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Six subjects wore lower-arch intra-oral appliances supporting plaque-covered enamel units in the left and right buccal sulci. Units on both sides received identical cariogenic challenges by intermittent immersion in 0.28 M glucose. When one side was treated, in addition, with a mouthrinse designed to enrich plaque with Ca, P, and F, there was a 76% reduction in the softening and a 96% reduction in the porosity, created in enamel by the glucose exposures. F dentifrice extract, used similarly, caused a 67% reduction in enamel softening and a 93% reduction in porosity. When the two treatments were compared in the same experiment, the mouthrinse had a significantly greater effect in limiting enamel softening, but the porosity measurement technique was not sensitive enough to confirm this finding. Use of the mouthrinse caused variable deposition of fluorhydroxyapatite in plaque, and scanning electron microscopy examination of enamel showed small adherent hard deposits in some subjects. The polished enamel surface enabled backscattered electron imaging which revealed preferential dissolution of the core and tail regions of the prism. The results suggest that plaque mineral enrichment may be even more effective than F dentifrice in preventing dental caries.

The surface morphology of human enamel treated with pulsed, infrared laser radiation was examined using reflected light and scanning electron microscopy. Thin (

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.

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 μm 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.

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.

Three topical fluoride agents deposited surface coatings of different morphology and thickness on intact human enamel surfaces. The agents studied were an acidic silane fluoride lacquer, a neutral NaF lacquer, and an APF gel. Each agent reacted with the enamel surface differently, producing its own distinctive etching pattern. The smallest particles observed in the surface coatings were from 20 to 30 nm in diameter and appeared to have indistinct morphologies. They often agglomerated into spherical globules ranging from 1-3 μ m in diameter.

The effect on structural defects of carbonate, zinc, strontium, fluoride and lead inclusions in synthetic apatites has been studied by high resolution transmission electron microscopy. Treatment of dental enamel by zinc and strontium solutions has been similarly investigated. Electron beam damage to crystal surfaces was always seen in unerupted enamel and short-term refluxed aqueous apatites, and occasionally in mature enamel, but was not observed in high temperature synthetic apatites or long-term refluxed aqueous apatites. Concentrated areas of calcium deficiency (15–40 A in diameter), probably related to screw dislocations, were observed in untreated normal dental enamel and all synthetic apatites except high temperature carbonate-free stoichiometric preparations. These deficient regions are related to carbonate inclusion and are important in the susceptibility or resistance of enamel crystals to acid attack during the dental caries process.

The mineral profiles of artificial caries-like lesions formed in intact human dental enamel and pretreated with pulsed, infrared laser radiation were determined using a longitudinal microhardness tech

The crystallographic structure of surface coatings produced by three topical fluoride agents deposited by a single application on intact human enamel surfaces was investigated by light- and dark-field transmission electron microscopy, as well as by electron and x-ray diffraction. The agents studied were an acidic silane fluoride lacquer, a neutral NaF lacquer, and an APF gel. The smallest coherently diffracting particles were CaF2 microcrystallites 4-15 nm in diameter. Large apatite-like crystals, approximately I μm in length, were also observed in the outer surface coating produced by the silane fluoride lacquer.

Three patients with a partial natural dentition in one jaw and a full denture in the other participated in this study. Enamel treated with APF gel, Duraphat or Fluor Protector and untreated controls were positioned in a full denture for periods up to 3 months. Plaque accumulation on the enamel blocks was evaluated by scanning electron microscopy. The results show that in all 3 patients studied the formation of CaF2 inhibited dental plaque accumulation.