GROWTH FACTORS AND GINGIVAL FIBROSIS

生长因子和牙龈纤维化

• 批准号: 7606224
• 负责人: PHILIP C TRACKMAN
• 金额: $ 1.39万
• 依托单位: BOSTON UNIVERSITY MEDICAL CAMPUS
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-01-03 至 2007-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7606224
• 关键词: Academic Medical Centers; Age; Apoptosis; Apoptotic; Biological Assay; Boston; Cells; Collagen; Computer Retrieval of Information on Scientific Projects Database; Control Groups; Crown Lengthening; Cyclic AMP; Dental; Dental Schools; Dinoprostone; Down-Regulation; Enrollment; Fibroblasts; Fibrosis; Funding; Genetic Transcription; Gingiva; Gingival Overgrowth; Gingivectomy; Grant; Growth Factor; Hospitals; Human; Immunohistochemistry; In Situ; Inflammation; Inherited; Institution; Measurement; Measures; Medicine; Metabolism; Methods; Microtubules; Operative Surgical Procedures; Patients; Pharmaceutical Preparations; Phenytoin; Procedures; Proliferating; Prostaglandin E Receptor; Recruitment Activity; Research; Research Personnel; Resources; Role; Source; Surgical Flaps; Tissue Sample; Tissues; United States National Institutes of Health; Universities; connective tissue growth factor; in vivo; wisdom tooth

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The objectives of this study are: 1. To determine the mechanisms of CTGF (Connective Tissue Growth Factor) activation of human gingival fibroblasts: identify functional domains of CTGF responsible for stimulating insoluble collagen accumulation, proliferation, and apoptosis. 2. To determine the mechanisms by which phenytoin increases CTGF levels in cultured human gingival fibroblasts: a) assess for deficient down-regulation of CTGF related to PGE2 and cAMP metabolism in gingival fibroblasts b) assess for phenytoin stimulated release of sequestered Smad's from microtubules, thereby increasing the level of CTGF transcription and expression. 3. Assay quantitatively human gingival tissue samples in situ to investigate in vivo the mechanisms and role of DTGF in contributing to inherited and drug-induced gingival overgrowth: a) measure the concentration of apoptotic cells, and proliferating cells, b) measure the expression of CTGF protein by quantitative methods and c) measure by quantitative immunohistochemistry PGE2 receptors d) measure the degree of fibrosis, and inflammation. All measurements will be performed in serial sections of the same tissues in inherited and drug-induced gingival overgrowth tissue samples compared to non-overgrown control gingival tissues. 250 subjects (ages 12-65) will be enrolled in the study. Patients undergoing routine periodontal flap surgery, crown lengthening procedures or surgery for impacted third molars will be enrolled in a control group. Patients undergoing gingivectomy surgery to treat gingival overgrowth will be recruited for the other four gingival overgrowth groups. All patients will be recruited from Boston University School of Dental Medicine, Boston University Medical Center, and affiliated hospitals and dental centers.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 本研究的目标是： 1. 确定 CTGF（结缔组织生长因子）激活人牙龈成纤维细胞的机制：确定 CTGF 负责刺激不溶性胶原积累、增殖和凋亡的功能域。 2. 确定苯妥英增加培养的人牙龈成纤维细胞中 CTGF 水平的机制： a) 评估牙龈成纤维细胞中与 PGE2 和 cAMP 代谢相关的 CTGF 下调缺陷 b) 评估苯妥英刺激微管中隔离的 Smad 释放，从而增加 CTGF 转录和表达水平。 3. 原位定量检测人牙龈组织样本，研究 DTGF 在体内导致遗传性和药物诱导的牙龈过度生长的机制和作用：a) 测量凋亡细胞和增殖细胞的浓度，b) 通过定量方法测量 CTGF 蛋白的表达，c) 通过定量免疫组织化学 PGE2 受体测量 d) 测量程度 纤维化和炎症。所有测量都将在遗传性和药物诱导的牙龈过度生长组织样本中的相同组织的连续切片中进行，与非过度生长的对照牙龈组织进行比较。 250 名受试者（12-65 岁）将参加该研究。 接受常规牙周瓣手术、牙冠延长手术或阻生第三磨牙手术的患者将被纳入对照组。 接受牙龈切除术治疗牙龈过度生长的患者将被招募到其他四个牙龈过度生长组中。 所有患者都将从波士顿大学牙科医学院、波士顿大学医学中心以及附属医院和牙科中心招募。