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Notes: Abstract. Home-use studies on dentine hypersensitivity have most commonly involved toothpastes and rarely have mouthrinses been employed. Potassium and/or fluoride toothpastes have been shown effective in the treatment of dentine hypersensitivity The aim of this study was to evaluate the effectiveness of a total formulation, containing potassium citrate, sodium fluoride, cetylpyridinium chloride mouthrinse compared to the base rinse minus actives in the reduction of dentine hypersensitivity. The study was a randomised placebo controlled, double blind parallel design. At a screening visit, 90 adult subjects were recruited who were suffering from dentine hypersensitivity from at least 1 tooth responding to tactile stimulation (45gm pressure) and had at least 2 teeth responding to evaporative stimulation (air blast). During a washout period of 28 days and throughout the 56-day study period, subjects used a soft filament toothbrush and standard fluoride toothpaste. At baseline (day 1), threshold sensitivities to incremental tactile (10 g to 70 g) and evaporative stimuli were determined. Gingival health was assessed by recording bleeding on probing at 25 g pressure at mesiobuccal and lingual sites. Plaque scores from buccal and lingual surfaces of disclosed teeth were also measured. Subjects then used the prescribed rinse. 10 ml for at least 30 s after brushing 2× per day returning on days 28 and 56 for rescoring of sensitivity, gingivitis and plaque. Data from 88 subjects were used with the intent to treat analyses and 83 in the completely evaluable analyses. Groups were well balanced for demographic data and product returns suggested good compliance. Both groups showed highly significant improvements in tooth sensitivity. The pattern was for greater improvement in the test compared to the control group (statistically significant for the plaque score), whereas bleeding scores, already low, showed no change in either group. By definition, the placebo rinse could not have exerted any therapeutic action; the study therefore provides clear direct evidence as to the magnitude (30%-40%) of the little studied, but assumed, placebo response in dentine hypersensitivity trials.

Notes: Abstract A considerable number of varied agents are apparently effective in the treatment of dentine hypersensitivity. In particular, the literature supports the efficacy of strontium, potassium and fluoride containing toothpastes. This study was a double-blind, randomised, parallel group comparison of three products, namely strontium- and potassium-based desensitising toothpastes both containing fluoride, and a conventional fluoride toothpaste. A total of 131 subjects entered a 4-week wash-in phase using the conventional fluoride toothpaste, of whom 120 entered a 6-week treatment phase. Sensitive teeth were evaluated at wash-in baseline, treatment baseline and after 2 and 6 weeks use of the treatment pastes. Dentine hypersensitivity was assessed with tactile and cold air stimuli together with an overall subjective assessment. Analysis of the findings was performed using non-parametric statistical methods. Of the original 120 subjects, 112 completed the trial. All 3 toothpaste groups showed reductions in sensitivity over the 6 weeks; however, no significant differences were found between the three products at any given time. Interestingly, there was no significant change in sensitivity between wash-in baseline and treatment baseline for the cold air stimulus with the fluoride-only-based paste. However, for the group using the same fluoride toothpaste, there was significant improvement between wash-in baseline and week 6, and treatment baseline and week 6 for this stimulus, suggesting a substantial placebo effect occurred. There is a need for further investigation of a wash-in period and examination of the placebo effect when evaluating dentine hypersensitivity trials.

Notes: summary  Fluoride is known to reduce enamel solubility during the caries process. The aim of this investigation was to determine whether fluoride preparations affect erosion attributed to citric acid and citric acid-based soft drinks. Flat enamel specimens embedded in epoxy resin were prepared from caries free, human third molar teeth extracted from patients aged 18–35 years. Specimens were polished to have a profile within a tolerance of ±0·3 μm measured on a profilometer. Specimens were taped to leave a 2 mm window of exposed enamel. Groups of specimens were exposed to citric acid and soft drinks with and without the addition of sodium fluoride or exposed to the same solutions after pre-treatment with fluoride products. Enamel loss was measured by profilometer after 10, 20 and 30 min of acid exposure. The different acidic solutions varied significantly in the amount of erosion produced both with and without the addition of fluoride. In addition, the different fluoride products differed significantly in the protective effect afforded. Both fluoride application methods reduced in mean terms, enamel erosion at all time points and by all acidic solutions. The majority of differences were 〈25% and as the study was powered to show differences as significant at or above this level few reached statistical significance. Fluoride applied to enamel either in acidic solutions or as a pre-treatment, reduces enamel erosion; however, the actual clinical benefit appears low. More studies are required, including investigations in situ.

Notes: The reported incidence of tooth erosion caused by acidic soft drinks has been increasingly documented. Citric and phosphoric acids are the two main dietary acids present in these soft drinks. Many variables need to be determined in order to assess risk factors for dental erosion caused by beverage consumption including pH, titratable acidity, pKa, buffering capacity, hence the aim of these in vitro investigations. Methodologies included profiling flat enamel and dentine samples (〈 ± 0·3 μm profile) from unerupted human third molars. Groups of five specimens were placed in acidic solutions adjusted with alkali over the available pH range; citric, phosphoric and hydrochloric acid were adjusted with sodium hydroxide and citric acid with trisodium citrate. Tissue loss was calculated by profilometry. Results showed that under these conditions citric acid caused far more erosion over the pH range employed than phosphoric acid for both tissue types. Citric acid compared with hydrochloric acid highlighted dissolution and chelation effects. Phosphoric acid caused minimal erosion over pH 3 for enamel and pH 4 for dentine. These factors could be considered in order to reduce the erosivity of acidic soft drinks.

Notes: Dentine exhibiting symptoms of dentine hypersensitivity has tubules open at the dentine surface and patent to the pulp. The mechanisms whereby dentinal tubules are exposed is ill understood but probably involves a variety of abrasive and/or erosive agents. This study in vitro examined the quantitative and qualitative effects of toothpastes, their solid and liquid phases and detergents on dentine and acrylic. Abrasion of dentine and acrylic were measured by surfometry. Morphological changes to dentine were assessed by scanning electron microscopy. Abrasion of dentine and acrylic by toothpastes increased with increasing brushstrokes with marked differences in the extent of abrasion between different pastes. Brushing dentine with water or detergents produced progressive abrasion but which appeared to plateau around 2 μm loss. Water and detergents produced minimal effects on acrylic. At 5000 strokes dentine abrasion by solid phases was less than the parent toothpastes but the ranking order of abrasivity was the same as the parent toothpastes. Loss of dentine produced by liquid phases was minimal and in the order of 1–2 μm. Observationally, all toothpastes removed at least the dentine smear layer to expose many tubules; with one desensitizing product leaving a particulate deposit occluding most tubules. The solid phases of the toothpaste produced identical morphological changes to the parent paste. The liquid phases and detergents all exposed dentinal tubules by 5000 strokes. Water had little or no effect on the dentine smear layer. It is concluded that toothpastes, solid phase, liquid phase and detergents have the potential to abrade or erode dentine to a variable degree and result in tubule exposure. The effects of the liquid phases and detergents appear limited to the removal of the smear layer. Such detrimental effects seen in vitro could have relevance to the aetiology and management of dentine hypersensitivity. Toothpaste formulations which despite exposing tubules have ingredients capable of occluding tubules may be an area of development for such products.

Notes: Although many people have exposed dentine, only a percentage exhibit symptoms of dentine hypersensitivity. This has been ascribed to opening and closing of the dentinal tubules by for example, smear layer changes or tubular occlusion. The aims of this study were to examine the surface morphological changes of etched and unetched dentine in vitro, attributed to the effects of toothbrushing with and without toothpastes designed for the alleviation of dentine hypersensitivity. A total of 96 etched and 96 unetched human dentine specimens were brushed with various toothpastes and water for 1, 2, 5 or 10-min periods in a toothbrushing machine and subsequently examined under scanning electron microscopy for surface changes. Analyses of brushed etched specimens demonstrated that time and treatment were significant variables (P 〈 0·05) for tubule occlusion. Further, the interaction between time and treatment was significant (P 〈 0·05). The artificial silica based paste was significantly better for all time intervals at occluding the dentine tubules. All toothpastes investigated caused dynamic changes to the smear layer of the unetched dentine, opening tubules. However, the artificial silica based paste resulted in occluded rather than patent tubules. All of the pastes evaluated had the capacity to remove the smear layer but some could then occlude tubules through the contained abrasives.

Notes: Sales of soft drinks has been increasing by 56% over the last 10 years and are estimated to keep rising at about 2–3% a year. Further, the reported incidence of tooth erosion has been increasingly documented. Whilst these factors could well be linked, many individuals with erosive diets are not presenting with erosion. This would suggest the effects of many variables, hence the aim of these investigations. Methodologies included preparing enamel and dentine samples from unerupted human third molars. Groups of five specimens were placed in citric acid over a temperature range of 5–60 °C for 10-min exposures; placed in citric, lactic, malic or phosphoric acid (0·05, 0·1, 0·5, and 1% (w/v)) for 10-min exposures; and placed in the same three organic hydroxy acids at 0·3% (w/v) or phosphoric acid at 0·1% (w/v) for 3×10-min exposures. Tissue loss was determined by profilometry. Results showed that increasing temperature, concentration and exposure time increased the erosion of dentine and enamel. This study has shown that under highly controlled conditions, erosion of dentine and enamel by dietary acids can be greatly influenced in vitro by temperature, concentration, type of acid and exposure time. These factors could be employed in order to reduce the erosivity of soft acidic drinks.

Notes: Epidermolysis bullosa simplex (EBS) is a blistering skin disease caused in most cases by mis-sense mutations in genes encoding the basal epidermal keratin (K) 5 and K14. The inheritance is usually autosomal dominant and the mutant keratin proteins appear to exert a dominant negative effect on the keratin intermediate filament cytoskeleton in basal keratinocytes. We report a child with a homozygous K14 mutation resulting in the complete absence of K14 protein in the epidermis; remarkably, he only had mild to moderate disease. Electron microscopy of a skin biopsy showed a marked reduction in numbers of keratin intermediate filaments in the basal keratinocytes. Immunofluorescence microscopy using monoclonal antibody LL001 against K14 showed no staining, suggesting a functional knockout of K14. Sequence analysis of genomic DNA revealed a homozygous mutation in codon 31 of K14 that resulted in a premature stop codon further downstream in exon 1. The child's mother, who is unaffected by the disease, is heterozygous for the mutation. The consanguineous father was unaffected and unavailable for testing. The resulting mRNA is predicted to encode a protein of 116 amino acids, of which the first 30 are identical to the normal K14 sequence, and the remaining 86 residues are mis-sense sequence. Four previously reported cases of autosomal recessive EBS with functional knockout of K14 were severely affected by blistering, in contrast to our patient in whom the predicted protein has only the first 30 amino acids of K14 and is therefore the closest to a true knockout of K14 protein yet identified.