10 and RANKL:osteoprotegerin ratios.     

吸烟与牙周病关系的研究

为研究吸烟与牙周病的关系，调查４３２名中老年男性的口腔卫生状况、牙周状况及吸烟习惯。结果表明吸烟者软垢指数与不吸烟者相同，龈炎区段数两者差异无显著性，吸烟者牙周炎区段数高于不吸烟者。重度吸烟者牙周炎区段数高于轻、中度吸烟者及不吸烟者。调查结果提示吸烟可能是牙周病流行的高危因素之一。     

Interleukin-11, interleukin-1beta, interleukin-12 and the pathogenesis of inflammatory periodontal diseases

Objectives: The balance between pro‐inflammatory and anti‐inflammatory cytokines may be crucial for determining the immunopathology of gingivitis (G) and periodontitis. This study aimed to analyse interleukin‐1β (IL‐1β), IL‐11 and IL‐12 levels in gingival crevicular fluid (GCF) of patients with G and chronic periodontitis (CP). Material and Methods: Fourty subjects including 12 CP, 14 G and 14 controls (C) were enrolled. GCF samples were collected from six maxillary sites per patient and analysed for IL‐1β, IL‐11 and IL‐12 by an enzyme‐linked immunosorbent assay. Results: Significantly lower concentrations of IL‐11 were detected in CP compared with both G and C groups (p<0.05). The CP group had a significantly higher total amount of IL‐12 and IL‐1β compared with the C group (p<0.05). The IL‐11:IL‐1β cytokine ratio was higher in both G and C groups compared with the CP group. The IL‐11:IL‐1β ratio became progressively lower with increasing probing depth (p<0.01). Conclusions: Our data showed that IL‐11 levels are significantly decreased in GCF from sites with periodontitis compared with G and healthy sites. Because of the possible preventive effect of IL‐11 on inflammation, IL‐11 may be an important factor in the therapeutic modulation of periodontal disease.     

口源性口臭与牙周病的相关性

口源性口臭与牙周病之间存在密切关系,本文将从口源性口臭的病因、检测、主要成分挥发性硫化物对牙周组织的影响以及治疗等几方面进行综述。     

The impact of diabetes on periodontal diseases

The susceptibility and severity of periodontal diseases is made more severe by diabetes, with the impact on the disease process inversely proportional to the level of glycemic control. Although type 1 diabetes mellitus and type 2 diabetes mellitus have different etiologies, and their impact on bone is not identical, they share many of the same complications. Studies in animals and humans agree that both forms of diabetes increase inflammatory events in periodontal tissue, impair new bone formation, and increase expression of RANKL in response to bacterial challenge. High levels of glucose, reactive oxygen species, and advanced glycation end-products are found in the periodontium of diabetic individuals and lead to increased activation of nuclear factor-kappa B and expression of inflammatory cytokines such as tumor necrosis factor and interleukin-1. Studies in animals, moreover, suggest that there are multiple cell types in periodontal tissues that are affected by diabetes, including leukocytes, vascular cells, mesenchymal stem cells, periodontal ligament fibroblasts, osteoblasts, and osteocytes. The etiology of periodontal disease involves the host response to bacterial challenge that is affected by diabetes, which increases the expression of RANKL and reduces coupled bone formation. In addition, the inflammatory response also modifies the oral microbiota to render it more pathogenic, as demonstrated by increased inflammation and bone loss in animals where bacteria are transferred from diabetic donors to germ-free hosts compared with transfer from normoglycemic donors. This approach has the advantage of not relying upon limited knowledge of the specific bacterial taxa to determine pathogenicity, and examines the overall impact of the microbiota rather than the presumed pathogenicity of a few bacterial groups. Thus, animal studies have provided new insights into pathogenic mechanisms that identify cause-and-effect relationships that are difficult to perform in human studies.     

The relationship between microbiological assays and the clinical signs of periodontal disease

Ninety-five patients with periodontal disease each had subgingival plaque samples collected from four sites (one from each quadrant) in their mouths. The relative proportions of spirochaetes, motile rods and cocci were determined using dark field microscopy and the proportion of anaerobic to aerobic micro-organisms calculated after culture. In addition, clinical recordings were made. The only significant correlations observed were between probing depth or attachment loss and the proportion of cocci in the plaque (negative association), probing depth or attachment loss and sites which were suppurating or displayed a radiolucent interdental crest (positive association), and the percentage of cocci and sites with a radiolucent interdental crest (negative association). Partial correlation analysis controlling for probing depth or attachment loss showed that a significant inverse association between the percentages of cocci and the presence of a radiolucent interdental crest remained. No significant associations were observed between clinical signs such as bleeding on probing or suppuration and the microbiological assays. Overall there was a poor correlation between many of the signs thought by some to indicate periodontal disease activity.