Based on studies in Northern Tanzania a new classification system of dental fluorosis is proposed. The classification system includes 10 scores designed to characterize the degree of dental fluorosis affecting buccal/lingual and occlusal surfaces. With aid of polarized and ordinary light microscopy the histologic features behind the individual scores are described. The macroscopic appearance of increasing degrees of dental fluorosis were well correlated to the degree of subsurface porosity. Above a certain level of subsurface hypomineralization various degrees of loss of surface enamel occurred, presumably as a result of posteruptively acquired injuries. Application of the new classification system to samples of children born in areas with 3.5, 6.0 and 21.0 parts/106 F‐ in the water supplies revealed that the distribution of dental fluorosis within the individual followed the same pattern irrespective of fluoride concentration in the water. While the classical Dean index was unable to distinguish between dental fluorosis in the 6.0 and the 21.0 parts/106 area it was possible with the new system to disclose that particularly the posterior teeth were significantly more affected in the latter area. Comparisons of degree of dental fluorosis with available measurements of enamel thickness proved that the within‐tooth as well as within‐dentition variations are determined by enamel thickness rather than length of exposure to body fluids. The limitations of the Dean index are discussed with special attention to its validity as a biological index in relation to current efforts to determine the minimal toxic effect of fluoride on the dental hard tissues.

Kuhn proposed in his Structure of Scientific Revolutions (1962) that the theoretical framework of a science (paradigm) determines how each generation of researchers construes a causal sequence. Paradigm change is infrequent and revolutionary; thereafter previous knowledge and ideas become partially redundant. This paper discusses two paradigms central to cariology. The first concerns the most successful caries-preventive agent: fluoride. When it was thought that fluoride had to be present during tooth mineralisation to ‘improve’ the biological apatite and the ‘caries resistance’ of the teeth, systemic fluoride administration was necessary for maximum benefit. Caries reduction therefore had to be balanced against increasing dental fluorosis. The ‘caries resistance’ concept was shown to be erroneous 25 years ago, but the new paradigm is not yet fully adopted in public health dentistry, so we still await real breakthroughs in more effective use of fluorides for caries prevention. The second paradigm is that caries is a transmittable, infectious disease: even one caused by specific microorganisms. This paradigm would require caries prevention by vaccination, but there is evidence that caries is not a classical infectious disease. Rather it results from an ecological shift in the tooth-surface biofilm, leading to a mineral imbalance between plaque fluid and tooth and hence net loss of tooth mineral. Therefore, caries belongs to common ‘complex’ or ‘multifactorial’ diseases, such as cancer, cardiovascular diseases, diabetes, in which many genetic, environmental and behavioural risk factors interact. The paper emphasises how these paradigm changes raise new research questions which need to be addressed to make caries prevention and treatment more cost-effective.

Substantial pH fluctuations within the biofilm on the tooth surface are a ubiquitous and natural phenomenon, taking place at any time during the day and night. The result may be recordable in the dental tissues at only a chemical and/or ultrastructural level (subclinical level). Alternatively, a net loss of mineral leading to dissolution of dental hard tissues may result in a caries lesion that can be seen clinically. Thus, the appearance of the lesion may vary from an initial loss of mineral, seen only in the very surface layers at the ultrastructural level, to total tooth destruction. Regular removal of the biofilm, preferably with a toothpaste containing fluoride, delays or even arrests lesion progression. This can occur at any stage of lesion progression, because it is the biofilm at the tooth or cavity surface that drives the caries process. Active enamel lesions involve surface erosion and subsurface porosity. Inactive or arrested lesions have an abraded surface, but subsurface mineral loss remains, and a true subsurface remineralization is rarely achievable, because the surface zone acts as a diffusion barrier. The dentin reacts to the stimulus in the biofilm by tubular sclerosis and reactionary dentin.

ABSTRACT:This review aims at discussing the pathogenesis of enamel fluorosis in relation to a putative linkage among ameloblastic activities, secreted enamel matrix proteins and multiple proteases, growing enamel crystals, and fluid composition, including calcium and fluoride ions. Fluoride is the most important caries-preventive agent in dentistry. In the last two decades, increasing fluoride exposure in various forms and vehicles is most likely the explanation for an increase in the prevalence of mild-to-moderate forms of dental fluorosis in many communities, not the least in those in which controlled water fluoridation has been established. The effects of fluoride on enamel formation causing dental fluorosis in man are cumulative, rather than requiring a specific threshold dose, depending on the total fluoride intake from all sources and the duration of fluoride exposure. Enamel mineralization is highly sensitive to free fluoride ions, which uniquely promote the hydrolysis of acidic precursors such as octacalcium phosphate and precipitation of fluoridated apatite crystals. Once fluoride is incorporated into enamel crystals, the ion likely affects the subsequent mineralization process by reducing the solubility of the mineral and thereby modulating the ionic composition in the fluid surrounding the mineral. In the light of evidence obtained in human and animal studies, it is now most likely that enamel hypomineralization in fluorotic teeth is due predominantly to the aberrant effects of excess fluoride on the rates at which matrix proteins break down and/or the rates at which the by-products from this degradation are withdrawn from the maturing enamel. Any interference with enamel matrix removal could yield retarding effects on the accompanying crystal growth through the maturation stages, resulting in different magnitudes of enamel porosity at the time of tooth eruption. Currently, there is no direct proof that fluoride at micromolar levels affects proliferation and differentiation of enamel organ cells. Fluoride does not seem to affect the production and secretion of enamel matrix proteins and proteases within the dose range causing dental fluorosis in man. Most likely, the fluoride uptake interferes, indirectly, with the protease activities by decreasing free Ca 2+ concentration in the mineralizing milieu. The Ca 2+ -mediated regulation of protease activities is consistent with the in situobservations that (a) enzymatic cleavages of the amelogenins take place only at slow rates through the secretory phase with the limited calcium transport and that, (b) under normal amelogenesis, the amelogenin degradation appears to be accelerated during the transitional and early maturation stages with the increased calcium transport. 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 reduction without a concomitant risk of dental fluorosis. Further efforts and research are needed to settle the currently uncertain ...

The way in which we conceptually consider dental caries determines our choice of preventive and treatment strategy. In this paper the definition of dental caries is discussed and the related problems concerning causality are addressed. Dental caries reflects symptoms of ongoing and past disease--not the disease itself. As such, it is important to record early stages of signs of the disease, i.e. non-cavitated stages of lesion development. The dynamic nature of the processes leading to net loss of mineral (hence a lesion) is emphasized, and appreciating that caries is ubiquitous in populations around the world and initiation and progression of lesions continues lifelong leads to the logical conclusion that we can control dental caries through a variety of measures--but not truly prevent the disease. We can prevent cavities by controlling the patho-physiological events which may result in a net loss of mineral. The relative role of dental plaque in caries control is discussed in relation to the role of the many determinants which influence the likelihood for lesion development. It is concluded that several paradigms about the nature of dental caries should be reconsidered to provide the most cost-effective dental services.

This study has shown that the exposure of human dental enamel to acid solutions in vitro produces three basic etching patterns. In the most common, called type 1 etching pattern, prism core material was preferentially removed leaving the prism peripheres relatively intact. In the second, type 2 etching pattern, the reverse pattern was observed. The peripheral regions of prisms were removed preferentially, leaving prism cores remaining relatively unaffected. In the type 3 etching pattern, there was a more random pattern, areas of which corresponded to types 1 and 2 damage together with regions in which the pattern of etching could not be related to prism morphology. These findings differ from previous studies in which the type 1 pattern was ascribed to acid action and type 2 etching pattern to attack by chelators. The results therefore suggest that there is no one specific etching pattern produced in human dental enamel by the action of acid solutions. Such differences produced by acids are difficult to explain on the basis of variation in chemical composition, and crystallite orientation. This further highlights the variation in structure that can occur in enamel not only from tooth to tooth, or surface to surface, but also from site to site on a single tooth surface.

This study comprised 1131 persons who constitute a stratified random sample of the entire population aged 15-65 years in Machakos District, Kenya. Each person was examined for tooth mobility, plaque, calculus, gingival bleeding, loss of attachment and pocket depth on the mesial, buccal, distal and lingual surface of each tooth. The oral hygiene was poor with plaque on 75-95% and calculus on 10-85% of the surfaces depending on age. Irrespective of age, pockets greater than or equal to 4 mm was seen on less than 20% of the surfaces, whereas 10-85% of the surfaces had loss of attachment greater than or equal to 1 mm. The proportion of surfaces per individual with loss of attachment greater than or equal to 4 mm or greater than or equal to 7 mm, and pocket depths greater than or equal to 4 mm or greater than or equal to 7 mm, respectively, showed a pronounced skewed distribution, indicating that in each age group, a subfraction of individuals is responsible for a substantial proportion of the total periodontal breakdown. The individual teeth within the dentition also showed a marked variation in the severity of periodontal breakdown. Our findings provide additional evidence that destructive periodontal disease should not be perceived as an inevitable consequence of gingivitis which ultimately leads to considerable tooth loss. A more specific characterization of the features of periodontal breakdown in those individuals who seem particularly susceptible is therefore warranted.

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.