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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.

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.

Developmental defects of enamel are visible deviations from the normal translucent appearance of tooth enamel resulting from enamel organ dysfunction. In the past, information about the activities of the ameloblasts has determined the terminology used to describe the lesions. Advances in our understanding of the complicated secretory and maturation phases of amelogenesis have required a re-appraisal of the concepts of defect formation. The phase of ameloblast activity, the duration of the disturbance, and its severity leading to temporary or permanent inactivity of the cells determine the appearance of the three common types of lesions--hypoplasia, and diffuse and demarcated opacities.

Upper incisor teeth from sheep infected with parasites or given 6 mg fluoride per kg bodyweight for 21 days during the period of tooth formation were examined with SEM and microradiography. It was found using both techniques that there had been a severe disturbance of the secretory ameloblasts leading to enamel hypoplasia. It is suggested that it is the severity rather than the cause of the insult to the ameloblasts which determines the degree of hypoplasia.

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.

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.

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).

Defects present in 12 human permanent teeth were classified on the basis of their macroscopic appearance as hypoplasia (three teeth), diffuse opacities (three teeth), white demarcated opacities (one tooth but two defects), or yellow demarcated opacities (five teeth but six defects). The hardness values and SEM appearance of the defective enamel were determined after the teeth were sectioned through the lesion(s) and were distinctive for each type of defect. The thin enamel of the hypoplastic lesions was either opaque (with reduced hardness values) or translucent (with near-normal hardness values and sometimes a change in prism orientation external to an incremental line). The enamel of the diffuse and demarcated opacities was of normal thickness. The changes in the macroscopic and SEM appearance, and the reduced hardness values of the diffuse patchy opacities, were restricted to the outer 150 microns of the enamel. The demarcated opacities varied in position and depth, and in places had a clearly marked boundary with the adjacent normal enamel. Hardness values were related to color change, with yellow lesions being softer than white. Although prism direction was normal within demarcated opacities, prism outlines were less distinct. The findings suggest that temporary and permanent dysfunction of ameloblasts can occur in both secretory and maturation phases, influencing the final appearance of the lesion.

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.

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.