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蔗糖在菌斑形成中的作用。

Role of sucrose in plaque formation.

作者信息

Rölla G, Scheie A A, Ciardi J E

出版信息

Scand J Dent Res. 1985 Apr;93(2):105-11. doi: 10.1111/j.1600-0722.1985.tb01317.x.

DOI:10.1111/j.1600-0722.1985.tb01317.x
PMID:3159073
Abstract

Results are presented which support the concept that the bacterial enzyme glucosyltransferase (GTF) plays a crucial role in sucrose induced plaque formation. GTF was shown to adhere strongly to anionic, hydrophobic and polysaccharide solid materials, and to be able to produce glucans in the adsorbed state. It appears conceivable that GTF adsorb to teeth and produce glucans. Glucan chains on the surface of the bacteria and glucans on the tooth surfaces interact (pack) and form a strong binding mechanism. The rigid alpha 1,3 linked glucans produced by Streptococcus mutans are particularly suited for interaction of this kind. This mechanism could account for sucrose-induced binding of bacteria to enamel, pellicle covered enamel and preformed plaque. S. mutans would adhere particularly strongly to tooth surfaces in the presence of sucrose, according to this model.

摘要

研究结果表明,细菌酶葡糖基转移酶(GTF)在蔗糖诱导的牙菌斑形成中起关键作用这一概念得到了支持。研究表明,GTF能强烈粘附于阴离子、疏水和多糖固体材料,并能在吸附状态下产生葡聚糖。GTF吸附到牙齿上并产生葡聚糖似乎是可以想象的。细菌表面的葡聚糖链与牙齿表面的葡聚糖相互作用(堆积)并形成强大的结合机制。变形链球菌产生的刚性α-1,3连接葡聚糖特别适合这种相互作用。这种机制可以解释蔗糖诱导的细菌与牙釉质、覆盖有薄膜的牙釉质和预先形成的牙菌斑的结合。根据这个模型,在蔗糖存在的情况下,变形链球菌会特别强烈地粘附在牙齿表面。

相似文献

1
Role of sucrose in plaque formation.蔗糖在菌斑形成中的作用。
Scand J Dent Res. 1985 Apr;93(2):105-11. doi: 10.1111/j.1600-0722.1985.tb01317.x.
2
Why is sucrose so cariogenic? The role of glucosyltransferase and polysaccharides.为什么蔗糖如此容易致龋?葡糖基转移酶和多糖的作用。
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Kinetic properties of glucosyltransferase adsorbed onto saliva-coated hydroxyapatite.吸附在唾液包被的羟基磷灰石上的葡糖基转移酶的动力学特性。
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[Glucosyltransferase (GTF) and immunization against dental caries in humans].
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10
Glucans synthesized in situ in experimental salivary pellicle function as specific binding sites for Streptococcus mutans.在实验性唾液薄膜中原位合成的葡聚糖可作为变形链球菌的特异性结合位点。
Infect Immun. 1992 Jan;60(1):284-95. doi: 10.1128/iai.60.1.284-295.1992.

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