氟化钠对大鼠门牙成牙细胞和牙本质超微结构的影响。

Shika gakuho. Dental science reports Pub Date : 1989-01-01
S Araki
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引用次数: 0

摘要

对体重100 g的年轻雄性Wistar大鼠皮下注射8.4 mg氟化钠。1、3、6、12、24 h及2、4 d后灌注固定大鼠;对上切牙进行光学显微镜、显微放射照相和电子显微镜检查。在某些情况下,为了观察酸-粘多糖的分布,在固定液或脱矿液中加入0.1%的钌红(RR)。1. 在成牙细胞中观察到以下变化:粗内质网肿胀,液泡形成,自噬液泡和高尔基液泡数量增加,细胞体-4异常积聚。所有这些变化在给药后24小时内趋于恢复。2. 在给药后1小时,非晶态物质的数量异常增加,并持续到给药后12小时。此后,增长逐渐放缓;对照组观察到的水平在给药后第四天恢复。RR染色显示该无定形物质含有大量酸性粘多糖。3.在前段提到的无定形物质中观察到两种类型的异常胶原蛋白——节段性胶原聚集体(SCA)和纤维性长间距胶原蛋白(FLS)。在纵截面上,SCAs长320 nm,宽200 nm;在它们内部可以看到对称排列的条纹。fls为长而粗的原纤维,具有约160 nm的周期性条纹。随着时间的推移,这些异常的胶原聚集体和原纤维从成牙本质的远端转移到牙本质,并嵌入其中。4. 异常胶原蛋白的矿化开始于针状或薄板状晶体的沉积。随着时间的推移,胶原蛋白被晶体完全覆盖。胶原蛋白分子结合的松动似乎是随着矿化和晶体生长的进展而发生的。5. 牙本质矿化异常,形成了高矿化层和高矿化层下的低矿化层。超矿化层含有密集分布的晶体。与低矿化界线清晰可见。然而,与规则牙本质的边界却在移动,模糊不清。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Ultrastructural changes in rat-incisor odontoblasts and dentin caused by administration of sodium fluoride].

Subcutaneous injections of 8.4 mg of sodium fluoride were administered to young male Wistar rats weighing 100 g each. After 1, 3, 6, 12, and 24 hours and then after 2 and 4 days, the rats were fixed by perfusion; and their upper incisors were subjected to optical microscopy, microradiography, and electron microscopy. In some instances, 0.1% ruthenium red (RR) was added to the fixing or demineralizing solution for the sake of observing acid-mucopolysaccharide distribution. 1. The following changes were observed in odontoblasts: swelling of the rough endoplasmic reticulum, vacuole formation, increased numbers of autophagic vacuoles and Golgi vacuoles, and abnormal accumulation of cytosome-4. All of these changes tended to have recovered by 24 hours after administration. 2. In the predentin, abnormal increases in amounts of amorphous substance occurred 1 hour after and continued until 12 hours after administration. Thereafter, increases gradually retarded; and the level observed in controls was restored by the fourth day after administration. RR staining showed this amorphous substance to contain large amounts of acid mucopolysaccharides. 3. Two types of abnormal collagen--segmental collagen aggregate (SCA) and fibrous long-spacing collagen (FLS)--were observed in the amorphous substance mentioned in the preceding paragraphy. In longitudinal sections, SCAs were 320 nm long and 200 nm wide; symmetrically arranged striations were visible within them. FLSs were observed as long, thick fibrils with periodic striations of about 160 nm. With the passing of time, these abnormal collagen aggregates and fibrils shifted from the distal end of the odontoblast toward the dentin, in which they became embedded. 4. Mineralization in the abnormal collagen commenced with deposition of needle-shaped or thin platelike crystals. As time passed, the collagen came to be completely covered with the crystals. Loosening of collagen molecular binding seems to occur following advances in mineralization and crystal growth. 5. Abnormality in dentin mineralization resulted in the formation of a hypermineralized layer and a hypomineralized layer beneath the hypermineralized layer. The hypermineralized layer contained densely distributed crystals. Its boundary with the hypomineralized was clearly observable. The boundary with teh regular dentin, however, was shifting and indistinct.

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