Bacterial penetration of the root canal of intact incisor teeth after a simulated traumatic injury.
Bacterial penetration of the root canal of intact incisor teeth after a simulated traumatic injury.
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模拟外伤后完整门牙根管内的细菌渗透。
DOI：
10.1111/j.1600-9657.1996.tb00529.x
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
R. Love
中科院分区：
文献类型：
--
作者：
R. Love
治疗外伤牙齿的目的之一是维持牙髓的活力或创造有利于牙髓血运重建的条件。然而，牙髓和根管系统的感染可能会阻止这种情况的发生。已经提出了许多允许细菌侵入根管系统的途径，但是这些途径中的大多数不能解释未对牙周附着造成损伤的牙齿中的牙髓感染。牙釉质/牙本质裂纹被认为是细菌侵入看似完整牙齿的门户，本研究的目的是确定细菌是否可以在模拟创伤事件后侵入根管系统。选择并准备了二十颗完整且健全的上中切牙。选择一颗牙齿作为无菌对照，其余 19 颗牙齿的外冠表面在细菌微渗漏模型中接受戈登链球菌感染。经过 7 天的时间，从根管系统中采集生长介质样本并进行细菌测试。十六颗牙齿在一段时间内没有表现出细菌入侵。然后，这些牙齿准备在摆锤冲击装置中进行测试，并受到不会使牙冠断裂或使牙齿从模拟牙槽中脱落的撞击。然后制备牙齿并在细菌微渗漏模型中进行测试。撞击后，其中 7 颗牙齿显示细菌侵入根管系统 (P = 0.002)。然后重新准备这些牙齿以在细菌微渗漏模型中进行测试。随机选择的五颗牙齿的牙冠涂有两层光固化未填充树脂，其余两层用作阳性对照。所有涂有树脂的牙齿均未表现出细菌侵袭（P = 0.00），而阳性对照则表现出细菌侵袭。结果表明，牙釉质/牙本质损伤是细菌侵入外伤牙齿根管系统的途径。在解剖冠上应用未填充的树脂可以防止感染。
One of the aims in treating traumatised teeth is to maintain the vitality of the pulp or allow conditions favourable for pulp revascularisation. However, infection of the pulp and root canal system may prevent this. A number of pathways have been proposed that allow bacteria to invade the root canal system, however most of these pathways cannot account for pulp infection in teeth that did not sustain injury to the periodontal attachment. Enamel/dentine cracks have been proposed as a portal for bacterial invasion of seemingly intact teeth and the aim of this study was to determine if bacteria could invade the root canal system after a simulated traumatic episode. Twenty intact and sound upper central incisors were chosen and prepared. One tooth was selected as a sterility control and the external crown surface of the remaining 19 teeth was subjected to infection with Streptococcus gordonii in a bacterial microleakage model. Over 7 days samples of growth media from the root canal system were taken and tested for bacteria. Sixteen of the teeth did not demonstrate bacterial invasion over the time frame. These teeth were then prepared for testing in a pendulum impact device and were subjected to a blow which did not fracture the crowns or dislodge the tooth from its simulated alveolus. The teeth were then prepared and tested in the bacterial microleakage model. After impact seven of the teeth demonstrated bacterial invasion of the root canal system (P = 0.002). These teeth were then reprepared for testing in the bacterial microleakage model. The crowns of five teeth, selected at random, were coated with two layers of light cured unfilled resin, the remaining two were used as positive controls. All the teeth coated with resin did not demonstrate bacterial invasion (P = 0.00), while the positive controls demonstrated invasion. The results suggested that enamel/dentine infractions were pathways for bacterial invasion of the root canal system of traumatised teeth. The application of unfilled resin to the anatomical crown prevented infection.