Using ApoE Genotyping to Promote Healthy Lifestyles in Finland - Psychological Impacts: Randomized Controlled Trial.

Common health recommendations often incite very little public response, as people instead require individualized information. The purpose of this study was to assess the psychological effects of personal genetic information, provided by different apoE genotypes, as a tool to promote lifestyle changes. This study was a one-year intervention study using healthy adults, aged 20-67 years (n = 107). Their experiences of state anxiety, threat and stage of change were measured three times over a 12 months period. These psychological experiences were assessed, during the genetic information gathering, for three groups: a high-risk group (Ɛ4+, n = 16); a low-risk group (Ɛ4-, n = 35); and a control group (n = 56). The psychological effects of personal genetic risk information were shown to be short-term, although the levels of state anxiety and threat experiences in the high-risk group both remained at a slightly higher level than in the baseline. Threat experiences differed almost significantly (alpha = 0.017) between the Ɛ4+ and Ɛ4- groups (p = 0.034). Information on the apoE genotype impacted the experience of cardiovascular threat; this effect was most intense immediately after genetic feedback was received. However, fears of threat and anxiety may not be an obstacle for using gene information to motivate healthy, stable adults towards making lifestyle changes. Further studies should thus focus on how to utilize genetic screening in prevention of lifestyle-related diseases.

Post-treatment effect of fluoride varnishes in children with a high prevalence of dental caries in a community with fluoridated water.

Children with a high prevalence of dental caries living in a community with fluoridated water had received semi-annual half-mouth applications of one of two fluoride varnishes for three years. Two years after the applications were discontinued, we studied the post-treatment effect of the varnishes. The absolute reduction in caries found during the treatment was retained, but the cariostatic effect did not continue after treatment. This finding suggests that fluoride varnish applications should not be discontinued after three years.

Caries prevention in rats by fluoride varnish treatment combined with addition of fluoride to dietary sugar.

Osborne-Mendel rats were fed a cariogenic diet containing 43% sucrose for 48 days. The control group received no additional treatment. The teeth of the second group received topical treatment with a sodium fluoride varnish which was applied twice onto newly-erupted molars. The third group received topical treatment with the sodium fluoride varnish combined with a NaF + Mg addition to the diet. In both treatment groups, caries was significantly reduced as compared with caries in the control group. Combined treatment was significantly more effective than was the varnish alone. In spite of the high fluoride concentration in the varnish, no changes in the oral mucosa were found at the end of the study.

Effect of chlorhexidine-fluoride applications without and with Sr and Zn on caries, plaque, and gingiva in rats.

Molar teeth of four groups of Osborne-Mendel rats, kept on a cariogenic diet, were treated once per day for 48 days with either distilled water (solution C), a solution containing 0.05% chlorhexidine gluconate and 0.04% NaF, pH 5.8 (solution CXF), CXF plus 1000 ppm Sr (solution CXFS), or CXFS plus 1000 ppm Zn (solution CXFSZ). Caries of the hemi-sectioned lower molars was scored according to grades of severity, and the extent of the buccal plaque was estimated. Inflammatory cell infiltration, vascularity, and thickness of the oral mucosa were estimated from stained sections of the buccal oral mucosa to detect possible adverse effects of the treatments. Fissure caries lesions with involvement of the dentin were reduced by 57% (p less than 0.01) with the CXF treatment and by 68% (p less than 0.001) with the CXFS treatment. The CXFSZ treatment reduced the fissure caries least (44%, p less than 0.05), but it appreciably reduced the extent of plaque. The mucosal changes were greatest in the group receiving the CXFSZ treatment, but they were generally small and at a non-pathological level. Supplementation of the CXF solution with Sr thus appeared beneficial for caries reduction.

Differences in PH fall, phosphorus content and dissolution of enamel in layers of the oral bacterium Streptococcus mutans deposited in vitro on bovine enamel granules with and without fluoride varnish.

Bovine enamel granules were treated with fluoride varnish for 24 h. Samples of F-treated and untreated control enamel were covered with maleic-acid-NaOH buffer (pH 5.8) previously saturated with enamel salts and containing a standard amount of fresh Strep. mutans cells plus KCl and MgCl2 (6 and 1 mM, respectively). The cells were centrifuged on the enamel; sucrose was added to the test and to control systems with fluoridated and non-fluoridated enamel; distilled water was added to non-fermenting controls. After incubation at 37 degrees C for intervals up to 2 h, fluoridation of the enamel had reduced the drop in pH of Strep. mutans plaque by 0.7 pH unit and reduced the release of Ca and P from enamel. Bacterial P levels were also significantly reduced in plaque in contact with fluoridated enamel. Magnesium concentrations outside the enamel were not altered.

Exchange of fluoride between bovine enamel and the surface-related cells of the oral bacterium Streptococcus mutans.

Standard areas of intact bovine enamel surface were fluoridated with dental F-varnish for 24 h and then cleaned from varnish residues and thoroughly rinsed with distilled water. Sucrose fermentation by a plaque-like layer of Streptococcus mutans cells covering such an enamel surface was accompanied by a rapid but transient accumulation of F of enamel origin by the Strep. mutans cells and by a pH drop in the plaque to pH 4.0. The uptake of F from the surface by the control cells, utilizing their carbohydrate stores and causing a smaller pH-drop, was slow but no release of F back to the cell exterior took place within 18 h. In a second experiment, F- varnished and placebo- varnished bovine enamel granules were used as above, but they were not thoroughly washed after being varnish-treated and cleaned. Both the sucrose-fermenting and the control layer of Strep. mutans rapidly released appreciable but equal amounts of fluoride from the F-treated enamel. The accumulation of F of enamel origin by the Strep. mutans cells with or without sucrose was rapid and of almost the same magnitude. In the model with the sucrose-utilizing Strep. mutans and the F-treated enamel granules, the plaque pH-drop was less and the dissolution of the enamel Ca and P completely prevented compared to the respective changes in the sucrose-utilizing model with placebo-treated enamel granules.

Enamel dissolution in relation to fluoride concentrations in the fluid of dental plaque-like layers of precultured Streptococcus sobrinus.

Two experiments were conducted to find out what concentration of fluoride (F), when added as NaF to the fluid of an in vitro caries model, would be sufficient for full protection of the underlying enamel during a long (20 or 40 h) fall in 'plaque' pH. An existing caries model with bovine enamel and Streptococcus sobrinus 'plaque' was employed, while the fluid phase was initially either fully or partially saturated with tricalcium phosphate. In the model with fully saturated and more strongly buffered fluid, a 10 parts/10(6) addition of F to the fluid phase caused no inhibition of the pH fall. In the model with partially saturated and weakly buffered fluid, prevention of the pH fall increased along with increase of added F from 2 to 20 parts/10(6). In each model, the 10 parts/10(6) addition of F was associated with complete prevention of the increase of calcium (Ca) in the fluid phase. In the partially saturated, weakly buffered model, findings on the inorganic P of the fluid phase agreed with findings on Ca. The findings for microhardness of the enamel surface indicated a complete prevention of the enamel softening through the 10 parts/10(6) F additive. Enamel F content was elevated by the fermentation, and even more so when F was added with sugar to the fluid phase. The Ca content of Strep. sobrinus cells was reduced when incubated with sucrose for 40 h and, especially, with sucrose and F.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of different strontium concentrations on the efficacy of chlorhexidine-fluoride-strontium gel in preventing enamel softening in vitro.

The effects were compared of strontium concentrations of 0, 15, 50 and 250 parts/10(6) in chlorhexidine(0.20%)-fluoride(0.16%) gel in preventing the softening of bovine enamel during bacterial fermentation. Fresh Streptococcus sobrinus cells were suspended in a buffer solution (pH 6.0) with 3.3% sucrose and centrifuged as a plaque-like layer on the top of enamel slabs covered with 10 microliters gel. AFter 24 h incubation, the pH fall of the fluid was significantly smaller in all test groups than in the placebo group. Strontium seemed to have an inhibitory effect on the pH fall. All test gels significantly prevented softening and dissolution of enamel during bacterial fermentation, which was directly related to strontium concentration. The amounts of calcium and phosphorus in the cells and fluid after incubation were the smallest in the group with 250 parts/10(6) strontium. In a second experiment without bacteria, new enamel slabs were covered with 10 microliters gel containing chlorhexidine and NaF with 0 and 250 parts/10(6) strontium to study the protective effect of strontium. After 24 h gel treatment, each enamel slab was dissolved in 1 ml 0.1 M lactic acid, pH 5.0, for 2 h. Significantly less calcium and phosphorus were dissolved from the enamel in both test groups than in the control and placebo groups. However, the placebo gel also prevented calcium and phosphorus dissolution significantly. These results suggest that the addition of strontium to chlorhexidine-fluoride gel improves the ability of this combination to prevent caries-like enamel softening. The inhibition of bacterial acid production by the strontium-containing gel may explain this enhanced protection of enamel.

Bovine enamel hardness and its Ca-, P-, Mg- and F-contents modified by the bacterium Streptococcus mutans, artificial dental plaque and fluoride.

A layer of cells from buffered Strep. mutans suspension (pH 5.8), with or without sucrose, was centrifuged on bovine enamel surfaces. Fluoride was added to a part of the samples (final F 25 parts/10(6]. Control and test samples were incubated at 37 degrees C for 18 h. The pH of the fermenting plaque dropped to 4.15. When F was present, the final pH was 4.45. Microhardness of the enamel surface was reduced by the presence of sucrose but less in the presence of F. Enamel Ca was liberated during fermentation, but only into the fluid and less in the presence of F. The weight ratio of Ca and P released by sugar fermentation was 3.14 and 1.91 when F was present. The F content of enamel surface was only slightly increased (130 parts/10(6]by the F in distilled water alone. Subsurface enamel gained more F (280 parts/10(6]. When artificial plaque was present, addition of F increased the F content of enamel surface by 450 parts/10(6) and F of subsurface by 210 parts/10(6). The addition of F increased the enamel F content to the greatest extent under the fermenting plaque, 680 parts/10(6) in surface and 400 parts/10(6) in subsurface enamel, compared to the values of the enamel under non-fermenting plaque.

Fluoride in sugar.

Results of caries model studies in vitro and in animals suggest that the tooth-protective potential of fluoride may be best utilized if fluoride is brought to the local caries milieu at the moment of each caries attack. Two clinical trials performed so far indicate that a reduction in caries increment of about 40 per cent can be obtained within 3 years through small (0.5-1.0 mg) daily intakes of fluoride when it is incorporated in highly cariogenic sucrose products or in tablets having a sucrose base. When incorporated in sucrose products, fluoride caused a complete arrest of caries during the third year. There was substantial accumulation of the supplemental fluoride in surface and subsurface enamel beneath the plaque fermenting the F-supplemented sucrose. This may be one of the preventive mechanisms involved. In plaque fluid, the supplemental fluoride, together with fluoride released from the plaque material and by the action of acid on the surface enamel of high fluoride content, may strongly reduce further enamel dissolution and promote its remineralization. Further metabolism of the plaque bacteria including their acid production may also be inhibited. Among the many advantages of using this principle are that: the supplemental fluoride in sugar automatically seeks the caries risk subjects who use sugary products; the amount of fluoride needed per kg of sugar may remain low and thus the risk of excessive intake of fluoride may also be low; the technical process is low in cost and easily performed; and the products are easily distributed nationwide. Furthermore, non-fluoridated sugary products may still be distributed to those who may continue to prefer them.

The role of magnesium in the aetiology and prevention of caries: some new findings and implications.

While some epidemiological studies seem to indicate that a high intake of magnesium should be associated with a low prevalence of dental caries, the results of experimental studies are mainly equivocal. Magnesium is probably not bound to the apatite lattice of dental enamel or dentine, or it is bound to a small degree only. It is mainly located in the hydration layer of the apatite crystallites. In the dental caries process it is preferentially dissolved together with the carbonate of the mineral phase. It is not known to what extent feasible dietary changes can modify tooth magnesium content during pre-eruptive tooth development. Animal experiments indicate that the elevation of dietary magnesium alone after tooth eruption has no definite capacity to modify the occurrence of dental caries. When fed in combination with small fluoride supplements in the diet magnesium and fluoride may support each other in preventing various calcium salt imbalances such as dental caries, arteriosclerosis and nephrocalcinosis. Although some recent in vitro findings indicate that extra magnesium in the fluid environment of cariogenic streptococci may protect them against the inhibitory action of fluoride, such magnesium changes do not seem possible in the human mouth under present or envisaged dietary conditions.

Seven weeks feeding of magnesium and fluoride modifies plasma lipids of hypercholesterolaemic rats in late growth phase.

Recent findings indicated that a low fluoride supplement, especially with a low magnesium supplement in the basically low magnesium diet of genetically hypercholesterolaemic male RICO rats, may prevent the generation of atherosclerotic serum lipid profile. In the present study, several plasma lipids/lipoproteins were measured in the same strain of rats after a later growth phase. The control group C was fed an adequate diet with 45 per cent sucrose plus some cholesterol while the dietary fluoride was very low (1.1 mg F/kg of diet). In diet of group D, the Mg content was reduced to about one seventh of Mg of group C, i.e. to 122 mg/kg. Diet of group E was as that of group D with F content elevated to 17.2 mg/kg. Diet of group G was as that of group E with Mg content elevated to 220 mg/kg. The feeding period was terminated at 12 h deprivation of food and following exsanquination. Total plasma cholesterol in group C was 4.5 mmol/L. The central factor in causing reduction in growth rate and several plasma lipids and their lipoprotein subfractions appeared to be the magnesium deficiency. However, the greatest significant reductions in plasma cholesterol, plasma free cholesterol, plasma and VLDL esterified cholesterol and also HDL cholesterol, HDL esterified cholesterol and plasma triglycerides from those levels of the control group C were found in group G (fluoride and magnesium supplements). Supplementation of fluoride alone in group E reduced only plasma and VLDL esterified cholesterol. In the present male RICO rats, low dietary F and Mg supplements, separately, and especially together, may participate in the regulation of the outcome of atherosclerosis via affecting several plasma lipid risk factors known to associate with the development of atherosclerosis.