Chronic fluoride toxicity: dental fluorosis.

Chronic fluoride toxicity: dental fluorosis.
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DOI:
10.1159/000327028
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发表时间:
2011
影响因子:
--
通讯作者:
Li W
Li W
中科院分区:
其他
文献类型:
--
作者:
DenBesten P;Li W

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氟斑牙是牙齿形成过程中摄入过量氟化物的结果。牙釉质氟中毒和原发性牙本质氟中毒只能在牙齿形成时发生,因此氟暴露(因为它与氟斑牙有关)发生在儿童时期。在恒牙列中,这将从下切牙开始开始,下切牙在大约2-3岁时完成矿化,并在第三磨牙矿化后结束。氟斑牙釉质的白色不透明外观是由釉质次表面矿化不足引起的;更严重的氟斑牙,会发生点蚀和釉质表面损失,导致继发性染色(表现为棕色)。氟化物引起的许多变化与牙齿形成时的细胞/基质/矿物质相互作用有关。在早期成熟阶段,氟牙釉质中釉原蛋白的相对量以剂量相关的方式增加。这似乎是由于釉质成熟时釉原蛋白的去除延迟所致。在体外,当氟化物被掺入矿物质中时,更多的蛋白质与形成的矿物质结合,蛋白酶去除蛋白质的时间被延迟。这表明改变的蛋白质/矿物质相互作用是部分负责釉原蛋白的保留和由此产生的低矿化,发生在氟牙釉质。氟化物似乎也会增强牙齿形成过程中的矿物质沉淀,导致釉质的高矿化带,然后是低矿化带。增强矿物沉淀与局部增加基质酸度可能会影响成熟阶段的成釉细胞调制,可能解释剂量相关的减少周期的成釉细胞调制从ruffleended平滑结束的细胞,发生在啮齿动物氟暴露。氟化物的特定细胞效应已经被牵连,但需要更多的研究来确定这些变化中的哪些与氟牙的形成有关。随着进一步的研究,我们将更好地了解氟斑牙的机制。
Dental fluorosis occurs as a result of excess fluoride ingestion during tooth formation. Enamel fluorosis and primary dentin fluorosis can only occur when teeth are forming, and therefore fluoride exposure (as it relates to dental fluorosis) occurs during childhood. In the permanent dentition, this would begin with the lower incisors, which complete mineralization at approximately 2–3 years of age, and end after mineralization of the third molars. The white opaque appearance of fluorosed enamel is caused by a hypomineralized enamel subsurface; with more severe dental fluorosis, pitting and a loss of the enamel surface occurs, leading to secondary staining (appearing as a brown color). Many of the changes caused by fluoride are related to cell/matrix/mineral interactions as the teeth are forming. At the early maturation stage, the relative quantity of amelogenin protein is increased in fluorosed enamel in a dose-related manner. This appears to result from a delay in the removal of amelogenins as the enamel matures. In vitro, when fluoride is incorporated into the mineral, more protein binds to the forming mineral, and protein removal by proteinases is delayed. This suggests that altered protein/mineral interactions are in part responsible for retention of amelogenins and the resultant hypomineralization that occurs in fluorosed enamel. Fluoride also appears to enhance mineral precipitation in forming teeth, resulting in hypermineralized bands of enamel, which are then followed by hypomineralized bands. Enhanced mineral precipitation with local increases in matrix acidity may affect maturation stage ameloblast modulation, potentially explaining the doserelated decrease in cycles of ameloblast modulation from ruffleended to smooth-ended cells that occur with fluoride exposure in rodents. Specific cellular effects of fluoride have been implicated, but more research is needed to determine which of these changes are relevant to the formation of fluorosed teeth. As further studies are done, we will better understand the mechanisms responsible for dental fluorosis.
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发表时间: 1975-01-01
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影响因子: 4.2
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DOI: 10.1016/s0003-9969(02)00117-6
发表时间: 2002-11-01
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