牙周病患者牙龈组织前列腺素E_2、血栓素B_2、6－酮－前列腺素F_（1α）水平的研究

采用ＲＩＡ对１１例健康牙龈组织（Ｈ）、１１名龈炎（Ｇ）患者的１７个牙、２６名成人牙周炎（ＡＰ）患者３６个牙和１４名青少年牙周炎（ＪＰ）患者的２０个牙的牙龈组织同时测定ＰＧＥ_２、ＴＸＢ_２、６－Ｋ－ＰＧＦ_（１α）的含量。结果以ＰＧＥ_２最多，ＴＸＢ_２次之，６－Ｋ－ＰＧＦ_（１α）最少；３种前列腺素（ＰＧｓ）均随病变严重程度而增加，除Ｇ组ＴＸＢ_２和６－Ｋ－ＰＧＦ_（１α）与Ｈ组相差显著（Ｐ＜０．０５）外，其余各病变组与Ｈ组比，３种ＰＧｓ均相差非常显著（Ｐ＜０．０１），ＡＰ组和ＪＰ组比Ｇ组也有非常显著升高（Ｐ＜０．００１），而ＡＰ和ＪＰ组间相差不显著（Ｐ＞０．０５），表明３种ＰＧｓ在牙周病发病中具有重要作用。     

龈沟液中弹性蛋白酶水平与白细胞数目的关系

目的初步探讨龈沟液（ｇｉｎｇｉｖａｌｃｒｅｖｉｃｕｌａｒｆｌｕｉｄ，ＧＣＦ）中细胞外弹性蛋白酶（ｅｌａｓｔａｓｅｉｎｔｈｅｓｕｐｅｒｎａｔａｎｔ，ＥＡｓ）、细胞内弹性蛋白酶（ｅｌａｓｔａｓｅｉｎｔｈｅｐｅｌｅｔ，ＥＡｐ）及中性多形核白细胞（ｐｏｌｙｍｏｒｐｈｏｎｕｃｌｅａｒｌｅｕｋｏｃｙｔｅ，ＰＭＮ）间的关系。方法先用滤纸条法取ＧＣＦ样本，以底物检测法分别测定其中的ＥＡｓ和ＥＡｐ水平；２４ｈ后在同一部位用龈沟灌洗法收集ＧＣＦ灌洗液，光镜下计数ＰＭＮ。结果ＥＡｓ与ＥＡｐ的总水平和ＰＭＮ数目三者间均呈正相关（Ｐ＜０．００１）。结论ＧＣＦ中弹性蛋白酶水平与ＰＭＮ数目一致，可以用ＥＡｐ的水平代表同一样本中ＰＭＮ的数量。     

牙周病患者龈组织中6－K－PGF_1a放免测定和免疫组化定位及定量分析

本实验采用放射免疫测定法（ＲＩＡ）测定了成人牙周炎（ＡＰ）、青少年牙周炎（ＪＰ）、龈炎（Ｇ）和健康人（Ｈ）（各１０例）龈组织中６－酮－前列腺素Ｆｉａ（６－Ｋ－ＰＧＦ＿１ａ）的含量，用免疫组织化学ＡＢＣ染色对同一标本中的６－Ｋ－ＰＧＦ＿１ａ定位，用显微分光光度计（ＭＳＰ）对染色标本定量，与ＲＩＡ结果比较，以探讨６－Ｋ－ＰＧＦ＿１ａ与牙周病的关系。ＲＩＡ结果表明：牙周病患者龈组织中６－Ｋ－ＰＧＦ１ａ含量从Ｈ、Ｇ、ＡＰ到ＪＰ呈递增趋势，各病变组与Ｈ皆有显著差异，ＪＰ与Ｇ组有显著差异，ＡＰ与Ｐ也有显著差异。ＡＢＣ染色表明龈组织中６－Ｋ－ＰＧＦ＿１ａ主要的分泌细胞为血管内皮细胞、巨噬细胞、浆细胞、多形核白细胞及个别的腺管内皮细胞等。对牙龈组织６－Ｋ－ＰＧＦ＿１ａ的ＭＳＰ定量结果与ＲＩＡ相似，两方法可相互补充。提示对６－Ｋ－ＰＧＦ＿１ａ与牙周病关系的研究有重要意义。     

牙周炎龈下菌斑胰蛋白酶样酶的检测

胰蛋白酶样酶（ＴＬＥ）由牙周主要致病菌牙龈卟啉菌，齿密螺旋体及福赛氏类杆菌合成，本文利用苯甲酰精氨酰萘酰胺（ＢＡＮＡ）检测成人牙周炎龈下菌斑ＴＬＥ活性，用间接荧光免疫技术及光学显微法计数菌斑中牙龈卟啉菌、螺旋体量。结果显示：ＢＡＮＡ阳性菌斑中两种菌量高于阴性菌斑，ＢＡＮＡ反应与临床指标ＧＩ、ＰＤ、ＰＬＩ呈正相关，与临床诊断相比，ＢＡＮＡ法较可靠。提示：龈下菌斑ＴＬＥ活性能反映临床牙周状态及相关微生物状态，适于作为牙周炎活动监测指标的研究。     

三种牙周炎患者龈沟液中IL—8的检测

目的：探讨ＩＬ－８与不同种类牙周炎的关系，比较三种牙周炎，即青少年牙周炎（ｊｕｖｅｎｉｌｅｐｅｒｉ－ｏｄｏｎｔｉｔｉｓ，ＪＰ），快速进展型牙周炎（ｒａｐｉｄｐｒｏｇｒｅｓｓｉｖｅｐｅｒｉｏｄｏｎｔｉｔｉｓ，ＲＰＰ）和成人牙周炎（ａｄｕｌｔｐｅｒｉｏｄｏｎｔｉｔｉｓ，ＡＰ）龈沟液（ｇｉｎｇｉｖａｌｃｒｅｖｉｃｕｌａｒｆｌｕｉｄ，ＧＣＦ）中ＩＬ－８浓度和检出率。方法：采集ＪＰ、ＲＰＰ和ＡＰ患者ＧＣＦ，用ＥＬＩＳＡ法对ＧＣＦ中ＩＬ－８进行检测。结果：ＡＰ患者ＧＣＦ中ＩＬ－８检出率为６７．８５％，明显高于ＪＰ组、ＲＰＰ组的检出率（分别为３４．４８％、２５％）；ＧＣＦ中ＩＬ－８浓度无明显差别。结论：ＪＰ、ＲＰＰ患牙ＧＣＦ中ＩＬ－８检出率低可能是造成此种牙周炎局部中性粒细胞趋化异常的原因之一。     

用放射免疫测定法分析豚鼠牙龈和牙槽骨中前列腺素E2含量…

将２０只豚鼠分为对照组和牙周炎组，每组１０只，用丝线缝扎十高糖食料喂养形成牙周炎，用放射免疫测定法（ＲＩＡ）分析牙周炎形成后两组牙龈和牙槽骨中前列腺素Ｅ２（ＰＧＥ２）含量。结果表明牙周炎组和对照组牙龈组织中ＰＥＧ２含量均高于牙槽骨中的含量，对照组牙龈组织中ＰＥＧ２（３９４．９７±１１８．２７ｐｇ／ｍｇ）为牙槽骨中（１８２．９１±３３．２９ｐｇ／ｍｇ）的２．１倍，牙周炎组龈组织中ＰＥＧ２（９４６．５     

牙周病患者龈组织中6—K—PGF1a放免测定和免疫组化定位及…

本实验采用放射免疫测定法（ＲＩＡ）测定了成人牙周炎（ＡＰ），青少上牙周炎（ＪＰ），龈炎（Ｇ）和健康人（Ｈ）（各１０例）龈组织中６－酮－前列腺素Ｆ１ａ（６－Ｋ－ＰＧＦ１ａ）含量，用免疫组织化学ＡＢＣ染色对同一标本中的６－Ｋ－ＰＧＦ１ａ定位，用显微分光光度计（ＭＳＰ）对染色标本定量，与ＲＩＡ结果比较，以探讨６－Ｋ－ＰＧＦ１ａ与牙周病的关系。ＲＩＡ结果表明：牙周病患者龈组织中６－Ｋ－ＰＧＦ１ａ含量从Ｈ，     

成人慢性牙周炎龈上皮中郎格罕氏细胞的观察

本文用 S-100蛋白和溶菌酶抗体的免疫过氧化物酶技术,对10例正常人和20例成人慢性牙周炎龈上皮中郎格罕氏细胞进行鉴定和计数观察。结果表明:牙周炎时龈上皮中郎格罕氏细胞的数目明显高于正常龈上皮(P<0.01),且随炎症细胞浸润程度的加重和菌斑指数记分值的升高而增多,呈显著正相关(P<0.05)。     

种植体周围炎龈下优势厌氧菌群的研究

目的：为了探讨种植体周围炎的病因及发病机制，明确其龈下优势厌氧菌群。方法：运用厌氧培养技术，对３９例种值体周围炎的龈下标本进行厌氧菌的分离与鉴定，另外还选取了２２例健康种植体及３０例牙周炎作对照。结果：种植体周围炎组厌氧菌检出率（８９．７％）显著高于健康对照组（６３．６％）（Ｐ＜０．０５），而与牙周炎组（９０％）则无显著性差异（Ｐ＞０．０５），并发现不同临床症状的种植体周围炎病例其龈下的所得厌氧菌株的构成比有显著性差异。结论：本文认为种植体周围炎是种植后细菌再定植过程中的一种菌群失调症，Ｇ－厌氧菌为其龈下优势厌氧菌群。     

DNA探针鉴定伴放线放线杆菌及其与牙周炎临床参数的关系

目的 评估ＤＮＡ探针鉴定伴放线放线杆菌（Ａａ）的价值，探讨Ａａ与牙周炎临床表现间的相关性。方法 ３２例成人牙周炎患者５９个部位龈下菌斑经Ａａ选择性培养后，菌落分别用ＤＮＡ探针法及生化法鉴定，并根据探针法的检出率探讨Ａａ感染与牙周炎临床参数间的关系。结果 ＤＮＡ探针法与培养法有一致性（Ｐ〈０．０１，ｒ＝０．７８但探针法的检出率（２６／５９）明显高于培养法（１９／５９）（Ｐ〈０．０５）；Ａａ的检出率与     

T cells and T-cell subsets in periodontal diseases

Acetone-fixed cryostat gingival tissue sections from marginal gingivitis (MG), juvenile periodontitis (JP), adult periodontitis (AP) patients and clinically healthy subjects (H) were immunohistochemically stained with monoclonal antibodies to aid in identification and quantification of T cells and T-cell subsets in the inflammatory infiltrates. T cells were present in all specimens studied. The number of T cells in the connective tissue (CT) zone of AP was much greater than in any other groups. The amounts of T cells in oral epithelium and sulcular (pocket) epithelium zones of diseased groups were larger than in the healthy group. There was a significant positive correlation between the number of T cells and the percentage of infiltrated connective tissue. While there were no significant differences between the mean ratios of T-helper/T-suppressor cells from diseased and healthy tissues, large individual variance existed in the three diseased groups. The existence of a high or low T4/T8 ratio in inflamed gingiva might be related to an abnormal immunoregulation.     

Real-time polymerase chain reaction quantification of human cytomegalovirus and Epstein-Barr virus in periodontal pockets and the adjacent gingiva of periodontitis lesions

BACKGROUND: Genomic sequences of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV), two herpesviruses, can frequently be detected in periodontal pockets of progressive periodontitis lesions, but the prevalence and load of the two viruses in gingival tissue are unknown. This study determined levels of HCMV and EBV DNA in the periodontal pocket and in the adjacent gingiva of periodontitis lesions using a real-time polymerase chain reaction (PCR) assay. MATERIAL AND METHODS: A total of 20 systemically healthy periodontitis patients participated in the study. Nine patients below 35 years of age were tentatively diagnosed as having aggressive (early onset) periodontitis, and 11 patients 36-56 years of age as having chronic (adult) periodontitis. Clinical parameters were evaluated using established methods. Using periodontal curettes, specimens were harvested from 6-10 mm periodontal pockets and from the adjacent inflamed periodontal pocket wall. A 5'-nuclease (TaqMan) real-time PCR assay was used to identify and quantify genomic copies of periodontal HCMV and EBV. RESULTS: HCMV DNA was detected in 78% of subgingival and 33% of gingival tissue samples from aggressive periodontitis lesions, but only in 46% of subgingival and 9% of gingival tissue samples from chronic periodontitis lesions. In aggressive periodontitis, HCMV subgingival and gingival tissue counts were positively correlated with periodontal pocket depth and probing attachment loss at sample sites (p6 mm, but none of 14 patients having mean pocket depth at sample teeth相似文献   

Comparison of scanning and transmission electron microscopy of the epithelial pocket wall in juvenile and adult periodontitis

Using scanning (SEM) and transmission (TEM) electron microscopy, this study compared fine structural features of the pocket walls in both juvenile and adult periodontitis (JP and AP, respectively) in 40 cases. Gingiva was also obtained from a control group consisting of periodontally noninvolved teeth. Clinical parameters were assessed in both JP and AP patients as well as in controls. Clinical findings showed low plaque accumulation, marked periodontal tissue destruction and less gingival inflammation in JP. Bone destruction and attachment loss were more marked in JP than in AP. AP had a higher plaque index and more evident gingival inflammation. SEM observations of JP as compared to AP showed gross distortions in pocket walls, an increased beaded appearance of microridges, and separation between pocket epithelial cells. TEM showed partially desquamated and separated superficial epithelial cells, but only in JP were fine granular precipitates observed in the intercellular spaces. The observations demonstrated structural features indicative of more prominent degenerative changes in JP than in AP. Also, these features were coincidental with a higher plaque index in AP than in JP, where clinical features (including a low plaque index) were not proportional to the epithelial destructive changes present.     

Polymorphonuclear neutrophils and their mediators in gingival tissues from generalized aggressive periodontitis.

BACKGROUND: Impaired polymorphonuclear neutrophil (PMN) functions were generally considered to be related to the onset of generalized aggressive periodontitis (GAgP). However, some research has indicated that the hyperreactivity of PMN seems to be involved in the inflammatory response of GAgP. The present study's main purpose was to provide more evidence about the role of PMN in the pathogenesis of GAgP by surveying PMN infiltration in gingiva and its relationship with the expression of their mediators including intercellular adhesion molecule-1 (ICAM-1), interleukin-8 (IL-8), interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha). The inflammatory response in GAgP was also compared with that in adult periodontitis (AP) and periodontally healthy subjects. Since these PMN mediators were reported to be produced mainly by macrophages, the association between the expression of these PMN mediators and the distribution of macrophages was also investigated. METHODS: A total of 25 gingival specimens were obtained from 10 GAgP patients, 10 AP patients, and 5 periodontally healthy subjects. Serial sections were obtained from each specimen, and the following techniques were adopted to investigate the distribution and interrelation of different cells and cytokines. Infiltration of PMN was observed by using hematoxylin and eosin staining. Distribution of the macrophages, identified as CD68+, was shown by using immunohistochemistry. Immunohistochemistry and in situ hybridization were used to detect the expression of ICAM-1, IL-8, IL-1beta, and TNF-alpha in gingival tissues. These techniques were performed in serial sections from each individual specimen. RESULTS: Large numbers of infiltrating PMNs were observed in gingiva from GAgP. In gingiva from both GAgP and AP, the strongest protein and mRNA expression of IL-8, ICAM-1, IL-1beta, and TNF-alpha were located in pocket epithelium and adjacent connective tissue with large numbers of infiltrating PMNs. In tissues without abundant PMN infiltration, the appearance of positive cells expressing IL-8, ICAM-1, IL-1beta, and TNF-alpha was scattered. CD68+ was distributed sparsely in connective tissue and was hardly seen in pocket epithelium with large numbers of PMN infiltration. The degree of leukocyte infiltration and connective tissue destruction in gingiva from GAgP patients was not distinctly different from that in gingiva from AP. The gingival specimens with heavy PMN infiltration from both GAgP and AP patients presented strong expressions of IL-1beta and TNF-alpha; showed more extensive inflammatory cell infiltration; had severe connective tissue destruction; and presented severe elongation and ulceration of pocket epithelium. In gingiva from healthy subjects, inflammation was minor with visually no PMN, CD68+, or the positive cells of IL-8, ICAM-1, IL-1beta and TNF-alpha expression. CONCLUSIONS: Enhanced accumulation of PMN, which is associated with the upregulation of IL-8, ICAM-1, IL-1beta, and TNF-alpha expression, relates to the severity and activity of GAgP. In addition to macrophages, PMN and/or epithelial cells might also be important sources of IL-8, IL-1beta, and TNF-alpha production in gingiva.     

Cells and cellular interactions in gingival crevice washings from patients with juvenile periodontitis

The cells and the cellular interactions in the gingival crevices of three patients with juvenile periodontitis (JP), three patients with adult periodontitis (AP) and one healthy control were studied using light and scanning electron microscopy (SEM). The cells were collected by the washing method. The washings were either 1) fixed for 30 min in 2.5% glutaraldehyde (GA), or 2) cytocentrifuged onto a Melinex-polyester film and fixed in GA. On the films the cells of interest were identified and light photomicrographs were taken before processing for SEM. Four types of cellular interactions were seen in SEM: between polymorphonuclear leukocytes (PMN) and epithelial cells, between PMNs and bacteria, between PMNs and between bacteria. Based on morphologic and structural interpretation, the PMNs in the local lesion in JP seemed 1) to have a different morphology from the PMNs of AP lesions, 2) to be capable of ingesting bacteria, 3) to accumulate in gingival pockets in numbers as high as in AP, and 4) to be overwhelmed by the challenge of bacteria and bacterial aggregates.     

Cells and cellular interactions in gingival crevice washings from patients with juvenile periodontitis

Abstract – The cells and the cellular interactions in the gingival crevices of three patients with juvenile periodontitis (JP), three patients with adult periodontitis (AP) and one healthy control were studied using light and scanning electron microscopy (SEM). The cells were collected by the washing method. The washings were either 1) fixed for 30 min in 2.5% glutaraldehyde (GA), or 2) cytocentrifuged onto a Melinex-polyester film and fixed in GA. On the films the cells of interest were identified and light photomicrographs were taken before processing for SEM. Four types of cellular interactions were seen in SEM: between polymorphonuclear leukocytes (PMN) and epithelial cells, between PMNs and bacteria, between PMNs and between bacteria. Based on morphologic and structural interpretation, the PMNs in the local lesion in JP seemed 1) to have a different morphology from the PMNs of AP lesions, 2) to be capable of ingesting bacteria, 3) to accumulate in gingival pockets in numbers as high as in AP, and 4) to be overwhelmed by the challenge of bacteria and bacterial aggregates.     

Bacterial penetration of pocket soft tissues in chronic adult and juvenile periodontitis cases

This study investigates bacterial invasion of the soft tissue walls of deep pockets from cases with adult (AP) and juvenile periodontitis (JP). Transmission electron microscopy was used to examine pocket soft tissue walls removed from extracted teeth from 5 patients with AP and 2 patients with JP. Bacteria were sparse throughout the epithelium and connective tissue, regardless of the level of tissue breakdown. However many inflammatory cells were seen, and these did appear to be located in regions of marked collagen loss. Accumulations of large numbers of bacteria were extremely rare and found only on the epithelial surface or in artefactual spaces within the deeper tissues. The findings indicate that the tissue destruction associated with periodontitis is not directly related to bacterial invasion. The sparse organisms within the pocket tissues probably result from passive entry rather than an invasive action. Under these circumstances, it would seem reasonable to suggest that bacterial metabolic products rather than the micro-organisms themselves penetrate the tissues in periodontitis.     

Subgingival temperature and microbiota in initial periodontitis

Abstract. The association between subgingival temperature, other clinical characteristics, and the subgingival microbiota was examined in adult subjects with initial periodontitis and differing levels of gingival inflammation, 43 subjects were measured at 6 sites per tooth for pocket depth, attachment level, presence of plaque, gingival redness, bleeding on probing and subgingival temperature at 3-month intervals for 1 year. Subgingival plaque was sampled from 15 initial active periodontitis sites (10 subjects), 121 gingivitis, sites (20 subjects) and 202 healthy sites (13 subjects), and included the 5 hottest and 5 coldest sites in each subject. Plaque samples were analyzed for 13 subgingival species using whole-genomic DNA probes. The major influences on the subgingival microbiota were the clinical status of sites, pocket depth, and the presence of supragingival plaque. No significant association between species and site temperature was observed. Initial active sites were associated with Bacteroides forsythus and Campylobacter rectus. and had a higher mean subgingival temperature and deeper mean pocket depth than inactive sites, A weak association between pocket depth and site temperature was noted. The major influence on subgingival temperature of sites was the anterior to posterior anatomical temperature gradient in the mandible and maxilla.     

Immunoshistochemical localization of epidermal growth factor receptors in human gingival epithelia

Epidermal growth factor (EGF) is a small molecular weight polypeptide which is thought to have important functions in epithelial growth and differentiation and in wound healing. EGF exerts its action on cells through binding to a cell surface receptor. Using immunohistochemistry and a monoclonal antibody (mAb) directed against the EGF receptor, we have examined gingival specimens of periodontally healthy individuals and patients with adult adult (AP) and juvenile periodontitis (JP), as well as epithelial cell rests of Malassez. EGF receptors were expressed at high levels on the cell surface of basal cell layers of gingival epithelium. In normal junctional epithelium, on the other hand, specific labeling was faint or negative, indicating that receptors are poorly expressed or absent in these cells. No differences were detected between uninflamed gingival specimens of periodontally healthy subjects and of patients with JP. Instead, in biopsies of inflamed tissue from AP patients, an intense cell surface labeling was revealed in proliferating epithelial cells. Moreover, the epithelial cell rests of Malassez bound the antibody intensely. The results suggest that EGF is involved in control of epithelial growth and differentiation in periodontal tissues.     

Syndecan‐1 immunohistochemical expression in gingival tissues of chronic periodontitis patients correlated with various putative factors

Kotsovilis S, Tseleni‐Balafouta S, Charonis A, Fourmousis I, Nikolidakis D, Vrotsos JA. Syndecan‐1 immunohistochemical expression in gingival tissues of chronic periodontitis patients correlated with various putative factors. J Periodont Res 2010; 45: 520–531. © 2010 John Wiley & Sons A/S Background and Objective: Limited information is available on the expression and distribution of syndecan‐1 within human gingival tissues/cells and on putative factors that might affect its expression. Therefore, the objective of the present study was to determine immunohistochemically the expression and distribution of syndecan‐1 in the gingival tissues of patients with chronic periodontitis and to examine the correlation of syndecan‐1 expression with various putative factors (environmental, patient/systemic and local factors). Material and Methods: Gingival specimens were surgically excised from the area of the junctional/pocket epithelium (study group 1, including 30 chronic periodontitis patients) or the gingival oral epithelium (study group 2, comprising another 30 chronic periodontitis patients), adjacent to teeth with poor prognosis. Standard two‐step immunohistochemistry and semi‐quantitative evaluation of immunohistochemical staining were used to determine syndecan‐1 expression. Statistical analyses on the impact of various putative factors were performed. Results: In the junctional/pocket epithelium or the oral epithelium, syndecan‐1 expression was weak to moderate in the suprabasal and basal epithelial cells and absent to weak in the internal basal lamina, external basal lamina and gingival connective tissue matrix. Syndecan‐1 expression in the junctional/pocket epithelium was statistically significantly stronger than in the oral epithelium in inflammatory cells within the underlying gingival connective tissue (primarily plasma cells and lymphocytes) and in scattered fibroblast‐like cells. Conclusions: Syndecan‐1 expression in the junctional/pocket epithelium or the oral epithelium can exhibit a significant positive correlation with the severity/degree of histologically evaluated local gingival inflammation, but in general is not significantly correlated with age, smoking, full‐mouth and local clinical (probing pocket depth and clinical attachment level) and radiographical parameters (radiographical bone loss) of periodontal status.