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Dental erosion shows a typical distribution pattern within the dental arches. Tooth protection from erosion by salivary pellicle has been shown in vitro, but the hypothesis that pellicle may differ quantitatively at sites of erosion has not been investigated. This study aimed to determine the thickness of acquired salivary pellicle within the dental arches, investigate the possible relationship of this thickness to the distribution and severity of erosion within the arches, and confirm the protective effect of pellicle against dental erosion. Eight enamel blocks were produced from each of 5 bovine incisors assigned to five volunteers. Each block was further cut into 2 slabs, producing control and experimental slabs. Pellicle developed on experimental slabs located on 8 intra-oral sites after 1 hr of exposure was stained by "sheep anti-human IgGAM-FITC". Slabs were then visualized, and pellicle thickness measured, by confocal laser scanning microscopy. Eroded enamel lesions were produced in experimental and control slabs by means of pure orange juice. The degree of erosion was quantified by transverse microradiography. Pellicle thickness varied significantly within the dental arches and among individuals. An inverse relationship (r = -0.96, p < 0.001) was observed between the degree of erosion and pellicle thickness. Significant differences in erosion were observed between slabs with and those without pellicle. This study has shown that the thickness of acquired salivary pellicle varies within the dental arches, which may be responsible for the site-specificity of dental erosion, and that pellicle does protect the teeth from erosion. [ABSTRACT FROM AUTHOR]

In 2 separate studies, plaque was harvested (i) from 15 smokers and 15 non-smokers after a 48-h period without oral hygiene, and (ii) from 15 smokers and 12 non-smokers after a 48 h hygiene-free period following complete plaque removal by toothbrushing. No significant association emerged between wet weight of accumulated plaque and cigarette smoking, in either study. In the second study, the mean plaque calcium concentration was raised in smokers compared with non-smokers, and significantly raised in 7 heavy smokers relative to non-smokers. In both instances, calcium concentration was significantly raised relative to (total) phosphorus concentration, which may indicate that the additional calcium was not in mineral deposits. These results may reflect an association between calcium concentration of plaque and tobacco consumption. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the aetiological factors and the prevalence of salivary gland hypo-function (SGH) in patients complaining of xerostomia. Design: Prospective, clinical study. Setting: Xerostomia clinic in the Department of Oral Medicine at Liverpool University Dental Hospital. Subjects: 100 consecutive patients, aged 60 years or older, referred for investigation of xerostomia. Interventions: Patients were asked specific questions concerning their complaint of oral dryness and associated orofacial symptoms. A detailed medical history was recorded and patients underwent a systematic examination of the head, neck and oral structures. All patients underwent haematological, biochemical, immunological investigations, urinalysis and sialometry. Further investigations and referrals to other specialists were undertaken when appropriate. Main outcome measures: The causes of xerostomia were established on the basis of clinical and laboratory findings and SGH was defined as an unstimulated whole salivary flow rate of <0.2ml/min. Results: The causes of xerostomia were identified as: Sjögren's Syndrome (40), iatrogenic <22), psychogenic (14), idiopathic (19), diabetes (1), candidosis (3) and alcohol (1). Sixty five percent of the patients studied had SGH. Conclusions: This study has shown that 65% of patients whose presenting complaint was xerostomia had objective evidence of SGH. Several aetiological factors were identified, the most common of which was Sjögren's Syndrome. The possibility of associated systemic diseases should be considered when establishing the aetiology of SGH. [ABSTRACT FROM AUTHOR]

A wide range of different methodologies and measurement techniques has been employed in laboratories around the world for the study of de- and remineralization of enamel and dentin in intra-oral systems. These different approaches are summarized and discussed in relation to the nature of the different research questions to be studied by means of the intra-oral model. [ABSTRACT FROM PUBLISHER]

Studies of the extracellular, free concentrations of substrates, growth factors, inhibitors, and end-products of metabolism to which the intact plaque microflora is exposed in situ can assist in the understanding of factors controlling plaque pathogenicity. Information is becoming increasingly available from analysis of fluid separated by centrifugation of plaques collected at various intervals after an intra-oral pulse of dietary or experimental substrate, or different procedures or treatments having cariostatic potential. Such analytical results give more information than those obtained by analysis of aqueous or other extracts, because they yield values of substrate concentration representing those occurring at the bacterial cell surface. The largest body of information concerns extracellular levels of acid end-products of sugar catabolism in relation to food quality or sequence, and of amino acids and other products of nitrogen metabolism, in relation to studies of the detailed metabolic events of the Stephan curve, and of the demineralizing effect of the plaque environment. Areas where little information is available and which merit further study include plaque clearance of salivary and other components with anti-caries activity (e.g., antibodies, enzymes, fluorides, cations, other antimicrobial, etc.), and substrate concentrations to determine gradients for diffusion into and out of plaque. [ABSTRACT FROM AUTHOR]

The objective of the study was to determine quantitatively the effect on the potential for in situ remineralization of artificial caries-like lesions in human enamel when sugar-free gum containing mainly sorbitol as sweetener was chewed after meals and snacks. Artificial white-spot lesions were created in extracted human premolars and divided into three parts. One part was used as reference and the other two worn consecutively for two 21-day periods by 10 volunteers in a cast silver band cemented on lower molar teeth and covered with gauze to promote plaque formation. During the experimental periods the subjects used fluoridated toothpaste twice daily, and consumed three meals (breakfast, lunch, and dinner) and two snacks (selected from chocolate bar, raisins, chocolate wafer, and iced cupcake). Sorbitol gum was chewed for 20 rain immediately after each meal or snack during one of the experimental periods. The three parts of the enamel lesions were then sectioned (≏80 µm) and examined together by means of quantitative microradiography and by polarized light microscopy. All estimates of mineral content indicated that significant remineralization occurred and was approximately doubled with gum-chewing. It is suggested that sorbitol gum stimulates salivation, which is responsible for the significantly enhanced remineralization, thus contributing to a therapeutic, caries-preventive effect. Because the gum was chewed immediately after meals and snacks, inhibition of demineralization may also have occulted. [ABSTRACT FROM AUTHOR]

Following reports of increased salivary gland size and increased function, induced by increased mastication in animals, the effects of long-term, frequent gum-chewing on resting and stimulated flow rates were studied in human volunteers in separate experiments in Newcastle upon Tyne and in Toronto. In both experiments, unstimulated and stimulated saliva flow rates were measured in student volunteers at intervals of one or two weeks over a baseline period. Approximately half of the subjects were then given sugarless gum to be chewed (four pieces per day) over the experimental period; controls refrained from vigorous mastication. During (and, in Newcastle, after) the experimental period, salivary flow rates were measured at intervals, as before. In Newcastle unstimulated, but not stimulated, flow rates increased in the gum-chewing group and were still elevated (compared with controls) eight weeks following the experiment. In Toronto, the mean results showed no effect of gum-chewing, but the seven gum-chewers among the 11 subjects with low baseline flow rates (<0.3 mL/min) showed a 43% rise in unstimulated flow rate (p ∼ 0. 05). The results suggest that increased mastication, in the form of gum-chewing, can increase unstimulated flow rates, especially in those with low salivary function. In addition to short-term beneficial effects of sugarless gum, these long-term effects indicate the possibility of a beneficial effect in caries prevention. [ABSTRACT FROM AUTHOR]

The primary aim of this study was to rank several reference foods (apple drink caramel chocolate, cookie, skimmed milk powder, snack cracker, and wheat flake) according to their plaque pH response as monitored in a panel of 12 volunteers by the plaque-sampling method for comparison with data previously reported with other methods used to assess cariogenicity potential Secondary experiments (using subsets of the panel of subjects) were undertaken in an attempt to elucidate some of the reasons for the observed plaque pH changes. Oral carbohydrate retention was measured at a single time period after food use as total anthrone-positive carbohydrate material, and as specific acidogenic sugars by gas-liquid chromatography after gel-exclusion chromatography. The concentrations of acid anions in the plaque fluid after food consumption were measured by isotachophoresis eight min after food use. According to the plaque pH response, apple-flavored fruit drink and chocolate were the most acidogenic foods and skimmed milk powder the least acidogenic. There were significant correlations (p < 0.05) between the plaque pH data and lactate-plus-acetate concentrations in plaque fluid, but the correlations between the pH data and any of the carbohydrate retention parameters were not significant. [ABSTRACT FROM AUTHOR]

Evaluation of cariogenicity from evidence provided by plaque pH data may be assisted if the duration as well as the extent of the pH fall is examined. Consumption of foods in sequence may alter the pH response to individual items. [ABSTRACT FROM AUTHOR]

Plaque pH in six adult subjects was monitored while they consumed a meal containing three foods. The marked fall in plaque pH caused by drinking sugared coffee was considerably reduced by eating the two non-sugary foods (egg and crisp-bread) before, during, or after the sugared coffee. This favorable action was negated by a pause between the sugary and non-sugary courses. [ABSTRACT FROM AUTHOR]

Previous reports in the literature indicate that smoking is associated with increased plaque accumulation and/or mineralization. This might be due to an effect of tobacco smoke on properties of saliva. The present study examined the stability of components in fresh and incubated saliva in smokers and non-smokers. Saliva from smokers: collected immediately after smoking a cigarette, did not differ significantly from that of non-smokers in the turbidity developing after incubation (24 h, 37°C) which may reflect aggregation of salivary components by mechanisms analogous to those involved in plaque formation. This finding is in agreement with our previous result (Macgregor, Edgar & Greenwood 1985) which showed that the rate of plaque formation did not differ between smokers and non-smokers. Although an intimation of higher initial calcium concentrations, greater precipitation of calcium and development of more turbidity during incubation was observed in the salivas of smokers than those of non-smokers, the major reason for the greater plaque accumulation and calculus in smokers is probably inadequate oral hygiene. [ABSTRACT FROM AUTHOR]