Identification of disease-susceptibility genes related to congenital missing or supernumerary tooth.

鉴定与先天性缺失或多生牙相关的疾病易感基因。

• 批准号: 15592158
• 负责人: MATSUMOTO Yoshiro
• 金额: $ 1.98万
• 依托单位: Tokyo Medical and Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2003
• 资助国家: 日本
• 起止时间: 2003 至 2004
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15592158/
• 关键词: supernumerary tooth; congenital missing; anomaly in tooth number; environmental factors; mechanical stress; 遺伝子; 罹患同胞対連鎖解析; 歯の移動; 歯根吸収; 開咬; 咬合機能低下; 咬合接触; ミニインプラント

For affected sib-pair analysis and SNPs related analysis, we selected and diagnosed patients with anomaly in tooth number such as supernumerary tooth or congenital missing, especially affected sib-pair, their consanguinities and normal control people. Affected sib-pair analysis was performed by gene typing concerned with chromosomes using samples of patients bloods and a fluorescence-labeled gene marker kit. But we could not identify the disease-susceptibility genes related to congenital missing or supernumerary tooth.Then we adopted the mechanical stress one of which environmental factors contrasted to hereditary factors. In order to clarify the biological response to the mechanical stimuli, we investigated using the molecular biological analysis in vivo and in vitro. When the occlusal stimuli were reduced in rats, the expression of IL-1 mRNA was increased in their hypofunctional periodontium using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Furthermore, the expression of IL-1 mRNA was increased after the mechanical stimuli were adopted to their molars. Mechanical tensional stress of low magnitude to the bovine periodontal ligament cells on the flexible bottomed culture plate induced the increase of both type I collagen and decorin mRNA expression without changing alkaline phosphatase (ALP) activity in periodontal ligament cells. Mechanical tensional stress of low magnitude to the stromal cell line (ST2) induced the increase of Cbfa1/Runx2 mRNA expression and ALP activity without changing type I collagen mRNA expression.These results suggest the possibility that environmental factors such as mechanical stimuli might induce anomaly in tooth number.

对多生牙、先天缺失等牙数异常患者，特别是受影响同胞及其血缘关系和正常对照人群进行受累同胞配对分析和SNPs相关分析。通过使用患者血液样本和荧光标记的基因标记试剂盒进行与染色体有关的基因分型，进行受影响的同胞对分析。但我们无法确定与先天性缺牙或多生牙相关的疾病易感基因，于是我们采用了机械应力，其中环境因素与遗传因素进行了对比。为了阐明生物对机械刺激的反应，我们利用体内和体外的分子生物学分析进行了研究。半定量逆转录聚合酶链式反应(RT-PCR)结果显示，当咬合刺激减少时，IL-1mRNA在功能低下的牙周组织中的表达增加。此外，对磨牙施加机械刺激后，IL-1mRNA的表达增加。在柔性底培养板上对牛牙周膜细胞施加低幅度的机械张应力，可诱导牙周膜细胞I型胶原和核心蛋白聚糖的表达增加，但不改变碱性磷酸酶(ALP)的活性。对基质细胞系(ST2)施加低幅度的机械张应力后，Cbfa1/Runx2基因表达增加，碱性磷酸酶(ALP)活性升高，而I型胶原基因表达无明显变化，提示机械刺激等环境因素可能导致牙数异常。

项目成果

Modulation of extracellular matrix synthesis and alkaline phosphatase activity of periodontal ligament cells by mechanical stress

• DOI: 10.1111/j.1600-0765.2004.00782.x
• 发表时间: 2005-04-01
• 期刊: JOURNAL OF PERIODONTAL RESEARCH
• 影响因子: 3.5
• 作者: Ozaki, S;Kaneko, S;Soma, K
• 通讯作者: Soma, K

Duration of Orthodontic Force Affecting Initial Response of Nitric Oxide Synthase in Rat Periodontal Ligaments.

正畸力的持续时间影响大鼠牙周膜中一氧化氮合酶的初始反应。

• 发表时间: 2004
• 期刊: J Med Dent Sci 51(1)
• 作者: 富沢美惠子;M.Tomizawa;富沢美惠子;Koike M;Ozaki S;Ozaki S;Koike M;Watarai H;Yoo SK
• 通讯作者: Yoo SK

Age-Related Changes and Possible Adaptability of Rat Jaw Muscle Spindles.

大鼠颌肌纺锤体的年龄相关变化和可能的适应性。

• 发表时间: 2004
• 期刊: Arch Histol Cytol 67(3)
• 作者: 富沢美惠子;M.Tomizawa;富沢美惠子;Koike M;Ozaki S;Ozaki S;Koike M;Watarai H;Yoo SK;Winarakwong L;Shibasaki K;Chung CJ;Shibasaki K;Cholasueksa P;Winarakwong L
• 通讯作者: Winarakwong L

T.Kameyama, Y.Matsumoto, H.Warita, K.Soma: "Inactive Periods of Constant Orthodontic Forces Related to Desirable Tooth Movement in Rats."Journal of Orthodontics. 30・1. 31-37 (2003)

T.Kameyama、Y.Matsumoto、H.Warita、K.Soma：“与大鼠理想牙齿运动相关的恒定正畸力的非活动期”。正畸学杂志 30・1（2003）。

Age-Related Changes and the Possible Adaptability of Rat Jaw Muscle Spindles.

年龄相关的变化和大鼠颌肌纺锤体的可能适应性。

• 发表时间: 2004
• 期刊: Arch Histol Cytol 67(3)
• 作者: 富沢美惠子;M.Tomizawa;富沢美惠子;Koike M;Ozaki S;Ozaki S;Koike M;Watarai H;Yoo SK;Winarakwong L
• 通讯作者: Winarakwong L