Fejerskov O, Larsen M J, Richards A, Baelum V
Department of Oral Anatomy, Dental Pathology and Operative Dentistry, Royal Dental College, Faculty of Health Sciences, University of Aarhus, Denmark.
Adv Dent Res. 1994 Jun;8(1):15-31. doi: 10.1177/08959374940080010601.
It is now well-established that a linear relationship exists between fluoride dose and enamel fluorosis in human populations. With increasing severity, the subsurface enamel all along the tooth becomes increasingly porous (hypomineralized), and the lesion extends toward the inner enamel. In dentin, hypomineralization results in an enhancement of the incremental lines. After eruption, the more severe forms are subject to extensive mechanical breakdown of the surface. The continuum of fluoride-induced changes can best be classified by the TF index, which reflects, on an ordinal scale, the histopathological features and increases in enamel fluoride concentrations. Human and animal studies have shown that it is possible to develop dental fluorosis by exposure during enamel maturation alone. It is less apparent whether an effect of fluoride on the stage of enamel matrix secretion, alone, is able to produce changes in enamel similar to those described as dental fluorosis in man. The clinical concept of post-eruptive maturation of erupting sound human enamel, resulting in fluoride uptake, most likely reflects subclinical caries. Incorporation of fluoride into enamel is principally possible only as a result of concomitant enamel dissolution (caries lesion development). At higher fluoride concentrations, calcium-fluoride-like material may form, although the formation, identification, and dissolution of this compound are far from resolved. It is concluded that dental fluorosis is a sensitive way of recording past fluoride exposure because, so far, no other agent or condition in man is known to create changes within the dentition similar to those induced by fluoride. Since the predominant cariostatic effect of fluoride is not due to its uptake by the enamel during tooth development, it is possible to obtain extensive caries reductions without a concomitant risk of dental fluorosis.
现在已经充分证实,在人群中氟化物剂量与牙釉质氟斑牙之间存在线性关系。随着严重程度的增加,牙齿整个表面下的牙釉质孔隙越来越多(矿化不足),病变向牙釉质内部扩展。在牙本质中,矿化不足会导致生长线增强。牙齿萌出后,较严重的形式会使表面受到广泛的机械破坏。氟化物引起的变化连续体最好用TF指数分类,该指数按顺序反映组织病理学特征和牙釉质氟浓度的增加。人类和动物研究表明,仅在牙釉质成熟期间接触氟化物就有可能发生氟斑牙。单独氟化物对牙釉质基质分泌阶段的影响是否能够产生与人类氟斑牙中描述的类似牙釉质变化,尚不明显。萌出健康人类牙釉质萌出后成熟的临床概念,导致氟摄取,很可能反映了亚临床龋齿。氟化物主要仅在牙釉质同时溶解(龋齿病变发展)的情况下才可能掺入牙釉质中。在较高的氟浓度下,可能会形成类似氟化钙的物质,尽管这种化合物的形成、鉴定和溶解远未解决。得出的结论是,氟斑牙是记录过去氟暴露的一种敏感方式,因为到目前为止,已知人类中没有其他因素或状况会在牙列中产生与氟化物引起的变化类似的变化。由于氟化物的主要防龋作用不是由于其在牙齿发育过程中被牙釉质摄取,因此有可能在不伴随氟斑牙风险的情况下大幅降低龋齿发病率。