published_or_final_version / Dentistry / Doctoral / Doctor of Philosophy

Indiana University-Purdue University Indianapolis (IUPUI) / Objective: To investigate the effect of the size of the space between the restoration and the dentinal wall of the tooth (i.e. the dentinal portion of the gap) on the development of secondary caries. Methods: Tooth-resin-matrix composite specimens were mounted on custom-made gap-model stages. Specimens were divided into four groups (n=10). Group 1 had a uniform gap size of 30μm throughout both enamel and dentin. Group 2 had a 30μm enamel gap size with a 530μm dentinal gap. Group 3 had 525μm gaps in both enamel and dentin. Group 4 had 525μm and 1025μm gaps in enamel and dentin, respectively. Specimens were attached to plastic Petri plates, gas-sterilized and then incubated in a microbial caries model with S. mutans TH16 in (1% sucrose tryptic soy broth for 1 h, 4 times/day, and with a buffer solution for the rest of the day). After 8 days of incubation, tooth specimens were sectioned and stained with a rhodamine B solution. Digital images were taken under a confocal microscope and analyzed for lesion size at the enamel outer lesion (EOL), enamel wall lesion (EWL), dentin wall lesion next to the DEJ (DWL-A) and dentin wall lesion at 750µm from the DEJ (DWL-B). Results: No difference in EOL size was found between the groups. DWL-A and -B were larger in group 3 than groups 1and 2. Larger DWL-B was found in group 3 than group 4. Group 4 had marginally significant larger EWL than groups 1 and 2 (p=0.0652 and p=0.0648, respectively). Also, group 4 had marginally significant (p=0.0607) larger DWL-B than group 1. Conclusions: Based on the results of this study, it can be concluded that the presence of additional space at the dentinal wall area did not affect secondary caries development as long as the enamel gap was small. However, with enamel gaps of ≈500 µm, the presence of the additional gap space at the dentinal wall led to the development of smaller dentinal wall lesions at the deeper parts of the simulated cavity. Also, in uniform gaps, the size of the interface was positively correlated with size of the dentinal wall lesions.

Indiana University-Purdue University Indianapolis (IUPUI) / The impact of tobacco smoking on human health is well documented. The influence of smoking on tooth loss and cardiovascular diseases was investigated in the current study via both epidemiology and in vitro studies. From analyzing the 2006 Behavioral Risk Factor Surveillance System (2006 BRFSS) database, we confirmed that smoking was significantly associated with the number of teeth lost in a dose-dependent manner and smoking cessation reduced the risk when compared to those subjects continuing to smoke. In addition, the virulence factors related to caries were compared between Streptococcus mutans and Streptococcus gordonii in response to cigarette smoking condensate (CSC) treatment. We observed that S. gordonii was more susceptible to CSC treatment than S. mutans. CSC significantly enhanced S. mutans sucrose-dependent and independent adherence. Western blot assays revealed that several bacterial surface proteins including glucosyltransferase (GTF), glucan-binding proteins and antigen I/II, were significantly upregulated for the treated S. mutans. These findings suggested that the oral environment with CSC may favor a cariogenic dominant composition, which may increase the risk for smokers to develop caries. We also found that smoking and oral health status modified each other and synergistically increased the risk of CVD and this joint effect was more pronounced among the youngest age group using the 2006 BRFSS database. To further understand the joint effect, we conducted an in vitro study to investigate bacterial attachment to fibronectin and endothelial cells in response to smoking condensate treatment. Our study clearly demonstrated CSC significantly enhanced S. mutans attachment to both soluble and immobilized fibronectin as well as endothelial cells. Furthermore, our data suggested that bacteria possessed several adhesins that bound to host tissues and endothelial cells also had multiple receptors for bacterial attachment. Among these adhesins, antigen I/II seemed essential for bacterial attachment to endothelial cells without CSC. The knowledge of bacterial attachment to host tissues in the presence of CSC may help in developing different preventive or therapeutic strategies against attachment and colonization of the host by S. mutans.