Thesis (Ph. D.)--University of Wisconsin--Madison, 1961. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (doctoral)--Universität Hamburg, 1979.

Thesis (Ph. D.)--University of Manitoba, 1971. / Typescript (Photocopy). Includes bibliographical references (leaves [176]-190).

Thesis (Ph. D.)--University of Manitoba, 1971. / Typescript (Photocopy). Includes bibliographical references (leaves [176]-190).

Indiana University-Purdue University Indianapolis (IUPUI) / Reports differ concerning the cariogenic potential of milk. Some authors indicate that plain milk can cause dental caries, while others believe that the disease results from adding carbohydrates to the milk. Still others suggest that milk has a protective effect and may contribute to caries prevention. The present study investigated the capability of human milk, plain bovine milk, a milk formula, and milk with honey to produce caries-like lesions in an environment which simulated the oral cavity. Four groups of eight sound bicuspids each, which had been extracted for orthodontic reasons, were mounted in a mouth simulator. The teeth and complete apparatus were sterilized with ethylene oxide. The teeth were then inoculated with human saliva and covered with linen cloth to facilitate bacterial colonization. Each day the various groups of study teeth were exposed to one of the four milk solutions during a 2, 4, or 8-hour period. After each period, a sterile chemical solution simulating human saliva was dropped (8-12 ml/hr) over the cloth to provide a mouth-like environment. A control group was not exposed to a milk preparation. The results indicate that after six weeks, all milk solution groups showed unequivocal signs of decalcification, with an intensity proportional to the period of exposure to the study solutions. Plain bovine milk produced the least decalcification, followed in order by milk formula, human milk, and milk and honey. It can be inferred, from these results, that milk itself, without addition of extra carbohydrates, has the potential to produce dental caries if left stagnant over the tooth surfaces for a sufficient time.

There are a number of unanswered questions regarding new caries preventive methods such as ozone treatment as well as novel caries detection methods that monitor and evaluate these preventive methods. This thesis seeks answers to some of these questions. Aims: Paper I investigates the in vitro sealing capacity of a novel ozone delivery system and its re-suction capacity. Paper II studies the in vitro antibacterial effect of ozone on cariogenic bacterial species with and without the presence of saliva and its possible effect on the saliva proteins. Paper III assesses the in vitro validity of laser-induced fluorescence (LF) measurements, visual inspection (colour), and tactile examination (surface texture) on root caries lesions and correlates these with histopathological measurements of lesion depths.  In addition, Paper III investigates how inter-device, inter-examiner, and intra-examiner levels influence LF reading agreements and whether lesion colour and surface texture influences LF readings. Paper IV evaluates the in vivo effect of ozone and fluoride varnish treatments on occlusal caries in primary molars. Material and methods: Paper I: Full ozone application cycles, including the re-suction period, and interrupted cycles with displacement of the cup during the delivery cycle were studied using an ozone air analyser. Paper II: Ozone gas was exposed to the bacteria in the solution’s buffer and saliva via a tube connected to the ozone generator for 10, 30, and 60 seconds. Paper III: Calibrated examiners assessed lesion colour and surface texture and performed measurements with two LF devices for three separate one-week intervals.  Sections (300µm thick) of 64 out of 93 teeth were obtained and examined under a microscope. Lesion depth was assessed with two references: from the delineated borderline of the original exposed root surface (ref I) or, if loss of surface continuity, the absolute lesion depth (ref II). Paper IV: The split mouth study was conducted in two parts. The participants in part A were children (mean age 4.8 years) with medium-high caries risk. Inclusion criteria were bilateral matched pairs of cavitated or non-cavitated occlusal lesions in primary molars (Ekstrand index score ≤ 3). Children in part B (mean age 4.5 years) with low-medium caries risk had pairs of non-cavitated lesions only (Ekstrand index score ≤ 2a). The assessments and treatments with ozone and fluoride varnish were performed at baseline and at three, six, and nine months. At the 12-month follow-up, only assessments were performed. Results: Paper I: Ozone leakage levels varied between 5.2 and 9.8 µg/m3. Paper II: In the salt buffer, 92%, 73%, and 64% of the initial numbers of A. naeslundii, S. mutans, and L. casei, respectively, were killed after 10 s ozone exposure and approximately 99.9% of the bacteria were dead after a 60 s exposure. After 10 and 30 s but not after 60 s exposure to ozone, S. mutans and L. casei were less efficiently killed in saliva compared to in the salt buffer. Various saliva proteins were degraded by ozone after the 60 s exposure. Paper III: The correlation between LF readings and histological depth was low with values ranging from 0.22 (p ˃ 0.05) to 0.31 (p < 0.05). The LF devices were significantly correlated with discolouration and with a surface texture denoted as hard. A significant correlation was found between colour and histological depth. No significant correlation was found between surface texture and histological depth. The reliability, evaluated as intra-class correlation coefficient, was 0.99 for intra-examiner, 0.97 for inter-examiner, and 0.98 inter-device level. Large differences were found between two consecutive measurements and high measurement errors indicated considerable deviation of individual measurements.Paper IV: In the first 15 pairs of part A, eight lesions treated with ozone and nine treated with fluoride, including all cavitated lesions, progressed to failure, i.e., required operative treatment during the study time. Due to non-acceptable results, the sample collection was discontinued because of ethical reasons. In part B, of 35 pairs, one of the ozone treated lesions failed at 12 months. A small shift towards increased VI scores was recorded for both ozone and fluoride lesions in this second part. Conclusions: - The ozone delivery system can be considered a safe system with low leakage levels in air, also with accidental displacements. - The cariogenic species S. mutans, L. casei, and A. naeslundii were sensitive to ozone gas treatment. The presence of saliva hampered the antibacterial effect of ozone. A low correlation between the LF readings and the histopathological depth of root caries lesions was shown. The LF device was found not to be appropriate for application to root caries diagnosis. - Neither ozone nor fluoride varnish treatments arrested the progression of cavitated occlusal caries lesions. In low and medium caries risk children non-cavitated occlusal lesions remained mainly unchanged during the study period.  No difference in the effect of ozone and fluoride varnish treatments on occlusal caries in primary molars was seen.

Thesis (doctoral)--University of Göteborg, 1993. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (doctoral)--University of Göteborg, 1993. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1957. / Typescript. Abstracted in Dissertation abstracts, v. 17 (1957) no. 10, p. 2146-2147. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Abstract High-sucrose diet and metabolic acidosis have some similar effects on bone and they both reduce the formation of dentine. This series of experiments was conducted in order to get information about the effects of acidosis and alkalosis on dentine during primary dentinogenesis and also to ascertain if high-sucrose diet affects dentine formation via acidosis. Chronic metabolic acidosis (0.25 mol/L of NH4Cl in drinking water), chronic metabolic alkalosis (0.25 mol/L of NaHCO3 in drinking water) and chronic respiratory alkalosis (atmospheric pressure equivalent to an altitude of 3000 m) were induced in the rats immediately after weaning for 6 and 7 weeks. One subgroup from each of the main groups was fed a high-sucrose (43%) diet and one a standard maintenance diet, each ad libitum. The control groups had the same diets, but normal drinking water and atmospheric pressure. All the rats were injected with tetracycline (to mark the onset of the experiment in dentine) and inoculated orally with Streptococcus sobrinus. The acid-base status was verified by blood gas analysis at the end of the experiments. After sacrifice, fissure caries was scored with Schiff reagent and the areas of dentinal lesions and tetracycline-marked new dentine were measured from sagittally sectioned mandibular molars. The mineral elements (Ca, Mg, F, Na, P and total mineral contents) of the dentine formed before and during the experiment were measured with an electron probe microanalyzer. With the high-sucrose diet, respiratory alkalosis and metabolic acidosis promoted the initiation and progression of caries while metabolic alkalosis slightly retarded it. With the standard diet, all the experimental conditions slowed the rate of dentine formation and metabolic acidosis had the most pronounced effect. The mineral analysis revealed a totally different pattern of mineralization when the rats with metabolic acidosis (increased calcium and total mineral content) were compared to the previously reported rats with a high-sucrose diet (decreased calcium and total mineral content). Besides this, metabolic alkalosis did not correct the effects of the dietary sucrose on dentine formation and blood gas analysis showed no acid-base disturbances in the sucrose diet group. Therefore, a high amount of sucrose in the diet slows the rate of dentine formation and reduces the ability of teeth to resist caries attack by mechanisms different from those of metabolic acidosis. Nevertheless, metabolic acidosis was found to be the most harmful state of disturbance in acid-base balance for the teeth of young rats, especially with a diet containing a high amount of sucrose.