The quality of dental care and modern achievements in dental science depend strongly on understanding the properties of teeth and the basic principles and mechanisms involved in their interaction with surrounding media. Erosion is a disorder to which such properties as structural features of tooth, physiological properties of saliva, and extrinsic and intrinsic acidic sources and habits contribute, and all must be carefully considered. The degree of saturation in the surrounding solution, which is determined by pH and calcium and phosphate concentrations, is the driving force for dissolution of dental hard tissue. In relation to caries, with the calcium and phosphate concentrations in plaque fluid, the ‘critical pH’ below which enamel dissolves is about 5.5. For erosion, the critical pH is lower in products (e.g. yoghurt) containing more calcium and phosphate than plaque fluid and higher when the concentrations are lower. Dental erosion starts by initial softening of the enamel surface followed by loss of volume with a softened layer persisting at the surface of the remaining tissue. Dentine erosion is not clearly understood, so further in vivo studies, including histopathological aspects, are needed. Clinical reports show that exposure to acids combined with an insufficient salivary flow rate results in enhanced dissolution. The effects of these and other interactions result in a permanent ion/substance exchange and reorganisation within the tooth material or at its interface, thus altering its strength and structure. The rate and severity of erosion are determined by the susceptibility of the dental tissues towards dissolution. Because enamel contains less soluble mineral than dentine, it tends to erode more slowly. The chemical mechanisms of erosion are also summarised in this review. Special attention is given to the microscopic and macroscopic histopathology of erosion.
Periodontal diseases and dental caries are the most common diseases of humans and the main cause of tooth loss. Both diseases can lead to nutritional compromise and negative impacts upon self‐esteem and quality of life. As complex chronic diseases, they share common risk factors, such as a requirement for a pathogenic plaque biofilm, yet they exhibit distinct pathophysiologies. Multiple exposures contribute to their causal pathways, and susceptibility involves risk factors that are inherited (e.g. genetic variants), and those that are acquired (e.g. socio‐economic factors, biofilm load or composition, smoking, carbohydrate intake). Identification of these factors is crucial in the prevention of both diseases as well as in their management. Aim To systematically appraise the scientific literature to identify potential risk factors for caries and periodontal diseases. Methods One systematic review (genetic risk factors), one narrative review (role of diet and nutrition) and reference documentation for modifiable acquired risk factors common to both disease groups, formed the basis of the report. Results & Conclusions There is moderately strong evidence for a genetic contribution to periodontal diseases and caries susceptibility, with an attributable risk estimated to be up to 50%. The genetics literature for periodontal disease is more substantial than for caries and genes associated with chronic periodontitis are the vitamin D receptor (VDR), Fc gamma receptor IIA (Fc‐γRIIA) and Interleukin 10 (IL10) genes. For caries, genes involved in enamel formation (AMELX, AMBN, ENAM, TUFT, MMP20, and KLK4), salivary characteristics (AQP5), immune regulation and dietary preferences had the largest impact. No common genetic variants were found. Fermentable carbohydrates (sugars and starches) were the most relevant common dietary risk factor for both diseases, but associated mechanisms differed. In caries, the fermentation process leads to acid production and the generation of biofilm components such as Glucans. In periodontitis, glycaemia drives oxidative stress and advanced glycation end‐products may also trigger a hyper inflammatory state. Micronutrient deficiencies, such as for vitamin C, vitamin D or vitamin B12, may be related to the onset and progression of both diseases. Functional foods or probiotics could be helpful in caries prevention and periodontal disease management, although evidence is limited and biological mechanisms not fully elucidated. Hyposalivation, rheumatoid arthritis, smoking/tobacco use, undiagnosed or sub‐optimally controlled diabetes and obesity are common acquired risk factors for both caries and periodontal diseases.
ETW is a clinical condition, which calls for the increased attention of the dental community and is a challenge for the cooperation with other medical specialities.
The advantages, limitations and potential applications of available methods for studying erosion of enamel and dentine are reviewed. Special emphasis is placed on the influence of histological differences between the dental hard tissue and the stage of the erosive lesion. No method is suitable for all stages of the lesion. Factors determining the applicability of the methods are: surface condition of the specimen, type of the experimental model, nature of the lesion, need for longitudinal measurements and type of outcome. The most suitable and most widely used methods are: chemical analyses of mineral release and enamel surface hardness for early erosion, and surface profilometry and microradiography for advanced erosion. Morphological changes in eroded dental tissue have usually been characterised by scanning electron microscopy. Novel methods have also been used, but little is known of their potential and limitations. Therefore, there is a need for their further development, evaluation, consolidation and, in particular, validation.
The aim of the study was to evaluate the relevance of cations in different fluoride compounds for their effectiveness as anti-erosive agents. Human enamel samples underwent a de- and re-mineralisation procedure for 10 days. Erosive demineralisation was performed with 0.05 Mcitric acid (pH 2.3) 6 × 2 min daily followed by immersion in the test solution 6 × 2 min each. Test solutions were: SnCl2 (815 ppm Sn; pH 2.6), NaF (250 ppm F; pH 3.5), SnF2 (250 ppm F, 809 ppm Sn; pH 3.5), amine fluoride (AmF, 250 ppm F; pH 3.5), AmF/NaF (250 ppm F; pH 4.3), and AmF/SnF2 (250 ppm F, 390 ppm Sn; pH 4.2). In the control group no fluoridation was performed. Mineral content was monitored by longitudinal microradiography. Finally, scanning electron microscopy was performed. The highest erosive mineral loss was found in the control group (48.0 ± 17.1 µm). Mineral loss was nearly completely inhibited by AmF/SnF2 (5.7 ± 25.1 µm; p ≤ 0.001) and SnF2 (–3.8 ± 14.4 µm; p ≤ 0.001) treatments. Groups treated with SnCl2 (17.6 ± 19.5 µm; p ≤ 0.001) and NaF (13.2 ± 21.7 µm; p ≤ 0.001) showed a decrease in erosive mineral loss, AmF (41.6 ± 16.0 µm) and AmF/NaF (27.7 ± 28.4 µm) had no significant effect on erosion progression. The results indicate considerable differences between the fluoride compounds tested. Treatment with solutions containing SnF2 was most effective.
Tin-containing fluoride solutions can reduce erosive tissue loss, but the effects of the reaction between tin and enamel are still not clear. During a 10-d period, enamel specimens were cyclically demineralized (0.05 M citric acid, pH 2.3, 6 x 5 min d(-1)) and remineralized (between the demineralization cycles and overnight). In the negative-control group, no further treatment was performed. Three groups were treated (2 x 2 min d(-1)) with tin-containing fluoride solutions (400, 1,400 or 2,100 ppm Sn2+, all 1,500 ppm F-, pH 4.5). Three additional groups were treated with test solutions twice daily, but without demineralization. Tissue loss was determined profilometrically. Energy-dispersive X-ray spectroscopy was used to measure the tin content on and within three layers (10 mum each) beneath the surface. In addition, scanning electron microscopy was conducted. All test preparations significantly reduced tissue loss. Deposition of tin on surfaces was higher without erosion than with erosion, but no incorporation of tin into enamel was found without demineralization. Under erosive conditions, both highly concentrated solutions led to the incorporation of tin up to a depth of 20 mum; the less-concentrated solution led to small amounts of tin in the outer 10 mum. The efficacy of tin-containing solutions seems to depend mainly on the incorporation of tin into enamel.
New toothpastes with anti-erosion claims are marketed, but little is known about their effectiveness. This study investigates these products in comparison with various conventional NaF toothpastes and tin-containing products with respect to their erosion protection/abrasion prevention properties. In experiment 1, samples were demineralised (10 days, 6 × 2 min/day; citric acid, pH 2.4), exposed to toothpaste slurries (2 × 2 min/day) and intermittently stored in a mineral salt solution. In experiment 2, samples were additionally brushed for 15 s during the slurry immersion time. Study products were 8 conventional NaF toothpastes (1,400–1,490 ppm F), 4 formulations with anti-erosion claims (2 F toothpastes: NaF + KNO3 and NaF + hydroxyapatite; and 2 F-free toothpastes: zinc-carbonate-hydroxyapatite, and chitosan) and 2 Sn-containing products (toothpaste: 3,436 ppm Sn, 1,450 ppm F as SnF2/NaF; gel: 970 ppm F, 3,030 ppm Sn as SnF2). A mouth rinse (500 ppm F as AmF/NaF, 800 ppm Sn as SnCl2) was the positive control. Tissue loss was quantified profilometrically. In experiment 1, most NaF toothpastes and 1 F-free formulation reduced tissue loss significantly (between 19 and 42%); the Sn-containing formulations were the most effective (toothpaste and gel 55 and 78% reduction, respectively). In experiment 2, only 4 NaF toothpastes revealed significant effects compared to the F-free control (reduction between 29 and 37%); the F-free special preparations and the Sn toothpaste had no significant effect. The Sn gel (reduction 75%) revealed the best result. Conventional NaF toothpastes reduced the erosive tissue loss, but had limited efficacy regarding the prevention of brushing abrasion. The special formulations were not superior, or were even less effective.
Professional recommendations for individual oral hygiene mostly include tooth brushing at least twice daily for 2-3 min with gentle force using the Bass technique or modifications of it. This study evaluated whether habitual tooth brushing actually meets these standards. Uninstructed adults (n = 103; mean age 31 +/- 6 years; 61 female, 42 male) with habitual manual tooth brushing were given a self-administered questionnaire about the frequency of brushing and a computer system recorded their brushing technique, duration and force. The majority (79.6%) of participants brushed twice daily. The mean brushing duration was 96.6 +/- 36.0 s, the mean brushing force was 2.3 +/- 0.7 N (max. 4.1 N), and no significant differences were found for quadrants. Most subjects (73.8%) brushed with circling, 8.7% with horizontal/scrubbing, 13.6% with horizontal/circling and 3.9% with vertical/sweeping movements. Modified Bass technique was not observed. When appropriate brushing habits were defined as brushing at least twice daily for 120 s with a brushing force of less than 3 N and with circling or vertical sweeping movements, only 25.2% of the participants fulfilled all criteria, emphasising the ongoing need for oral hygiene education.
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