Richards A, Kragstrup J, Josephsen K, Fejerskov O
J Dent Res. 1986 Dec;65(12):1406-9. doi: 10.1177/00220345860650120501.
The aim of this study was to test whether dental fluorosis can be produced by administration of chronic doses of fluoride during only the post-secretory stage of enamel mineralization. Eight control and eight experimental pigs matched by weight and litter were fed a low-fluoride diet (less than 0.05 mg F-/kg b.w. daily) from weaning to slaughter at 14 months. The test group received an oral dose of 2 mg F-/kg b.w. per day from 8 months of age. Lower fourth pre-molars were at the post-secretory stage at the start of fluoride administration (confirmed by tetracycline marker) and were just erupting at slaughter. All of the fourth pre-molar teeth from the test group developed diffuse enamel hypomineralization indistinguishable from human fluorosis. No such lesions were seen in any of the teeth from the control animals. It was concluded that enamel fluorosis may be caused by fluoride exposure in the maturation phase only. The pathogenic mechanism may be an effect either on the selective loss of protein or on the influx of mineral, both of which occur during the post-secretory or maturation stage of enamel formation.
本研究的目的是测试仅在釉质矿化的分泌后阶段给予慢性剂量的氟化物是否会导致氟斑牙。将八只对照猪和八只按体重和窝别匹配的实验猪从断奶到14个月屠宰期间喂食低氟饮食(每日低于0.05 mg F⁻/kg体重)。测试组从8月龄开始每天口服2 mg F⁻/kg体重。在开始给予氟化物时(通过四环素标记确认),下颌第四前磨牙处于分泌后阶段,在屠宰时刚萌出。测试组所有的第四前磨牙均出现了与人类氟斑牙难以区分的弥漫性釉质矿化不全。对照动物的任何牙齿均未观察到此类病变。得出的结论是,釉质氟斑牙可能仅由成熟阶段的氟暴露引起。致病机制可能是对蛋白质选择性丢失或矿物质流入的影响,这两者均发生在釉质形成的分泌后或成熟阶段。