The severity of dental fluorosis in children exposed to water with a high fluoride content for various periods of time.

Inhabitants of the Ikeno district of Japan were accidentally exposed to drinking water containing 7.8 ppm fluoride (F) for 12 years, after which water with 0.2 ppm F was substituted. Dental examinations of local inhabitants revealed that only children aged seven years or less at the introduction or aged 11 months or more at the removal of the high-F water had fluorosis. Regular inspections were made of the 86 children between those age limits. The severity of fluorosis in three tooth types (first permanent molars, upper central incisors, and first premolars) was assessed and related to the period of use of the high-F water. Continuous exposure throughout tooth development resulted in severe changes in all three tooth types. With limited exposure, the age at the beginning and at the end was an important factor in determining the severity of the fluorosis. The pattern of change from normal to severe fluorosis differed in the three tooth types, influenced by their respective times of formation. Two 'at-risk' periods for the production of moderate or severe fluorosis were evident. One started at birth and ended early in tooth development, while the other started later and ended at eruption. The duration of F exposure, although determining the initial degree of fluorosis, did not influence the rate of post-eruptive enamel loss.

The appearance of tooth enamel in children ingesting water with a high fluoride content for a limited period during early tooth development.

Sixteen Japanese children, inadvertently exposed to drinking water containing 7.8 ppm fluoride (F) from birth, were aged 11 to 42 months when a low-F water supply was substituted. The appearance of the enamel of their permanent teeth was assessed 11 years later (children aged 12-15 years) and recorded using Dean's and the FDI indices. All grades of Dean's classification were seen. The enamel lesions were more severe in the older than in the younger children, in the incisal compared with the gingival halves of the teeth, and in the early- compared with the late-forming teeth. Small, localized, chalky-white areas of enamel were found at or close to the incisal margins of the anterior teeth of six children. The characteristics and the distribution of the lesions in this study add to our knowledge of the mechanism by which fluoride produces dental fluorosis.

Differential diagnosis of dental fluorosis.

Differentiating between fluorotic and non-fluorotic defects of dental enamel is an important diagnostic decision in epidemiology and public health dentistry. The commonly accepted diagnostic criteria for fluorosis discriminate between non-discrete symmetrical and asymmetrical distributions of opacities of dental enamel. These criteria appear to identify most cases of dental fluorosis. However, it is not yet confirmed that the pattern and distribution of dental fluorosis are a unique phenomenon. Metabolic, physiological, other trace elements, and malnutrition have been reported to induce bilateral symmetrical developmental enamel opacities. Misdiagnosis of non-fluoride-induced opacities remains a possibility. Reports of unexpectedly high population prevalence and individual cases of fluorosis, where such diagnoses are incompatible with the known fluoride history, indicate the need for a more precise definition and diagnosis of dental fluorosis. A more discriminating diagnostic procedure is recommended. This calls for a positive identification of the levels of fluoride available to communities and individuals before a diagnosis of fluorosis is confirmed. We believe a more critical approach to the diagnosis of fluorosis will be helpful in the rational use and control of fluorides for dental health, and in the identification of factors associated with inducing developmental defects of enamel.

The pattern of mineralization of traumatically-induced developmental defects of sheep enamel assessed by microhardness and microradiography.

An earlier study showed that some of the variation in appearance of defects of enamel in sheep incisor teeth induced by trauma during tooth development was related to the phase of activity of the ameloblasts at the time of injury. In the present study, sixteen selected defects were examined by microhardness and microradiography. It was found that in some of the fully formed teeth, the defects had retained the pattern of mineralization present at the time of trauma, i.e., mineralization had ceased. In other teeth, further mineralization of the defects occurred after trauma, resulting in well-mineralized enamel, although sometimes of incomplete thickness. It was concluded that the trauma, depending on its severity, leads to either permanent or temporary dysfunction of the ameloblasts, which also influences the appearance of the resulting lesions.

Etiological factors influencing the prevalence of developmental defects of dental enamel in nine-year-old New Zealand children participating in a health and development study.

Over 1000 children, participating in a longitudinal study of health and development, possess documented medical histories based on birth records and regular assessments starting at age 3. A dental examination at age 5 of 923 participants recorded their exposure to fluoride and evidence of trauma to the deciduous teeth. The prevalence of developmental defects of dental enamel in 696 of the children when aged 9 was reported as 56% (Suckling et al., 1985). For the present study, a number of illnesses, accidents, and other experiences were selected from the recorded information as possible etiological factors for any defect, demarcated and diffuse opacities, and hypoplasia. Despite extensive statistical testing, positive and strong associations were few. The prevalence of hypoplasia, seen in 15% of the sample, was higher in those children who had chicken pox before age 3 and, as reported previously, in those children with a history of trauma to their deciduous incisors. This study illustrates the difficulty of establishing the etiology of enamel defects, even when medical and dental histories are available.

Histological, macroscopic and microhardness observations of fluoride-induced changes in the enamel organ and enamel of sheep incisor teeth.

When aged 8.5 months, 10 sheep born in the same week were given 4 mg fluoride (F)/kg body weight orally for 26 days. Three sheep received no F. Sheep were killed at the end of the treatment period and later at selected stages of tooth development. The macroscopic changes in the enamel of one incisor were related to the cellular changes in the enamel organ of the contralateral tooth. A break in enamel continuity, hypoplasia, was seen on the labial enamel of 9 of the 10 F-treated sheep. Pitting of the enamel was associated with shortening of some ameloblasts and aggregations of cysts affecting cells late in their secretory phase in the first-killed sheep. In sheep killed later, these changes were associated with cells which had progressed into their maturation phase. A more extensive absence of enamel with ledge formation cervically, seen in one sheep, was associated with displacement or death of almost all the cells in their secretory phase during F treatment and consequent retention of the organic matrix. The hypoplastic lesions resulted from secretory-cell reaction during the period of F dosing. Diffuse patchy opacities, characterized by an irregular hypomineralized surface zone, were only apparent in the enamel of the later-killed sheep and were associated in one sheep with abnormal ameloblast regression in the contralateral tooth. These defects possibly resulted from the long-continued release of F stored in the bones during the period of F dosing.

The macroscopic appearance and associated histological changes in the enamel organ of hypoplastic lesions of sheep incisor teeth resulting from induced parasitism.

Twenty-one penned female sheep were infected with a high dose of nematodes (200,000 Trichostrongylus vitrinus and 25,000 Ostertagia circumcincta) during first incisor development when aged 7-8 months. Three sheep were infected with 200,000 T. vitrinus only; 10 sheep were untreated. Anorexia, lassitude and severe diarrhoea were seen in 14 of the infected sheep after 21-26 days. Anthelmintic was given to sheep showing undue distress to end the infection and to all remaining sheep on day 33. Animals were killed at 3 stages: during the infection, at intervals during later tooth development, and at the time of eruption of the incisor teeth, 7-8 months after the parasites were given. Hypoplasia of the labial enamel of 15 out of 19 teeth from sheep killed after recovery from the infection was classified according to the extent and depth as pits, grooves or larger areas of missing enamel with ledge-formation cervically. The amount of missing enamel related to the severity of the systemic disturbance which affected the secretory ameloblasts. During the period of active infection, some secretory ameloblasts showed vacuolization or were shorter than in controls; some cells were no longer adjacent to the organic matrix; some continued to function but abnormally and later became separated from the retained organic matrix by connective tissue. Cervically-placed ledges resulted either from the recovery and resumption of activity of some ameloblasts or from differentiation of new secretory cells after the infection ended.

The production of developmental defects of enamel in the incisor teeth of penned sheep resulting from induced parasitism.

Thirty-four sheep were infected with nematode parasites (Trichostrongylus spp. and Ostertagia circumcincta) during central incisor formation. The tooth enamel was examined for defects of mineralization at eruption and compared with that of 14 control sheep. The type and number of parasites given, the duration of the infection and the age of the sheep were varied. Sheep receiving high doses of parasites e.g. 200,000 T. vitrinus + 20,000 O. circumcincta showed severe systemic effects (debilitation, scouring and weight loss) which were of short duration (7-10 days) as the infections were terminated by anthelmintic treatment. Hypoplastic enamel (a break in continuity) was induced in all 5 sheep infected at 8 1/4-9 months of age and demarcated opacities (an alteration in the translucency) in 3 out of 4 sheep infected at 10 months of age. Sheep given 150,000 or 40,000 T. colubriformis showed less obvious systemic effects although the weight loss continued in some sheep for up to 54 days. Although opacities of the enamel in the form of parallel lines, sometimes with localized increase in width or with a diffuse opacity superimposed, were seen by microscopic examination (X 10) of teeth in this group, many of the teeth from the control sheep showed similar lesions. Only the hypoplastic lesions can be attributed with confidence to the experimental manipulations.

The macroscopic and scanning electron-microscopic appearance and microhardness of the enamel, and the related histological changes in the enamel organ of erupting sheep incisors resulting from a prolonged low daily dose of fluoride.

The hypothesis that diffuse opacities in enamel result from a chronic, mild disturbance to ameloblast activities was tested using fluoride. Three sheep (HF) were dosed orally with 0.5, and 3 (LF) with 0.2 mg fluoride/kg body weight daily for 6 months. A control sheep (C) received no additional fluoride. The 7 sheep were killed at or close to the time of emergence of their permanent central incisors. One tooth from each sheep was sectioned longitudinally. The enamel related to the secretory (S) and maturation (M) phases of ameloblast activity at the start of fluoride dosing was determined from a tetracycline marker. The pattern of mineralization of the outer 150 micron of the cut labial enamel was assessed using microhardness testing. The SEM appearance of the acid-etched outer enamel was compared in S and M zones in 5 teeth. The enamel of the C tooth was translucent. Diffuse opacities, similar in appearance to human fluorosis, were present in all fluoride-treated teeth. Hardness values in the outer 70 micron of the enamel decreased as the fluoride dose increased and, in the HF teeth, were lower in the S zone than in the M zone. Fluoride given during the M phase induced a surface hypomineralization which increased in degree and depth when fluoride was also given during the S phase. The SEM appearance of M and S enamel was similar in 2 LF and 1 HF teeth but, in the other HF tooth, S enamel but not M enamel had a disordered prism structure and loosely-packed crystals in an abnormal organic matrix. Histological examination revealed that ameloblasts remained in only 4 of the 7 teeth and that their regression and the formation of the cementum adjacent only to the labial enamel were progressing abnormally.

Proton microprobe assessment of the distribution of fluoride in the enamel and dentine of developing central incisors of sheep and changes induced by daily fluoride supplements.

Ten sheep were given 0.5 mg fluoride (F) and 10 sheep 0.2 mg F/kg body wt orally for periods of 1-6 months while 8 sheep received no additional F. One incisor from each sheep was sectioned longitudinally in the midline and, using the proton microprobe, multiple scans for calcium and F were made across the enamel and dentine. F was determined by proton-induced gamma-ray emission and calcium by X-ray emission. Tooth length and hence the stage of ameloblast activity for each of the 28 teeth at the start of the experiment was determined using a tetracycline marker. In addition, the stage of enamel development of the eight control teeth (no dietary F) at the time of their extraction was assessed from their macroscopic appearance. Continuous changes in F levels occurred in both enamel and dentine throughout tooth development and also in the mature enamel and associated dentine after ameloblast regression. All scans for all stages of tooth development and all F treatments showed a high F concentration at the enamel surface. Early in the secretory phase, a wide-based F peak occupied the entire width of the enamel with a similar F peak in the dentine. In the control teeth, no consistent increase in F concentration occurred at the enamel surface during later development. When F supplements were started early in the maturation phase an increase in F concentration only at the enamel surface was recorded. When F supplements were also given during the secretory phase, higher F concentrations were recorded not only at the enamel surface but also for the inner enamel and dentine plateau. These findings, based on a small number of sheep, indicate that further research is needed to clarify the method and control of F uptake and to determine the changes in these processes during the different stages of tooth development.

Proton microprobe determination of fluorine profiles in the enamel and dentine of erupting incisors from sheep given low and high daily doses of fluoride.

Developmental defects in incisors were induced by daily oral ingestion of sodium fluoride solutions. Teeth extracted at eruption from sheep that had been subjected to four different fluoride regimens--0.2 or 0.5 mg F/kg body weight daily for 6 months, 2 or 6 mg F/kg body weight daily for 21 days--were analysed for fluorine by gamma emission using a proton microprobe. Calcium and zinc profiles were also measured using proton-induced X-ray emission. Diffuse opacities, similar in appearance to mild human fluorosis, were produced by the first two regimens, whereas the last two produced hypoplastic lesions. Different distributions of fluoride were found in the unerupted enamel and dentine, and these patterns reflected variations in both the duration and concentration of the fluoride dose used to induce the fluorotic lesions.

Developmental defects of enamel in a group of New Zealand children: their prevalence and some associated etiological factors.

The prevalence of developmental defects of enamel was assessed in 243 children aged 12-14 yr using the FDI Index. The teeth were not cleaned or dried prior to examination for which fibre optic lighting was used. At least one tooth with defective enamel was seen in 63% of children with a demarcated white opacity present in 44% of children. The enamel was abnormal in 11.7% of teeth, diffuse patchy opacities and demarcated white opacities occurring in 4.4 and 4.2%, respectively. Although defects were found most frequently in the maxillary central incisors, the ranking order of prevalence and the distribution for demarcated and diffuse opacities was quite different. Sex, residence, and the common childhood illnesses did not alter the prevalence of defects which was, however, increased significantly in 22 children with a history of a serious illness or accident (0.01 greater than P greater than 0.001). The prevalence of the diffuse opacities was significantly increased with increased exposure to fluoride either in tablets or in the drinking water (0.01 greater than P greater than 0.001).

Stability of fluoride levels in surface layer of normal enamel during a 21-month fluoride mouthrinsing program.

A 21-month trial of the caries-preventive effect of a 0.2% NaF mouthrinse included monitoring changes in the concentration of F in normal enamel. Subsamples of 25 children were randomly selected from groups receiving either normal dental treatment (Control group); additional fortnightly professional prophylaxes (Test group); or prophylaxes plus fortnightly 2-min fluoride rinses (Test + F group). At the start of the trial the sound labial surface of tooth 24 (occasionally 23 or 22) was etched with 2 N HCL and the etchant analysed for F, Ca and phosphate. The contralateral tooth was sampled at the end of the trial. The caries increments (DFS) for the three groups over 21 months were Control, 2.88; Test, 2.51 and Test + F, 1.77, the last being significantly less than the others (P less than 0.05). The average sound enamel surface F concentrations were similar for the three groups at the start and the end of the trial. F parameter calculations showed that all differences were non-significant. Thus this factor could not explain the reduced caries increment due to F mouthrinsing. F biopsies for the purpose of predicting likely clinical effectiveness of neutral 0.2% NaF mouthrinsing will find little application in public health dentistry.

The assessment of non-carious defects of enamel.

Developmental defects of dental enamel are very common with at least one in every three individuals having one or more teeth with obvious non-carious defect. The more common defects are opaque areas, hypoplasias (missing enamel) and discoloured enamel; the variety in form, severity and combination of defects is extensive. The lesions are sequelae of systemic, traumatic or genetic events during tooth development. A review of past and current terminologies, and classifications of developmental defects of enamel, reveals ambiguities, deficiencies and lack of uniformity in methods and criteria used in their study. The principal objective for collecting and recording observations on enamel defects is to determine their frequency, severity and distribution for the purpose of assessing the magnitude of the clinical problem they generate and their aetiology. Hence, an internationally recognized classification of developmental enamel defects and recording procedure would increase the value and comparability of future studies. An acceptable uniform terminology and a simple procedure for classifying the more commonly observed defects, defined by their visual characteristics, would achieve these aims. A classification is proposed which identifies and defines the type, number and location of developmental defects affecting tooth enamel on the buccal and lingual surfaces of all teeth. The procedure has been designed for easy interpretation and simple evaluation. It may be modified for use with much less extensive clinical examination.

Fluoride uptake into the developing enamel and dentine of sheep incisors following daily ingestion of fluoridated milk or water.

Incomplete availability of fluoride from fluoride compounds when added to milk is claimed to reduce the effectiveness of fluoridated milk in caries prevention in humans. This study attempts to add to the understanding of the systemic bioavailability of fluoride ingested with milk compared with water, by measuring its uptake into developing incisors of sheep. Twenty-five sheep, aged approximately 10 months, were randomised into five groups and farmed under identical conditions. They were dosed orally each day for 22 weeks with fluoride as sodium fluoride in water or bovine milk. The doses of fluoride were 0.5 or 0.2 mg/kg body weight in milk or water; a control group received no additional fluoride. Tooth length was labelled at the start of dosing with intramuscular injection of tetracycline. After sacrificing, incisors were removed, sectioned, and analysed for fluoride and calcium by proton microprobe scans from the enamel surface to the pulp. Concentrations of ionised fluoride in the milk samples were 30 percent and 20 percent respectively for added fluoride at concentrations of 300 and 750 micrograms/ml. The mean fluoride concentrations in surface enamel, deep enamel, and dentine were dependent on the daily fluoride dose and independent of the carrier (milk or water). The teeth of sheep receiving the higher fluoride dose (0.5 mg/kg body weight) had significantly higher fluoride than those receiving the lower fluoride dose (0.2 mg/kg body weight), which were significantly higher than in the teeth of the control sheep. It was concluded that the bioavailability of fluoride from sodium fluoride mixed with milk or water was similar following metabolism, despite 20-30 percent and 100 percent ionisation in milk and water respectively.