Microleakage related to restorative procedures.

C F Cox
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引用次数: 0

Abstract

A current Med-line search from 1966 to present cited over 344 juried publications employing the term microleakage. Dentistry recognizes microleakage as a multifaceted biological phenomenon. Brännström et al. (1967), Trowbridge (1982), Närhi (1983), and others have reported the sensory component of microleakage as a consequence of hydrodynamic fluid movement within the dentinal tubule complex. This movement of dentinal fluid has been demonstrated to displace nociceptive receptors which stimulate the nerves of the Group A fibers which run and terminate within the odontoblastic layer (see Matthews 1992). Penetration of oral fluids, bacteria and their toxic products within the preparation-material interface following material insertion accounts for the pathological component of microleakage (Browne and Tobias 1986). Continued microleakage of bacterial infiltrates eventually present as an inflammatory process which may initially signal the dentin complex to respond by deposition of a hypermineralized or sclerotic dentin. The pulp-dentin interface will repair with a specialized zone of reparative dentin. An overwhelming carious lesion often results in pulp infection and eventual necrosis. Vital dentin is an extension of the pulp, presenting the first line of defense to the consequences of microleakage. Recent publications have demonstrated that microleakage of dental materials in non-exposed and exposed pulps is a function of controlling bacterial infection. In an exposed mature dental pulp, the mesenchymal tissue permits the reorganization of pulp tissue and regeneration of a new dentin bridge in the presence of a biological seal. New odontoblastoid cells appear to regenerate from deeper pulpoblasts in the presence of various dental materials, apparently without an epithelial stimulating factor (Yamamura 1985). This inherent healing of the dental pulp and regeneration of a new dentin bridge is expressed in the presence of various dental materials, but only in the absence of bacterial infection. Data which evaluates the biological deposition of reparative and dentin bridges as either repair or regeneration are presented as a basis for considering the clinical selections of dental materials. Recent data demonstrate that dentin and pulp healing are ensured when a proper biological seal is provided to control and prevent microleakage.

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与修复程序有关的微渗漏。
从1966年到现在,一个当前的中线搜索引用了超过344份使用术语微泄漏的受损出版物。牙科认识到微渗漏是一个多方面的生物现象。Brännström等人(1967)、Trowbridge(1982)、Närhi(1983)等人报道了微渗漏的感觉成分是牙本质小管复合体内流体动力运动的结果。牙本质液体的这种运动已被证明取代了伤害感受器,这种感受器刺激在成牙细胞层内运行和终止的A群纤维的神经(见Matthews 1992)。在材料插入后,口腔液体、细菌及其有毒产物在制备-材料界面内的渗透是微渗漏的病理成分(Browne和Tobias 1986)。细菌浸润的持续微渗漏最终表现为炎症过程,这可能最初向牙本质复合体发出信号,通过沉积高矿化或硬化的牙本质来做出反应。牙本质与牙髓的界面会被修复牙本质的特殊区域修复。严重的龋齿病变常导致牙髓感染并最终坏死。重要牙本质是牙髓的延伸,是防止牙髓微渗漏的第一道防线。最近的出版物表明,未暴露和暴露的牙髓中牙材料的微泄漏是控制细菌感染的一个功能。在暴露的成熟牙髓中,间充质组织允许牙髓组织的重组和新的牙本质桥在生物密封的存在下再生。新的成牙母细胞似乎在各种牙科材料存在的情况下从更深的成牙髓细胞再生,显然没有上皮刺激因子(Yamamura 1985)。这种牙髓的内在愈合和新牙本质桥的再生是在各种牙科材料存在的情况下表现出来的,但只有在没有细菌感染的情况下。评估修复和牙本质桥的生物沉积作为修复或再生的数据被提出作为考虑牙科材料临床选择的基础。最近的数据表明,当提供适当的生物密封来控制和防止微泄漏时,可以确保牙本质和牙髓的愈合。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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Function of masticatory system after surgical-orthodontic correction of maxillomandibular discrepancies. The Finnish Family Competence Study: young fathers' views on health education. Oral health status in a Finnish village. Trigeminal foraminal patterns in "skeletal" Class II and Class III adults--a radiocephalometric study. Comparison of dental arch dimensions in children from southern and northern Finland.
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