乳牙深龋的临床诊断牙髓血象和组织病理的比较研究

本文将临床诊断为深龋拟作活髓切断的７４例乳磨牙，作了牙髓血象和组织病理学检查。结果为：牙髓血涂片白细胞分类中淋巴细胞高于４０％的有５８例（７８．４％），冠髓组织病理为不同程度慢性炎症的有６１例（８２．４％），表明临床诊断为深龋的乳磨牙，绝大多数冠髓已为慢性炎症表现，本研究结果对了解乳深龋的牙髓状态及治疗方法的选择和用药具有临床指导意义。     

乳牙Carisolv去龋的扫描电镜观察

目的:用扫描电镜技术对化学机械去龋法和传统去龋法去除乳牙龋损牙本质后的微观形态进行比较.方法:选取12个深龋的离体乳磨牙,随机分为对照组、机械法去龋组、Carisolv去龋组,去龋后用扫描电子显微镜分别观察3组乳磨牙窝洞底部形态.结果:对照组牙本质崩解破坏,可见碎屑和残渣,牙本质小管形态不完整;机械法去龋组牙本质表面有不规则的颗粒和碎片,有玷污层形成,牙本质小管口堵塞;Carisolv去龋组未见碎屑和残渣以及玷污层,牙本质小管清楚可见.结论:Carisolv去龋法对乳牙的牙本质龋效果优于机械法去龋组.     

隐血试验法诊断不显性露髓的探讨

<正> 在深龋治疗中,由于过多削除非感染软化牙本质或健康牙本质,造成露髓,继发牙髓病变。露髓分显性露髓和不显性露髓。显性露髓肉眼能直观地察看,露髓点有明显探痛并有渗血。不显性露髓是肉眼见不到的、相当于髓角位置的微小点孔,造成牙髓与髓腔外界相通状态,其临床特点是肉眼见不到露髓点、无明显渗血点、探痛明显却无准确位置。所谓假性露髓亦属不显性露髓的范畴。假性露髓指牙本质发生进行性脱矿,牙本质小管软化和扩大而牙本质髓侧壁无继发性牙本质生成,窝洞髓壁与牙髓间隔微薄,已经软化和扩大的牙本质小管使窝洞与牙髓潜性连通。作者在本文中把不显性露髓和假性露髓并为一论。     

Carisolv去龋对牙本质粘结界面影响的实验研究

目的:研究Carisolv去龋对牙本质粘结界面的影响。方法:24颗新鲜拔除的中度龋损的第三磨牙,随机分成ABCD4组。每个牙的龋洞分成两半,一半用Carisolv去龋,另一半用涡轮车针去龋后,做如下处理:A组不处理;B组320ml/L磷酸酸蚀,扫描电镜观察牙本质表面形态;C组不酸蚀,DyractAP复合体充填;D组320ml/L磷酸酸蚀后复合树脂充填,扫描电镜观察牙本质-充填体界面。结果:A组:Carisolv去龋后牙本质表面玷污层少,大部分牙本质小管口开放,清晰可见,表面粗糙不平;涡轮车针去龋后牙本质表面覆盖较厚玷污层,牙本质小管口堵塞,很少见到开口。B组:Carisolv去龋组和涡轮车针去龋组均去除了玷污层,牙本质小管口开放,但Carisolv组牙本质小管无管塞,而涡轮车针组牙本质小管残留部分管塞。C组:观察牙本质-复合体界面见Carisolv去龋组有较多树脂突形成,深入牙本质小管及管周;而涡轮车针去龋组未见明显树脂突起形成。D组:观察牙本质-树脂界面见2组树脂突的密度和长度无明显差异,但Carisolv去龋组树脂突之间的侧枝连接较涡轮车针去龋组多见。结论:Carisolv去龋后牙本质表面玷污层少,牙本质小管口开放,表面粗糙不规则,利于粘结,尤其在使用不需酸蚀的复合体充填时优势突出。     

髓腔内使用牙本质小管阻塞剂封闭牙本质小管的实验研究

目的 比较髓腔内使用两种牙本质小管阻塞剂阻塞牙本质小管的效果。方法 选择90颗离体单根管牙经常规根管清理成形后,随机分为3组(其中1组为对照组),两实验组在髓腔内使用草酸钾或光固化粘接剂,用染料渗透法观察比较染料浸入牙本质的情况。结果 两实验组与对照组相比其染料浸入牙本质的情况有极为显著性差异(P<0.01)。结论 在髓腔内使用牙本质小管阻塞剂可以有效地阻止染料渗入牙体。     

年轻恒牙深龋盖髓失败原因浅析

年轻恒牙尤其是萌出不久的恒牙髓腔大,髓角高,牙本质薄,牙本质小管粗大,其深龋易及牙髓,且治疗过程中较易发生意外穿髓。在临床上,我们对年轻恒牙深龋均采用间接盖髓术,意外穿髓采用直接盖髓术治疗。现将近五年收治的３６例盖髓失败病例进行分析。临床资料３６例失...     

前牙前磨牙龋性牙髓病临床和组织病理学的研究

<正> 本文的目的是通过100例前牙前磨牙龋性牙髓病的临床资料和组织病理学观察来研究其有无特性。为了观察前牙前磨牙深龋与慢性牙髓炎的关系,本研究中也收集了深龋的病例。材料和方法多年来随意收集需去除全部牙髓的病员86人100例牙。去髓原因:1.根据临床诊断标准诊断为龋性牙髓病患者74例。2.去除龋蚀时意外穿髓或去净龋蚀后洞底很近髓腔者26例。其中男性38人48例牙,女性48人52例牙。年龄14～65岁,平均40.25岁。上牙77例:中、侧切     

丁香油过敏1例

患者女，２５岁，因左下后牙疼痛１周，加重２ｄ来诊。查：３６面深龋，龋洞内有少量腐败牙本质，探痛（），叩痛（＋），未穿髓，冷诊（＋），热诊（），诊断：３６慢性牙髓炎急性发作。涡轮机钻开髓，见３６髓腔内有多量脓血性分泌物流出。止血后，丁香油棉球安抚...     

根尖周围炎治疗时对碘过敏一例报告

患者李某某,女,42岁,工人。因右下磨牙龋洞,经常疼痛伴牙龈肿胀约3年求治。检查:(?)引近中邻(牙合)深龋,穿髓,探痛(—),叩痛(+～(?)),颊侧牙龈充血、水肿。(?)线片示根尖周骨质有明显破坏,其范围未超过根长1/3。处理:去除(?)软化牙本质,开髓,去冠髓,3%双氧水及生理盐水冲洗髓腔,置樟脑酚棉球,暂封丁香油     

牙髓炎症中降钙素基因相关肽阳性神经纤维的变化

本研究的目的在于探讨牙髓炎症及修复过程的分子生物学机理。在大鼠磨牙制备近髓窝洞，封入新鲜龋坏组织，建立了大鼠牙髓炎模型。用免疫组织化学方法观察正常牙髓及炎症４天、８天、１４天牙髓降钙素基因相关肽（ＣＧＲＰ）阳性神经纤维的变化。结果表明，ＣＧＲＰ阳性神经纤维广泛存在于正常牙髓中，大量阳性纤维进入牙本质小管；炎症４天组的牙髓中及进入牙本质小管内的阳性神经纤维均明显增多；炎症８天组冠髓部分坏死，阳性神经纤维包绕坏死区周围，根髓阳性神经纤维显著增多并可见大量“出芽”（ｓｐｒｏｕｔｉｎｇ）；炎症１４天组牙髓已大部分坏死，尖周膜腔阳性神经纤维聚集。结果提示，ＣＧＲＰ可能参与了牙髓炎症及其修复过程。     

Tissue response to dental caries

Abstract Caries still represents the most widespread human disease. The pulp tissue sequelae of den tin caries are of utmost importance, because prevention of pulpal damage considerably reduces the need for extensive restorations and endodontic therapy. There is, however, considerable disagreement in the literature regarding how early the pulpal response to caries can be detected. The material in this article, gathered from the author's and his coauthors' earlier investigations, deals with pulp reactions from initial caries to increasingly extensive caries; caries in combination with attrition; the effect of carious den tin in experimental cavities of intact dentin; the effect of medicaments, restorative procedures and materials, and indirect pulp capping in the treatment of deep caries; microbiologic aspects of dentin caries; diagnosis criteria for treatment; light and electron microscopic study of teeth with carious exposure; periodontal disease and root caries in the geriatric population; pulp biopsies of teeth with periapical lesions, and the breakdown of the remaining pulp and its periapical sequelae. Pulpal reactions to initial caries detected as early as bacteria reach the dentinal tubules arc also discussed. As in medium and deep caries, this can be reversible following the removal of the infected dentin, except for irritation dentin and calcifications on the canal walls or free in the lumen. Bacteria remaining in dentinal tubules combined with iatrogenesis may be the reason for pulpal disintegration under deep restorations. Indirect pulp capping is not an acceptable procedure. Pain (or lack thereof) is not a predictable indicator of the inflammatory stage of the pulp. Root caries must be treated early to prevent pulpal destruction. Vital pulp tissue can be found in the roots of teeth with periapical radiolucencies that will ultimately show the presence of bacteria.     

Effect of pulpal inflammation on bacterial penetration of acid-etched and non-etched dentin

Abstract Bacterial invasion of acid-etched and non-acid-etched dentin was compared in teeth with intact pulps and in teeth with experimentally induced pulpal inflammation. In 37 pairs of teeth from 3 dogs, class V cavities were prepared. In 1 tooth from each pair, pulpal inflammation was induced by the application of a strong thermal irritant to the floor of the cavity. In 18 pairs of teeth the cavity floor was treated with orthophosphoric acid, and in 19 pairs with normal saline. The cavities remained open to oral microflora for a period of either 3 or 7 d. All the teeth with acid-etched dentin and only 9 teeth with non-acid-etched dentin exhibited slight invasion of the dentinal tubules by gram-positive or gram-negative bacteria. This invasion had no relationship to the histopathological findings in the pulp     

Bacterial invasion of non-exposed dental pulp

Anaerobic procedures were adopted to demonstrate the early bacterial invasion of non-exposed dental pulps, and to isolate and identify the bacteria. Of 19 freshly extracted teeth which originally exhibited deep dentinal lesions, clinical examination and electric pulp testing showed that nine of them had no pulpal exposure. Thus the pulps of these teeth were covered by clinically sound dentine beneath the carious lesion. Bacteria were found to have invaded the pulps of six of these nine teeth. The predominant bacteria were obligate anaerobes belonging to the genera Eubacterium, Propionibacterium and Actinomyces. Other obligate anaerobes were Lactobacillus, Peptostreptococcus, Veillonella and Streptococcus. The bacterial composition resembled that of the deep layers of dentinal lesions described previously, suggesting that the bacteria isolated in this study had passed through some individual dentinal tubules, to invade the dental pulp.     

Is hard tissue formation in the dental pulp after the death of the primary odontoblasts a regenerative or a reparative process?

Objectives

Conceptually, two types of tertiary dentine may be produced in response to caries and environmental irritations: “reactionary dentine” that is secreted by existing primary odontoblasts and “reparative dentine”, formed after the death of the odontoblasts by proliferation and differentiation of progenitor cells into odontoblast-like cells. Because histologic evidence for tubular dentine generated by newly differentiated odontoblast-like cells is lacking in human teeth, the present study examined pulpal cellular changes associated with caries/restorations, in the presence or absence of pulpal exposures.

Methods

Ninety-six extracted human teeth were histologically processed and serial sectioned for light microscopy: 65 contained untreated enamel/dentine caries; 20 were heavily restored and 11 had carious exposures managed by direct pulp-capping.

Results

Sparsely distributed, irregularly arranged dentinal tubules were identified from the tertiary dentine formed in teeth with unexposed medium/deep caries and in restored teeth; those tubules were continuous with the tubules of secondary dentine; in some cases, tubules were absent. The palisade odontoblast layer was reduced to a single layer of flattened cells. In direct pulp-capping of pulp exposures, the defects were repaired by the deposition of an amorphous dystrophic calcified tissue that resembled pulp stones more than dentine, sometimes entrapping pulpal remnants. This atubular hard tissue was lined by fibroblasts and collagen fibrils.

Conclusions

Histological evidence from the present study indicates that reparative dentinogenesis cannot be considered as a regenerative process since the so-formed hard tissue lacks tubular features characteristic of genuine dentine. Rather, this process represents a repair response that produces calcified scar tissues by pulpal fibroblasts.

Clinical significance

Formation of hard tissue in the dental pulp after the death of the primary odontoblasts has often been regarded by clinicians as regeneration of dentine. If the objective of the clinical procedures involved is to induce healing, reduce dentine hypersensitivity, or minimise future bacteria exposure, such procedures may be regarded as clinical success. However, current clinical treatment procedures are not adept at regenerating physiological dentne because the tissues formed in the dental pulp are more likely the result of repair responses via the formation of calcified scar tissues.     

深龋乳牙根管细菌学分析

目的本研究的目的是对患有深龋的乳牙根管内细菌进行分析。方法选择12颗深龋乳牙，其中3颗有冷热刺激痛，其余9颗无临床症状。分别在微需氧(80％N2，10％H2，10％CO2)及厌氧条件(90％N2，10％CQ)下进行患牙根管细菌分离和鉴定。结果结果显示有症状牙的菌落形成单位(Colony Fomation Unit，简称CFU，下同)比无症状牙高，但二者间的差异无显著性。在这两组中，根管细菌的组成相似，并且与深龋的细菌组成相似。变链菌和乳杆菌占可培养细菌的比例比其它细菌高，差异有显著性，而且变链菌和乳杆菌的检出率比其它细菌高，差异亦有显著性。专性厌氧菌，如消化链球菌、韦荣氏菌、梭杆菌和普氏菌也有所检出，但其检出率和占可培养菌百分比均很低。结论微需氧致龋菌是乳牙龋源性牙髓炎的主要致病菌。     

Micromorphology of mineralization deposits in the pulps of human teeth

Summary. The dental pulp may contain a considerable amount of calcified material. This originates from the pulp and takes the form of rods or tubules in the radicular pulp, or concentric spherical deposits in the coronal pulp. Chains of oval deposits may also form at the coronal end of the radicular pulp.
Obliteration of the root canal may be due to dentinogenesis or to a massive diffuse pulpal calcification which has a herring-bone structure and contains small spaces which could harbour bacteria. Growths of tubular dentine may be observed which take the form of flakes along the walls of the root canal and nodules around the walls of the coronal pulp chamber. These tubular excrescences may be observed invading the diffuse pulpal calcification to form a complicated cross-linked calcified structure.     

A morphometric analysis of the cross-sectional area of dentine occupied by dentinal tubules in human third molar teeth

The number and the mean percentage tubular cross-sectional area of dentinal tubules per square millimetre were calculated in specimens of coronal dentine of 13 intact human third molar teeth from patients 18 to 28 years of age. The dentine was fractured at various known distances from the dentino-enamel junction. Near the dentino-enamel junction the number of tubules per square millimetre was 22 000 and the mean tubular cross-sectional area was 3.6%. Midway between the pulpal wall and the dentino-enamel junction the number of tubules was 37000 mm^?2 and the mean tubular cross-sectional area was 6.2%. Close to the pulp the number of dentinai tubules was 48000 mm^?2 and the mean cross sectional area of tubules was 10.2 percent. The number of tubules per square millimetre more than doubled and the area occupied by tubules increased threefold from the dentine close to the dentine -enamel junction, to that close to the pulp. These differences in tubular patterns at different depths in dentine are clinically significant in dentine permeability, the treatment of traumatized teeth, and pain transmission in dentine.     

Reaction of the human dental pulp to silver amalgam restorations. The effect of enclosing amalgam of initially high plasticity in intermediate depth or deep cavities.

From earlier studies using amalgam of known physical and sealing properties it was concluded that the initially high mercury content was the main reason for pulpal changes and that clinical leakage had been less important. The purpose of the present investigation was to study how a possible sealing insufficiency may contribute to the pulpal changes beneath restorations of silver amalgam. The influence of bacteria at the tooth/filling interface upon pulpal changes was also studied. The material consisted of 21 contralateral pairs of premolars. Intermediate depth cavities were prepared in 13 pairs and deep cavities in 8 pairs. All cavities were filled with silver amalgam by the wet technique. The restoration in one tooth of each pair was sealed off by glued metal foil protected by a cemented orthodontic band. After 1 week the teeth were extracted and examined histologically. In the pulp of teeth with restorations exposed to the oral environment, the frequency of dilated capillaries and inflammatory cells in the odontoblast - cell-rich zone boundary, associated with the dentinal tubules involved in the cavity preparation, was insignificantly higher statistically than in those with seal-off restorations. A few scattered bacteria were found on the cavity wall in some cases. It was concluded that, in the short run, the pulp reaction was influenced by sealing insufficiency, which may develop during the experimental period as a result of external factors such as tooth deformation and/or changes in temperature. No influence from bacteria on the cavity wall could be established.     

The pulpal origin of immunoglobulins in dentin beneath caries: an immunohistochemical study

Immunoglobulins localized in uninfected dentin beneath caries are thought to be protective, but their origin remains controversial. We reasoned that the localization and dominance of serum IgG1 would support the pulpal origin of the immunoglobulins while a predominance of secretory component (SC) bearing IgA1 and IgA2 would support their salivary origin. The prevalence and staining intensity of IgG1, IgA1, IgA2, IgM, and SC in uninfected dentinal tubules beneath shallow, deep caries, and noncaries teeth were examined immunohistologically. SC was only localized in caries, and IgG1 was the predominant subclass in uninfected dentinal tubules beneath shallow and deep caries, followed by IgA1. In noncaries teeth, IgG1 was localized on the pulpal end. The intensity of IgG1 was significantly higher than either IgA1 or IgA2 in both shallow and deep caries. Our data support the serum origin of immunoglobulins in uninfected dentin beneath caries.     

The effects on pulp tissue of microleakage in resin composite restorations

The purpose of this study was to evaluate histopathologically the effect on pulp tissue of microleakage in resin composite restorations. Seventy-two class V cavities were prepared on buccal surfaces of monkeys and divided into 3 groups, F, O, and S. Every cavity was etched with 37% phosphoric acid. In group F cavities, each cavity was restored with photo-curable composite without any dentin adhesives. In group O, the cavities were left unfilled. In group S, each cavity was treated with a dentin adhesive system and restored with a restorative composite. After 3, 30, or 90 days, animals were sacrificed and the subjected teeth were immediately removed, then fixed and decalcified. Following sectioning and staining with hematoxylin and eosin or Taylor's modified bacteria staining, each sample was examined with a light microscope. In most teeth with group S cavities, bacterial invasion was not found indicating excellent marginal sealing. The pulpal reaction was much less than that in other groups. In group F as well as in group O, bacteria were frequently observed in the cavity; however, bacteria penetrated into dentinal tubules more in group F than in group O at 30 and 90 days. A correlation between the presence of bacteria and pulpal inflammation was strongly indicated. It was suggested that a leaky restoration was more harmful to the pulp than an open prepared cavity without restoration.