正常人,龋病和牙髓炎患者牙髓组织中一氧化氮含量的检…

目的：正常人，龋病和牙髓炎病患者牙髓组织中一氧化氮（Ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）含量进行检测，初步探讨ＮＯ在牙髓组织自身修复中的作用。方法：采用荧光分光光度法检测其中亚硝酸根（ＮＯ２）含量，以间接确定ＮＯ含量。结果：正常牙髓组织中ＮＯ无性别差异（Ｐ〉０．０５），浅龋组与对照组ＮＯ无显著性差异（Ｐ〉０．０５），而深龋伴慢性牙髓炎组ＮＯ含量则显著高于对照组（Ｐ〈０．０５）。结论：牙髓组织中ＮＯ含量的     

牙髓组织中超氧化物歧化酶及丙二醛的研究

本研究目的为通过对超氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ，ＳＯＤ）活性和丙二醛（ｍａｌ－ｏｎｙｌｄｉａｌｄｅｈｙｄｅ，ＭＤＡ）含量的测定，进一步探讨了炎症牙髓组织和氧自由基的关系。作者从１２～６４岁做牙髓摘除术和根管治疗术的患者中，采集正常牙髓９份，炎症牙髓１２份，分别检测ＳＯＤ活性和ＭＤＡ含量。结果发现炎症牙髓中的ＳＯＤ活性有非常显著增高（Ｐ＜０．０１），ＭＤＡ含量也明显升高（Ｐ＜０．０５）。这表明牙髓炎与脂质过氧化物反应有密切关系，牙髓炎症中脂质过氧化的速率和强度均有增强和加快，ＳＯＤ活性增高说明牙髓组织具有内源性防御机制，保护牙髓组织免受反应性过氧化媒介物的毒性作用。     

炎症人牙髓组织渗出液中IL-8含量的检测

目的：检测人正常和炎症牙髓组织渗出液中ＩＬ－８的含量,揭示ＩＬ－８与牙髓炎的关系。方法：用滤纸条浸润法采集正常和临床诊断为急性或慢性牙髓炎患牙牙髓组织渗出液。用ＥＬＩＳＡ方法检测其ＩＬ－８含量。结果：正常牙髓组织渗出液中检测不到ＩＬ－８,而炎症牙髓组织渗出液中均有较高水平的ＩＬ－８（０．３３～１．０μｇ／Ｌ）,且在急性牙髓炎中的水平高于慢性牙髓炎（Ｐ〈０．０１）。结论：ＩＬ－８参与了牙髓炎的发生和     

正常和炎症人牙髓组织Cu，Zn─SOD活性比较研究

本文分别对正常和慢性炎症人牙髓组织各１５例、急性炎症牙髓组织５例，进行Ｃｕ，Ｚｎ─ＳＯＤ活性测定。。结果显示，Ｃｕ，Ｚｎ─ＳＯＤ活性均数，正常牙髓为１５１．０３±５８．３４Ｕ／ｇ（湿重），慢性炎症牙髓为１２１．７２±７７．９６Ｕ／ｇ（湿重），急性炎症牙髓为２１３．２８±４６．５７Ｕ／ｇ（湿重）．提示Ｃｕ，Ｚｎ─ＳＯＤ活性在慢性炎症牙髓组织中比在正常牙髓中显著降低（ｐ＜０．０５），而在急性炎症牙髓组织中则比正常牙髓显著升高（ｐ＜０．０１）。这为研究急、慢性牙髓炎ｃｕ，Ｚｎ─ＳＯＤ活性变化规律提供了依据。     

热休克蛋白70在人正常牙和龋坏牙牙髓中的免疫定位

目的：观察热休克蛋白７０（ｈｅａｔｓｈｏｃｋ ｐｒｏｔｅｉｎ ７０ ,ＨＳＰ７０）在人正常和龋坏牙牙髓组织中免疫定位,并通过对比研究,检测ＨＳＰ７０ 的分布变化。方法：选取人正常牙、浅龋牙和深龋牙的组织切片标本进行免疫组织化学染色,并通过计算机图像分析对比３ 种牙髓中ＨＳＰ７０ 量的不同。结果：ＨＳＰ７０ 于３ 组牙髓组织中普遍表达,分布于成牙本质细胞及细胞突、牙髓成纤维细胞、血管内皮细胞及管壁平滑肌细胞中。牙髓神经阴性。深龋组成牙本质细胞或成牙本质细胞样细胞中含量显著增加（ Ｐ＜ ０．０５） 。浅龋组观察到阳性细胞核数目增加。结论：提示ＨＳＰ７０ 维持成牙本质细胞、牙髓细胞功能,参与牙髓组织的自身修复。     

正常和炎症牙髓组织中超氧化物歧化酶的活性研究

从１２～６４岁做牙髓摘除术和根管治疗的患者中，采集正常牙髓９份，炎症牙髓１２份，冰浴下匀浆、离心，用黄嘌呤氧化酶法测定超氧化物歧化酶（ＳＯＤ）的活性。正常牙髓组织中ＳＯＤ活性为１８．９６～３０．９９ＮＵ／ｍｇ蛋白，炎症牙髓组织中ＳＯＤ活性为３５．５０～４５．１６ＮＵ／ｍｇ蛋白，两组有高度显著性差异（Ｐ＜０．０１）．说明人牙髓组织具有内源性防御机制，保护牙髓组织免受反应性过氧化媒介物的毒性作用。本研究还发现，不论是正常牙髓还是炎症牙髓都存在着ＳＯＤ的增龄变化，即随着年龄的增高，ＳＯＤ的活性逐渐下降．     

正常,炎症牙髓中肿瘤坏死因子—α的免疫组化研究

目的：通过对比研究检测正常、炎症牙髓中肿瘤坏死因子－α（ＴＮＦ－α）的分布变化。方法：取临床拔除的正常、龋牙和慢性炎症的第三磨牙牙髓，用ＡＢＣ法进行免疫组织化学染色，并用计算机图像分析方法对比３种牙髓中ＴＮＦ－α量的不同。结果：正常牙髓组织中存在少量ＴＮＦ－α；龋牙、炎症牙髓ＴＮＦ－α含量明显增加（Ｐ＜０．０１），其在牙髓中的分布也发生变化。结论：提示ＴＮＦ－α在牙髓组织中可能发挥重要的生理和病理作用。     

儿童唾液成分与龋齿关系的分析

本实验对１０７名４－６岁乳牙儿童取混合唾液检测流速（Ｖ），唾液钙（Ｃａ），磷（Ｐ）唾液总蛋白（ＴＰ），及唾液免疫球蛋白ＩｇＧ，ＩｇＡ的含量进行分析，探讨其与龋齿的关系，结果显示：１，唾液的ＴＰ，ＩｇＧ，ＩｇＡ含量无龋组低于患龋线两组均数之间有显著性差异（Ｐ〈０．０５，Ｐ〈０．０１，Ｐ〈０．０１），２．唾液的Ｖ和Ｃａ，Ｐ含量，无龋组与患龋组两组均数之间无显著性差异（Ｐ〉０．０５），３无龋组快于唾液Ｖ     

人牙髓中6—酮—前列腺素F1α,血栓素B2浓度的放射免疫 …

目的：观察正常、龋病、慢性牙髓炎、慢性牙髓炎急性发作患者的牙髓中６－酮－前列腺素Ｆ１α、血栓素Ｂ２的含量，揭示ＰＧＩ２和ＴＸＡ２的作用。方法：放射免疫检测法检测。结果：龋病、慢性牙髓炎、慢性牙髓炎急性发作三组中６－酮－ＰＧＦ１α和ＴＸＢ２水平明显高于正常组（Ｐ〈０．０１）。慢性牙央炎组中ＴＸＢ２水平高于龋病组（Ｐ〈０．０１），慢性牙髓炎急性发作组中６－酮－ＰＧＦ１α水平明显高于其它组（Ｐ〈０．０１     

龋病患者唾液中几种成分含量分析

目的：了解多龋患者和无龋者唾液中碱性磷酸酶、总蛋白、Ｋ＋、Ｃｌ－含量是否有差别。方法：碱性磷酸酶、总蛋白含量采用ＢＰＣ生化分析仪,Ｋ＋、Ｃｌ－含量用９０３电解质分析仪。结果：多龋患者唾液中碱性磷酸酶、Ｋ＋含量显著高于无龋者（Ｐ＜０．０５）,总蛋白、Ｃｌ－含量与无龋者比较无显著差异（Ｐ＞０．０５）。结论：唾液中碱性磷酸酶、Ｋ＋含量增高与龋齿有一定关系。     

Quantitative analysis of substance P, neurokinin A and calcitonin gene-related peptide in pulp tissue from painful and healthy human teeth

AIM: The purpose of this study was to investigate the levels of substance P (SP), neurokinin A (NKA) and calcitonin gene-related peptide (CGRP) in painful and healthy human dental pulps. METHODOLOGY: Forty-six samples of pulp tissue were collected from extracted or endodontically treated painful teeth and 20 from clinically healthy teeth extracted for orthodontic reasons. All pulp samples were boiled in 0.5 m acetic acid for 10 min, centrifuged and the supernatant collected. SP, NKA and CGRP levels were measured using radioimmunoassay. RESULTS: Substance P and CGRP were present in all samples and NKA was detected in 96% of the pulps. CGRP was present in much higher concentrations than SP and NKA in both painful and non-painful teeth. The painful teeth had significantly higher concentrations of SP (P = 0.02), NKA (P < 0.001) and CGRP (P = 0.03) than non-painful teeth. The concentration of CGRP was significantly higher in the pulps of smokers compared with non-smokers (P = 0.02). CONCLUSIONS: Elevated levels of these neuropeptides in pulps from painful teeth indicate that they may play an important role in the process of pulpal inflammation and pain. Further investigation of the association between these neuropeptides and pulpal status may help to improve our understanding of pulpal inflammation and dental pain.     

Innervation of human tooth pulp in relation to caries and dentition type

The neural status of carious teeth, particularly those associated with a painful pulpitis, is largely unknown. This study sought to determine differences in the innervation density of human primary and permanent teeth and whether caries or painful pulpitis was associated with anatomical changes in pulpal innervation. Coronal pulps were removed from 120 primary and permanent molars with a known pain history. Teeth were categorized as intact, moderately carious, or grossly carious. Using indirect immunofluorescence, we labeled sections for the general neuronal marker, protein gene product 9.5. Using image analysis, we found permanent teeth to be significantly more densely innervated than primary teeth. While there was no significant correlation with reported pain experience, neural density in both dentitions increased significantly with caries. Analysis of these data suggests that caries-induced changes in neural density may be functionally more important in the regulation of pulpal inflammation and healing than in the processing and perception of dental pain.     

Effect of nitric oxide synthase inhibitor (L-NAME) on substance P-induced vasodilatation in the dental pulp

AIM: To investigate the vasodilator mechanisms of pulpal vessels, especially the involvement of nitric oxide (NO), during pulpal inflammation. METHODOLOGY: Eleven cats were prepared for intra-arterial administration of test agents through a lingual artery. The pulpal blood flow was measured by laser Doppler flowmetry from ipsilateral mandibular canine teeth. By using the NO synthase (NOS) inhibitor N(G)-nitro L-arginine methyl ester (L-NAME), the effects of L-NAME on various vasodilators, such as Substance P (SP)-, calcitonin-gene related peptide (CGRP)-, and papaverine-induced vasodilatation, were compared in vivo in 11 feline dental pulps. RESULTS: L-NAME pretreatment potentiates SP-induced vasodilatation for a duration of approximately 5 h. The increase of pulpal blood flow ranged from 91.47 to 109.91%, which was significantly different from SP injection alone (48.79%, P < 0.05). Other vasodilators such as CGRP and papaverine did not respond to L-NAME pretreatment. CONCLUSIONS: This study demonstrates that NOS inhibitor L-NAME administration alone has insignificant effects on pulpal blood flow, although L-NAME pretreatment can potentiate SP-induced vasodilatation, probably via increased activity in the enzyme guanylate cyclase. CGRP and papaverine did not respond to L-NAME pretreatment, indicating that they are not mediated via an endothelium-dependent mechanism.     

The Effect of Hyperglycemia on Pulpal Healing in Rats

Diabetes mellitus (DM) may impede healing of dental pulps. In this study, the effect of hyperglycemia on pulpal healing was determined in exposed rat pulps capped with mineral trioxide aggregate. Two groups of 11 rats received injections of saline (control group) or streptozotocin to induce hyperglycemia (DM group). The pulps of the maxillary first molars of all rats were exposed and capped. Intact teeth and teeth with exposed pulps without restorations served as positive and negative controls, respectively. Histologic samples were prepared and evaluated for dentin bridge formation and pulpal inflammation. Data were analyzed by using Fisher exact, Mann-Whitney U, and Spearman correlation tests. Dentin bridge formation was inhibited in diabetic rats (p = 0.029) along with more inflammation in these pulps (p = 0.005). There was an inverse association between dentin bridge formation and inflammatory cell infiltration (p = 0.001). Based on these results, it appears that hyperglycemia adversely affects pulpal healing in rats.     

龋病病变程度与牙髓中TNF-α、IL-8含量关系的研究

目的探讨龋病进展过程中牙髓组织中TNF-α（肿瘤坏死因子-α）、IL-8（白细胞介素-8）含量变化的特点以及龋病病变程度与上述细胞因子（cytokine,CK）三者间的关系。方法用ELISA方法检测正常、釉质龋和牙本质浅龋、中龋、深龋牙髓组织中TNF-α、IL-8的含量。结果除正常组和釉质龋组比较牙髓组织中TNF-a、IL-8含量无显著性差异,牙本质浅龋和中龋组牙髓组织中IL-8水平比较无显著性差异外,随着龋齿深度的增加,牙髓组织中两种细胞因子的含量均呈显著增加的趋势。相关性分析结果表明龋坏程度与TNF-a之间、龋坏程度与IL-8之间、TNF-a与IL-8之间均呈正相关关系。偏相关分析显示：龋坏程度与TNF-a关系最为密切,其次是TNF-a与IL-8。结论牙本质浅、中和深龋的牙髓组织中均存在TNF-a和IL-8,其含量可反应龋病进展过程中的牙髓健康状态及其免疫防御功能。     

Expression of calcitonin gene-related peptide (CGRP) in irreversible acute pulpitis

The main goal of this study was to evaluate tissue levels of calcitonin gene-related peptide (CGRP) in human pulpal samples collected from teeth with a clinical diagnosis of acute irreversible pulpitis, normal pulps, and teeth with induced pulpal inflammation. All the pulp tissue was mechanically separated, collagenase digested to release individual cells, and labeled with FITC detection of an anti-CGRP polyclonal antibody. Detection of CGRP was possible in these cells due to a binding of the antibody to CGRP that was itself bound to its cell surface receptor. Flow cytometry analysis indicated that the labeled pulp cells were located in a region of low size and complexity according to their forward (FSC) and side scatter (SSC) properties. Significant statistical differences were found between the percentages of CGRP expression in healthy pulps and pulps with induced inflammation and between healthy pulps and pulps with acute irreversible pulpitis. No significant statistical differences were found between pulps with induced inflammation and pulps with acute irreversible pulpitis. These findings support the hypothesis that the CGRP system is active in human pulpal inflammation and may modulate the inflammatory response.     

Natural modifiers of the inflammatory process in the human dental pulp.

Concentrations of the protease inhibitors alpha 1-antitrypsin and alpha 2-macroglobulin were determined in normal and inflamed human dental pulps. Carious pulpal exposure which is associated with polymorphonuclear leukocyte infiltration and release of lysosomal enzymes was chosen as the point of verifiable inflammatory activity in the pulp. Normal samples were collected from nondiseased third molar teeth treatment planned for extraction and inflamed human pulps were collected from teeth with deep carious lesions. One half of each sample was assayed for concentration of protease inhibitors by enzyme-linked immunosorbent assay and the remaining half was examined histologically to verify the clinical diagnosis and categorize the extent of the inflammatory process. alpha 1-Antitrypsin and alpha 2-macroglobulin were detected in normal and inflamed human dental pulps in the nanogram per milliliter range. Statistically significant differences were found in the concentrations of alpha 2-macroglobulin (p less than 0.01) in moderate to severe inflammation versus normal pulp categories and between mildly inflamed pulps and moderate to severely inflamed pulps (p less than 0.05). Although differences in concentrations of alpha 1-antitrypsin were seen between inflamed and normal pulps, the differences were not statistically significant. The presence of these two protease inhibitors in the human dental pulp tissue and the increase in their concentration in acute inflammation indicates that these proteins play a role in the pathogenesis of pulpal inflammatory disease.     

Pulp capping of dental pulp mechanically exposed to oral microflora: a 1–2 year observation of wound healing in the monkey

Four adult Rhesus monkeys provided 120 teeth for buccal Class V cavities. Twenty-nine were non-exposed controls and 91 were exposed for 3 intervals. All 120 teeth were capped with a hard set Ca(OH)₂, medicament, restored with amalgam, 57 evaluated after 1 year and 63 after 2 years. Of the 91 exposed pulps, 45 showed complete healing, 25 showed pulpal inflammation varying from acute to chronic, 12 showed severe pulpal breakdown and abscess formation and 9 were necrotic. No difference was observed in the healing response between the 3 exposure times. New hard tissue formed at, or subjacent to, the medicament in 77 of 91 exposed pulps with a tunnel defect frequently present, running from the medicament interlace to the pulp. This study demonstrates that recurring pulp inflammation observed after 1 & 2 year direct pulp capping, is associated with bacterial contamination.