Analysis of Destruction Mechanisms of Dental Biofilm by Laser and Its Clinical Application

激光破坏牙齿生物膜的机制分析及临床应用

• 批准号: 12557196
• 负责人: KOSEKI Takeyoshi
• 金额: $ 6.4万
• 依托单位: Tohoku University (2002)Kyushu Dental College (2001)National Institute of Infectious Diseases (2000)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2000
• 资助国家: 日本
• 起止时间: 2000 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-12557196/
• 关键词: Laser; Dental Biofilm; Periodontitis; Dental Plaque; Calculus; Fluorescence; バイオフィルム

Dental plaque is the most important etiologic agent of two major dental diseases, dental caries and periodontal diseases. This consists of bacterial cells and their extracellular products and forms the microbial biofilm which adheres sticky to the tooth surfaces. Dental plaque is divided to two parts according to the location to the gingival margin, supragingival plaque and subgingival plaque. Supragingival plaque is easy to remove and to control by toothbrushes expect which is located in interdental area. Subgingival plaque is located inside the periodontal pockets and is difficult to remove completely without visual observation. In the clinics, dental calculus is also major target to eliminate from the tooth surfaces because their rough surfaces are possible retainers of a significant amount of dental plaque. To destroy and to remove dental biofilm and calculus from tooth surfaces completely, we analyzed the physiological resistance of microbial viability of the dental biofilm against the chemical reagents and physiological stresses. We established the assessment method of dental biofilm model to analyze the bactericidal efficiency of various debridement methods. Next, we analyzed the detection method of subgingival calculus by using autofluorescence properties of dental hard tissues. We found subgingival calculus and dentine caries showed characteristic autofluorescence excited by laser irritation, but sound dentine and enamel did not. This method provides us the new diagnosis device for diseased root surfaces without direct visualization. Understanding the physiological properties of dental plaque and calculus, we would established the easy, safe and effective method for tooth cleaning and debridement, to prevent the oral diseases, especially for elderly people who need to care for daily life.

牙菌斑是龋齿和牙周病两大口腔疾病最重要的病因。它由细菌细胞和它们的细胞外产物组成，形成粘在牙齿表面的微生物生物膜。牙菌斑根据离牙龈边缘的位置分为龈上菌斑和龈下菌斑两部分。龈上菌斑除位于牙间区外，较容易用牙刷清除和控制。龈下菌斑位于牙周袋内，不经肉眼观察很难完全清除。在诊所中，牙结石也是牙齿表面清除的主要目标，因为它们粗糙的表面可能是大量牙菌斑的固定物。为了彻底破坏和清除牙表面的牙生物膜和牙石，我们分析了牙生物膜微生物活力对化学试剂和生理应激的生理抵抗力。建立口腔生物膜模型评价方法，分析各种清创方法的杀菌效果。接下来，我们分析了利用牙硬组织自身荧光特性检测龈下结石的方法。我们发现牙龈下结石和牙本质龋在激光刺激下表现出特征性的自身荧光，而正常的牙本质和牙釉质则没有。该方法提供了一种无需直接可视化的根面病变诊断新方法。了解牙菌斑和牙石的生理特性，建立简单、安全、有效的牙齿清洁和清创方法，预防口腔疾病的发生，尤其适用于需要自理生活的老年人。

项目成果

Sato T, Koseki T, Yamato K, Saiki K, Konishi K, Yoshikawa M, Ishikawa I, Nishihara T.: "p53-independent expression of p21^<CIP1/WAF1> in plasmacytic cells during G_2 cell cycle arrest induced by Actinobacillus actinomycetemcomitans cytolethal distending t

Sato T、Koseki T、Yamato K、Saiki K、Konishi K、Yoshikawa M、Ishikawa I、Nishihara T.：“Actinobacillus actinomycetemcomitans 诱导的 G_2 细胞周期停滞期间，浆细胞中 p21^<CIP1/WAF1> 的 p53 独立表达

Nakahara T, Tominaga K, Koseki T, Yamamoto M, Yamato K, Fukuda J, Nishihara T.: "Growth/differentiation factor-5 induces growth arrest and apoptosis in mouse B lineage cells with modulation by Smad"Cell Signal. 15(2). 181-187 (2003)

Nakahara T、Tominaga K、Koseki T、Yamamoto M、Yamato K、Fukuda J、Nishihara T.：“生长/分化因子-5 在 Smad 的调节下诱导小鼠 B 谱系细胞生长停滞和凋亡”细胞信号。

Sato, T., et al.: "p53-independent expression of p21 (CIP1/WAF1) in plasmacytic cells during G(2) cell cycle arrest induced by Actinobacillus actinomycetemcomitans cytolethal distending toxin"Infection and Immunity. 70. 534-582 (2002)

Sato, T., et al.：“在放线杆菌伴放线菌细胞致死膨胀毒素诱导的 G(2) 细胞周期停滞期间，浆细胞中 p21 (CIP1/WAF1) 的 p53 独立表达”感染和免疫。

Yamato, K. et al.: "Activation of the p21^<CIP1/WAF1> promoter by bone morphogenetic protein-2 in mouse B lineage cells"Oncogene. 20. 4383-4392 (2001)

Yamato, K. 等人：“小鼠 B 谱系细胞中骨形态发生蛋白 2 激活 p21^<CIP1/WAF1> 启动子”癌基因。

Yamato,K., et al: "Dissociation of bone morphogenetic protein-mediated growth arrest and apoptosis of mouse B cells by HPV-16 E6/7"Experimenal Cell Research. 257. 198-205 (2000)

Yamato,K. 等人：“HPV-16 E6/7 解离骨形态发生蛋白介导的小鼠 B 细胞生长停滞和凋亡”实验细胞研究。