| Summary: | 碩士 === 國立嘉義大學 === 生化科技學系研究所 === 100 === Tooth decay account for 54.1% of patients with oral diseases; those affected by sensitive teeth account for 25% and dental calculus account for 23%. Plaque is the main cause factor. Tooth decay starts with plaque - a thin, sticky substance that forms naturally on all teeth. Plaque contains bacteria which react with sugars and starches present in our daily diet to form acid substances that are harmful to teeth. If plaque isn’t regularly removed, it will attach to teeth. The plaque bacteria produce acid substance, which will enrode tooth's protective enamel surface. Eventually, acid erodes the soft layer of the tooth resulting in holes or cavities.
The formation of dental caries is a dynamic process. Demineralization and remineralization have a crucial impact on the hardness and strength of tooth enamel. Healthy tooth dependents upon the balance between demineralization and remineralization. Acid oral environment which is undersaturated with mineral ions, relative to a tooth’s mineral content will cause demineralization. The enamel crystal, which consists of carbonated apatite, is dissolved by organic acids (lactic and acetic) that are produced by the cellular action of plaque bacteria in the presence of dietary carbohydrates. Remineralization allows the subsequent loss of calcium, phosphate, and fluoride ions to be replaced by fluorapatite crystals.
Dental caries are dangerous and can cause extreme illness when it other vital organs are affected. Tooth infection can affect major organs such as heart and brain. Also, it can affects every other organ when the infection is in the blood. In extreme cases, the untreated infection can eventually lead to death. Literature indicates that dental caries induced endotoxemia elevates level of serum pro-inflammatory cytokines such as interleukin-1 beta 、 tumor necrosis factor-alpha. ICAM-1 (Intracellular Cell Adhesion Molecule-1)、VCAM-1 (Vascular Cell Adhesion Molecule-1)、COX-2， Interleukin EX. IL-1、IL-8 expression. Under the decay condition, the gum tissue usually produces inflammation. However, it remains unknown whether tooth decay bacteria invasion of human gingival fibroblasts (HGF) is related to inflammation inducement.
The purpose of the study is to investigate the level of inflammation after tooth decay bacteria invade HGF causing expression of inflammatory factor cyclooxygenase -2 (COX-2). We use dental caries plaque clinical samples which were taken from 21 patients of the bacteria number with MOI = 20 (OD660 = 1 is equivalent to 1 ×109) to invade HGF cell to explore the level of toxicity. The results showed that the number 3 and 5 patients with dental caries plaque invasivity is low, and the number 8 and 11 patients with dental caries plaque invasivity is hight. Therefore, this study will further explore the invasive toxicity discrepancy between these four patients and COX-2、IL-1、IL-8、VCAM、ICAM performance expression.
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