Streptococcus mutans glutamate binding protein (GlnH) as antigen target for a mucosal anti-caries vaccine.

BACKGROUND: In recent years, several studies have demonstrated that bacterial ABC transporters present relevant antigen targets for the development of vaccines against bacteria such as Streptococcus pneumoniae and Enterococcus faecalis. In Streptococcus mutans, the glutamate transporter operon (glnH), encoding an ABC transporter, is associated with acid tolerance and represents an important virulence-associated factor for the development of dental caries. RESULTS: In this study, we generated a recombinant form of the S. mutans GlnH protein (rGlnH) in Bacillus subtilis. Mice immunized with this protein antigen elicited strong antigen-specific antibody responses after sublingual administration of a vaccine formulation containing a mucosal adjuvant, a non-toxic derivative of the heat-labile toxin (LTK63) originally produced by enterotoxigenic Escherichia coli (ETEC) strains. Serum anti-rGlnH antibodies reduced adhesion of S. mutans to the oral cavity of naïve mice. Moreover, mice actively immunized with rGlnH were partially protected from oral colonization after exposure to the S. mutans NG8 strain. CONCLUSIONS: Our results indicate that S. mutans rGlnH is a potential target antigen capable of inducing specific and protective antibody responses after immunization. Overall, these observations raise the prospect of the development of mucosal anti-caries vaccines.

The Effects of Fluoride Treatment Time and Concentration on In Vitro Caries Lesion Demineralisation and Remineralisation.

PURPOSE: To investigate the possible interaction between fluoride treatment time and concentration on enamel caries lesion de-/remineralisation. MATERIALS AND METHODS: The study design followed a three (fluoride concentration: 0, 275, 1250 ppm as sodium fluoride) x four (treatment time: 10, 30, 60, 120 s) factorial design. Caries lesions were created in bovine enamel and the extent of demineralisation determined using Vickers surface microhardness (VHN). Lesions were pH cycled (18 days) with the daily schedule consisting of two fluoride treatments, a 4-h demineralisation period and exposure to artificial saliva at all other times. VHN was determined again after pH cycling and changes to baseline values calculated (∆VHN). Enamel fluoride uptake (EFU) was determined using the microbiopsy technique. Data were analyzed using two-way ANOVA. RESULTS: The concentration x treatment time interaction was significant for ∆VHN (p < 0.0001) and EFU (p = 0.0298). Dose-response relationships were observed for both variables for fluoride concentration and treatment time. ∆VHN: higher fluoride concentration compensated for shorter treatment time (e.g. ∆VHN [mean ± SD] = 85.5 ± 60.6 for 30 s with 1250 ppm fluoride vs ∆VHN = 84.3 ± 26.9 for 120s with 275 ppm fluoride). EFU data were similar but highlighted a greater ability to discern between fluoride concentrations (e.g. EFU = 4364 ± 1166 ppm vs 8538 ± 9531 ppm; above examples). Although ∆VHN and EFU correlated well (r = 0.723; p < 0.001), lesion demonstrated a greater ability to acquire fluoride than to remineralise. CONCLUSIONS: Behavioural aspects relating to caries can be studied in vitro, although model limitations must be considered. Adequate exposure times to cariostatic concentrations of fluoride are important in maximising caries prevention.

Fluoride and Oral Health.

The discovery during the first half of the 20th century of the link between natural fluoride, adjusted fluoride levels in drinking water and reduced dental caries prevalence proved to be a stimulus for worldwide on-going research into the role of fluoride in improving oral health. Epidemiological studies of fluoridation programmes have confirmed their safety and their effectiveness in controlling dental caries. Major advances in our knowledge of how fluoride impacts the caries process have led to the development, assessment of effectiveness and promotion of other fluoride vehicles including salt, milk, tablets, toothpaste, gels and varnishes. In 1993, the World Health Organization convened an Expert Committee to provide authoritative information on the role of fluorides in the promotion of oral health throughout the world (WHO TRS 846, 1994). This present publication is a revision of the original 1994 document, again using the expertise of researchers from the extensive fields of knowledge required to successfully implement complex interventions such as the use of fluorides to improve dental and oral health. Financial support for research into the development of these new fluoride strategies has come from many sources including government health departments as well as international and national grant agencies. In addition, the unique role which industry has played in the development, formulation, assessment of effectiveness and promotion of the various fluoride vehicles and strategies is noteworthy. This updated version of 'Fluoride and Oral Health' has adopted an evidence-based approach to its commentary on the different fluoride vehicles and strategies and also to its recommendations. In this regard, full account is taken of the many recent systematic reviews published in peer reviewed literature.

Single oral acute fluoride exposure causes changes in cardiac expression of oxidant and antioxidant enzymes, apoptotic and necrotic markers in male rats.

Several studies have shown that acute fluoride (F(-)) exposure impairs cardiac function, but the molecular mechanism is not clear. In order to study this, male Wistar rats were treated with single oral doses of 45 and 90 mg/kg F(-) for 24 h. A significant accumulation of F(-) was found in the serum and myocardium of experimental rats. F(-) treatment causes myocardial necrosis as evident from increased levels of myocardial troponin I, creatine kinase, lactate dehydrogenase and aspartate transaminase. In addition, F(-) induces myocardial oxidative stress via increased reactive oxygen species, lipid peroxidation, protein carbonyl content and nitrate levels along with decreased in the levels of enzymatic (superoxide dismutase 2, catalase, glutathione peroxidase and glutathione s transferase pi class) and non-enzymatic (reduced glutathione) antioxidants. Notably, F(-) triggers myocardial apoptosis through altered Bax/Bcl2 ratio and increased cytochrome c, caspase 3p20 and terminal deoxynucleotidyl transferase dUTP nick end labeled positive cells. An increased cardiac expression of Nox4 and p38α MAPK in F(-) treated rats indicates the oxidative and apoptotic damage. Moreover, ultra-structural changes, histopathological and luxol fast blue staining demonstrates the degree of myocardial damage at subcellular level. Taken together, these findings reveal that acute F(-) exposure causes cardiac impairment by altering the expression of oxidative stress, apoptosis and necrotic markers.

Vitamin A deficiency: An oxidative stress marker in sodium fluoride (NaF) induced oxidative damage in developing rat brain.

Fluoride induced oxidative stress through depletion in levels of various anti-oxidants such as glutathione, superoxide dismutase (SOD), fat soluble vitamins (D and E) with increased levels of lipid peroxidation (LPO) and fluoride aggravate the damage in rodents as well as in humans. Vitamins A, a fat soluble vitamin possess antioxidant property which plays a significant role in scavenging the free radicals species similar to vitamin D and E. Vitamin A is involved in neural tissue development and plasticity. The growing evidence about vitamin A being antioxidant in different biological reactions formed the basis to determine the effect of fluoride on its levels. The present study was conducted in Wistar rat pups. The pregnant wistar rats were dosed with 20 ppm sodium fluoride (NaF) from day one of pregnancy till the pups were aged day 30. The serum was collected from developing rat pups on regular intervals (14th, 21st, 30th day) and vitamin A levels were analyzed by High performance liquid chromatography (HPLC). Body weights, Behavioural studies and spectrophotometric estimation of SOD, LPO in brain lysates were also performed. The results showed significant decrease (p<0.001) in vitamin A in fluoride induced samples in comparison to the control samples suggesting that decreased levels of vitamin A can be used as another marker in fluoride induced toxicity studies.

Renal excretion of fluoride after fluoride mouth rinses in children.

AIM: This study was conducted to determine if there was an increase in the urinary excretion of fluoride, after the use of fluoride mouth rinses in children. MATERIALS AND METHODS: The sample consisted of 58 children aged 5-8 years, randomly selected, residents in non-fluoridated water areas. Urine samples were collected prior to mouthwash and also 2 hours after use. The control sample, which received no treatment, consisted of 16 children of equivalent age and from the same community. Urinary excretion of fluoride was analysed by determining the pH, creatinine, F- ion and fluoride (mg)/creatinine (g) (F/Cr) ratio in urine. Results In the studied sample, the mean F/Cr ratio before fluoride mouth rinse was 0.26 mg/g and it rose to 1.58 mg/g 2 hours after mouth rinse. This difference of 1.33 mg/g was statistically highly significant (p<.001). In the control group no significant changes occurred. The average 2 hours afterward F/Cr ratios were 0.29 and 0.27 respectively (p=0.426). CONCLUSION: After the use of a fluoride mouthwash, in children, there is a statistically significant increase of fluoride ion in urine, which can be attributed to the application of this product.

Total fluoride intake and excretion in children up to 4 years of age living in fluoridated and non-fluoridated areas.

Fractional fluoride retention is important during the early years of life when considering the risk of development of dental fluorosis. This study aimed to measure fractional fluoride retention in young children. The objectives were to investigate the relationships between fractional fluoride retention and total daily fluoride intake, age, and body mass index (BMI). Twenty-nine healthy children, up to 4 yr of age, participated; 14 lived in a fluoridated area (0.64 µg ml(-1) of fluoride in drinking water) and 15 lived in a non-fluoridated area (0.04 µg ml(-1) of fluoride in drinking water). The total daily fluoride intake of each child was calculated from the daily dietary fluoride intake and toothpaste ingestion (if fluoride toothpaste was used). Total daily fluoride excretion was measured by collecting voided urine and faeces over a 24-h period, and fractional fluoride retention was calculated by dividing the amount of fluoride retained in the body (total daily fluoride intake minus total daily fluoride excretion) by the total daily fluoride intake. Nine children were excluded from data analysis because of suspected invalid samples. Mean (range) fractional fluoride retention for the remaining 20 children was 0.61 (0.06-0.98). There were no statistically significant correlations between fractional fluoride retention and either age or BMI. However, fractional fluoride retention was correlated with total daily fluoride intake: fractional fluoride retention = 1 - exp (-C × total daily fluoride intake), where C = 28.75 (95% CI = 19.75-37.75). The wide variation in fluoride retention in young children could have important implications when recommendations for fluoride use are being considered.

Fluoride balance in infants and young children in the U.K. and its clinical relevance for the dental team.

This paper provides an overview of the main sources of fluoride (F) in children and discusses the importance of assessing F exposure at an individual and community level. It describes some of the methods used to assess F exposure by estimating F intake and excretion, together with the development and use of biomarkers for F and their importance. The paper focuses on what recent F research has shown in terms of significant sources of dietary F intake in U.K. infants and young children and the proportion of F intake that derives from F ingestion of toothpaste. This information is considered in the context of clinical dental practice and the implications of this research for oral health discussed.

Physical exercise ameliorates the toxic effect of fluoride on the insulin-glucose system.

Daily intake of water with fluoride concentrations >1.5 mg/l produces insulin resistance (IR). On the other hand, physical activity increases insulin sensitivity in the muscle. Therefore, the aim of this study was to evaluate the effect of physical activity on IR in rats treated with sodium fluoride (NaF) in drinking water. Sprague-Dawley rats were divided into three groups (n=10/group): Control (drinking water without NaF), NaF (drinking water with NaF 15 mg/l for 30 days), and Exercise (daily running on a treadmill for 60 min at 2.25 m/min and drinking water with NaF 15 mg/l for 30 days). IR was evaluated with the homeostasis model assessment-IR (HOMA-IR) index using fasting plasma levels of glucose and insulin. IR increased in rats treated with 15 mg/l NaF in drinking water. A decrease in IR was observed in rats that performed physical activity and drank water with 15 mg/l NaF; the Exercise group also showed an increase in the amounts of bone fluoride. The variation in the HOMA-IR values could be the consequence of variation in the sensitivity of tissues to insulin or decrease in plasma fluoride levels due to bone fluoride intake. These findings indicate that the performance of daily physical activity could reduce the negative effects of the chronic ingestion of NaF on glucose homeostasis.

The cariogenic characters of xylitol-resistant and xylitol-sensitive Streptococcus mutans in biofilm formation with salivary bacteria.

Streptococcus mutans metabolize carbohydrates, such as glucose and sucrose, to produce acid and enhance biofilm formation with the early colonizing bacteria to induce dental caries. Xylitol has been used as a reliable substitute for carbohydrate to inhibit the acid production of S. mutans. However, long-term xylitol consumption leads to the emergence of xylitol-resistance in S. mutans. The aim of this study was to investigate the cariogenic trait of Xylitol-resistant (X(R)) S. mutans using biofilm formation and coaggregation of xylitol-sensitive (X(S)) and X(R) S. mutans with salivary bacteria and their glucosyltransferases expression. When X(S) or X(R) S. mutans were incubated in brain heart infusion broth with bacteria from human saliva, X(R)S. mutans exhibited reduction in biofilm formation in comparison to X(S) S. mutans. The coaggregation between X(R) S. mutans and S, gordonii, S. mitis, S. oralis or S. sanguinis was less pronounced than that of X(S) S. mutans in the presence of sucrose. However, there was no difference in the coaggregation between X(R) and X(S) S. mutans in the sucrose-free condition. The level of gtfB and gtfC mRNA expression of X(R) S. mutans was lower than that of X(S) S. mutans, whilst the level of gtfD mRNA expression did not differ between the two strains. The reduction of biofilm formation in X(S) S. mutans due to decrease in glucosyltransferases expression suggests that X(R) S. mutans may be less cariogenic than X(S) S. mutans.

Metabolomic effects of xylitol and fluoride on plaque biofilm in vivo.

Dental caries is initiated by demineralization of the tooth surface through acid production from sugar by plaque biofilm. Fluoride and xylitol have been used worldwide as caries-preventive reagents, based on in vitro-proven inhibitory mechanisms on bacterial acid production. We attempted to confirm the inhibitory mechanisms of fluoride and xylitol in vivo by performing metabolome analysis on the central carbon metabolism in supragingival plaque using the combination of capillary electrophoresis and a time-of-flight mass spectrometer. Fluoride (225 and 900 ppm F(-)) inhibited lactate production from 10% glucose by 34% and 46%, respectively, along with the increase in 3-phosphoglycerate and the decrease in phosphoenolpyruvate in the EMP pathway in supragingival plaque. These results confirmed that fluoride inhibited bacterial enolase in the EMP pathway and subsequently repressed acid production in vivo. In contrast, 10% xylitol had no effect on acid production and the metabolome profile in supragingival plaque, although xylitol 5-phosphate was produced. These results suggest that xylitol is not an inhibitor of plaque acid production but rather a non-fermentative sugar alcohol. Metabolome analyses of plaque biofilm can be applied for monitoring the efficacy of dietary components and medicines for plaque biofilm, leading to the development of effective plaque control.

Fluoride metabolism.

Knowledge of all aspects of fluoride metabolism is essential for comprehending the biological effects of this ion in humans as well as to drive the prevention (and treatment) of fluoride toxicity. Several aspects of fluoride metabolism - including gastric absorption, distribution and renal excretion - are pH-dependent because the coefficient of permeability of lipid bilayer membranes to hydrogen fluoride (HF) is 1 million times higher than that of F(-). This means that fluoride readily crosses cell membranes as HF, in response to a pH gradient between adjacent body fluid compartments. After ingestion, plasma fluoride levels increase rapidly due to the rapid absorption from the stomach, an event that is pH-dependent and distinguishes fluoride from other halogens and most other substances. The majority of fluoride not absorbed from the stomach will be absorbed from the small intestine. In this case, absorption is not pH-dependent. Fluoride not absorbed will be excreted in feces. Peak plasma fluoride concentrations are reached within 20-60 min following ingestion. The levels start declining thereafter due to two main reasons: uptake in calcified tissues and excretion in urine. Plasma fluoride levels are not homeostatically regulated and vary according to the levels of intake, deposition in hard tissues and excretion of fluoride. Many factors can modify the metabolism and effects of fluoride in the organism, such as chronic and acute acid-base disturbances, hematocrit, altitude, physical activity, circadian rhythm and hormones, nutritional status, diet, and genetic predisposition. These will be discussed in detail in this review.

An in vitro scanning microradiography study of the reduction in hydroxyapatite demineralization rate by statherin-like peptides as a function of increasing N-terminal length.

Enamel demineralization is slowed by salivary proteins that inhibit calcium hydroxyapatite (HA) demineralization. Statherin (StN43), a 43-residue phosphorylated salivary protein with primary sequence similarities to osteopontin and caseins, binds calcium and HA. The aim of this study was to identify the minimum length of the functional domain of the statherin molecule required for cariostatic function by measuring the efficacy of peptides of progressively shorter length (i.e. containing only the N-terminal 21 (StN21), 15 (StN15), 10 (StN10), or 5 (StN5) residues) to reduce HA demineralization rates (RD(HA) ). Porous HA blocks were used as enamel analogues, and were exposed to 0.1 M acetic acid at pH 4 for 120 h, rinsed, and treated with StN21, StN15, StN10, or StN5 peptides (1.88 × 10(-5) M) for 24 h, then demineralized for a further 120 h. The RD(HA) was measured, before and after peptide treatment, using scanning microradiography. Hydroxyapatite blocks treated with StN21 and StN15 demonstrated a 50-60% reduction in the RD(HA) . However, no reduction in the RD(HA) was observed following treatment with either StN10, StN5, or buffer only. The mechanism by which statherin-like peptides reduce RD(HA) may be associated with their binding to HA surfaces. Comparisons with previously published binding energies of statherin to HA also suggest that statherin-like peptides containing 15 N-terminal residues or more, are required for binding, suggesting a link between binding and demineralization reduction.

Fingernail may not be a reliable biomarker of fluoride body burden from dentifrice.

Fingernail has been suggested as a biomarker of fluoride (F) body burden, but there is no consensus if it would be a reliable indicator of F exposure from dentifrice. Therefore, the present study was conducted to investigate if fingernails would have sensitivity to detect F exposure from dentifrice in young children. Twenty-three 1-3-year-old children living in the city of Piracicaba (0.72 ppm F in water), Brazil, were enrolled in two phases of different F exposure: in phase A (1st to 11th week), they were exposed to the combination of F from diet (solids and liquids) and dentifrice (1,500 microg F/g as MFP), and in phase B (12th to 29th week), only to F from diet (the use of F dentifrice was interrupted). Fingernails were weekly clipped during 35 weeks for F determination. F intake from diet and dentifrice in each phase was also determined. Both analyses were made with ion-specific electrode. F intake (Mean +/- SD) was significantly higher (p<0.01) when the children were exposed to F from diet+dentifrice than only to F from diet (0.086 +/- 0.032 and 0.040 +/- 0.009 mg F/day/kg body weight, respectively). However, F concentrations in nails collected during the whole experimental period of 35 weeks presented great variation with no trend of decreasing after F dentifrice intake interruption. The findings suggest that fingernail may not be a reliable F biomarker of body burden from dentifrice.

Molecular mechanisms of fluoride toxicity.

Halfway through the twentieth century, fluoride piqued the interest of toxicologists due to its deleterious effects at high concentrations in human populations suffering from fluorosis and in in vivo experimental models. Until the 1990s, the toxicity of fluoride was largely ignored due to its "good reputation" for preventing caries via topical application and in dental toothpastes. However, in the last decade, interest in its undesirable effects has resurfaced due to the awareness that this element interacts with cellular systems even at low doses. In recent years, several investigations demonstrated that fluoride can induce oxidative stress and modulate intracellular redox homeostasis, lipid peroxidation and protein carbonyl content, as well as alter gene expression and cause apoptosis. Genes modulated by fluoride include those related to the stress response, metabolic enzymes, the cell cycle, cell-cell communications and signal transduction. The primary purpose of this review is to examine recent findings from our group and others that focus on the molecular mechanisms of the action of inorganic fluoride in several cellular processes with respect to potential physiological and toxicological implications. This review presents an overview of the current research on the molecular aspects of fluoride exposure with emphasis on biological targets and their possible mechanisms of involvement in fluoride cytotoxicity. The goal of this review is to enhance understanding of the mechanisms by which fluoride affects cells, with an emphasis on tissue-specific events in humans.

Kinetics of monofluorophosphate hydrolysis in a bacterial test plaque in situ.

Models to evaluate the anticaries potential of fluoride (F) formulations containing monofluorophosphate (MFP) should consider the release of F ion to the oral environment by its enzymatic hydrolysis. This was tested in situ, using a test plaque of a strain of Streptococcus mutans which presents high MFPase activity at pH 5.0. The test plaque was exposed to non-F or MFP (1,450 microg F/g) dentifrices and the fluid phase of the plaque was analyzed after 15, 30, 45 and 75 min. MFP concentration in the plaque fluid decreased over time after exposure to MFP dentifrice, but F ion reached 134.9 +/- 32.0 microM at 15 min and decreased significantly only at 75 min, suggesting continuous MFP hydrolysis by the test plaque.

Fingernail may not be a reliable biomarker of fluoride body burden from dentifrice

Fingernail has been suggested as a biomarker of fluoride (F) body burden, but there is no consensus if it would be a reliable indicator of F exposure from dentifrice. Therefore, the present study was conducted to investigate if fingernails would have sensitivity to detect F exposure from dentifrice in young children. Twenty-three 1-3-year-old children living in the city of Piracicaba (0.72 ppm F in water), Brazil, were enrolled in two phases of different F exposure: in phase A (1st to 11th week), they were exposed to the combination of F from diet (solids and liquids) and dentifrice (1,500 µg F/g as MFP), and in phase B (12th to 29th week), only to F from diet (the use of F dentifrice was interrupted). Fingernails were weekly clipped during 35 weeks for F determination. F intake from diet and dentifrice in each phase was also determined. Both analyses were made with ion-specific electrode. F intake (Mean ± SD) was significantly higher (p<0.01) when the children were exposed to F from diet+dentifrice than only to F from diet (0.086 ± 0.032 and 0.040 ± 0.009 mg F/day/kg body weight, respectively). However, F concentrations in nails collected during the whole experimental period of 35 weeks presented great variation with no trend of decreasing after F dentifrice intake interruption. The findings suggest that fingernail may not be a reliable F biomarker of body burden from dentifrice.

As unhas têm sido consideradas um biomarcador para a exposição ao flúor (F), mas não há consenso se é um indicador confiável para exposição ao F a partir do dentifrício. Vinte e três crianças, com idade entre 1 a 3 anos, moradoras de Piracicaba (0,72 ppm F na água), Brasil, foram submetidas a duas fases de diferentes exposição ao F: fase A (1a a 11a semanas), as crianças foram expostas à combinação de F a partir da dieta (sólidos e líquidos) e dentifrício (1500 µg F/g como MFP); e na fase B (12ª a 29ª semanas), apenas ao F da dieta, uma vez que usaram dentifrício não fluoretado. As unhas das mãos foram coletadas semanalmente durante 35 semanas para determinação de F. A exposição ao F a partir da dieta e dentifrício foi também determinada. Ambas análises foram feitas com eletrodo específico para F. A exposição ao F foi significativamente maior (p<0,001) quando as crianças foram expostas ao F da dieta + dentifrício que ao F da dieta (0,086 ± 0,032 e 0,040 ± 0,009 mg F/kg corpóreo/dia, respectivamente). Entretanto, a concentração de F nas unhas coletadas durante todo o período experimental não diminuiu após a interrupção da ingestão do F a partir do dentifrício. Os resultados sugerem que as unhas das mãos não são um biomarcador confiável para refletir a exposição ao F pelo dentifrício.

Dental caries: a dynamic disease process.

Abstract Dental caries is a transmissible bacterial disease process caused by acids from bacterial metabolism diffusing into enamel and dentine and dissolving the mineral. The bacteria responsible produce organic acids as a by-product of their metabolism of fermentable carbohydrates. The caries process is a continuum resulting from many cycles of demineralization and remineralization. Demineralization begins at the atomic level at the crystal surface inside the enamel or dentine and can continue unless halted with the end-point being cavitation. There are many possibilities to intervene in this continuing process to arrest or reverse the progress of the lesion. Remineralization is the natural repair process for non-cavitated lesions, and relies on calcium and phosphate ions assisted by fluoride to rebuild a new surface on existing crystal remnants in subsurface lesions remaining after demineralization. These remineralized crystals are acid resistant, being much less soluble than the original mineral.

Influence of salivary macromolecules and fluoride on enamel lesion remineralization in vitro.

The aim of this study was to investigate the influence of salivary macromolecules on enamel lesion remineralization in the presence or absence of fluoride. Paraffin-stimulated whole saliva was centrifuged, and the supernatant was dialyzed in 1,000 molecular-weight cutoff dialysis tubes, first against a phosphate buffer and then against a mineral solution containing Ca and phosphate. Artificial subsurface lesions of human enamel, created in pH 4.5 acetate buffer, were remineralized for 28 days in 4 remineralizing solutions: group C--mineral solution as a control; group S--mineral solution + dialyzed saliva; group F--mineral solution + 1 ppm F; group SF--mineral solution + dialyzed saliva + 1 ppm F. Changes in relative mineral concentration in the lesions were assessed by transverse microradiography. The results showed statistically significant mineral gains in the lesion body in groups C (DeltaZ = 3,254 +/- 1,562% x microm) and SF (DeltaZ = 2,973 +/- 1,349% x microm), but not in groups S (DeltaZ = 5,192 +/- 1,863% x microm) and F (DeltaZ = 4,310 +/- 1,138% x microm) compared with the baseline group (DeltaZ = 5,414 +/- 461% x microm). It was also found that the mineral density at the surface layer in group F (75.0 +/- 15.7%) was greater than that in the baseline group (30.1 +/- 12.3%) with statistical significance, but not in group SF (39.9 +/- 16.5%). It was concluded that the macromolecules inhibited lesion remineralization fundamentally but that these molecules, in the presence of fluoride, seemed to play an important role in the continuation of remineralization by reducing mineral gains at the surface layer.

The role of bitewing radiographs--a review of current guidelines.

This article sets out guidelines on the use of bitewing radiographs for the detection of dental caries, with suggested risk factors and recall intervals. It describes a case in which extensive carious lesions were not detected clinically, but were revealed when radiographs were taken during an orthodontic assessment.