Hua Fang, Zhang Lu, Chen Zhi
Key Laboratory for Oral Biomedical Engineering of Ministry of Education, School and Hospital of Stomatology, Wuhan University, 237# Luo Yu Road, Wuhan, Hubei, China.
Med Hypotheses. 2007;69(6):1222-4. doi: 10.1016/j.mehy.2007.04.012. Epub 2007 Jun 8.
Delayed tooth eruption (DTE) is the emergence of a tooth into the oral cavity at a time that delays significantly from norms. It causes a significant impact on a patient's oral health. Some methods have been suggested to rescue the delayed tooth eruption. However, no approach aims to accelerate the biological process of tooth eruption and rescue these eruption disorders. Recent researches have shown that tooth eruption depends on the presence of osteoclasts to create an eruption pathway through the alveolar bone. We postulate a new approach that targets osteoclast formation and activation to accelerate the eruption of the affected tooth. These strategies include stimulating osteoclastogenesis by applying the cytokines or small molecules, such as TNF-alpha, IL-1 alpha and MCP-1; triggering osteoclast differentiation by applying molecules associated RANKL signaling, such as RANKL-Fc and OPG antibody; enhancing the function of osteoclasts by applying proteinases, such as CTSK. For the clinical point of view, we can inject these molecules in the oral mucosa of the affected tooth to induce bone resorption, then to rebuild the pathway of tooth eruption.
迟发性牙齿萌出（DTE）是指牙齿进入口腔的时间明显晚于正常标准。它会对患者的口腔健康产生重大影响。已经提出了一些方法来挽救迟发性牙齿萌出。然而，目前尚无旨在加速牙齿萌出的生物学过程并挽救这些萌出障碍的方法。最近的研究表明，牙齿萌出依赖于破骨细胞的存在，以通过牙槽骨形成萌出通道。我们提出了一种新方法，该方法针对破骨细胞的形成和激活来加速患牙的萌出。这些策略包括通过应用细胞因子或小分子（如肿瘤坏死因子-α、白细胞介素-1α和单核细胞趋化蛋白-1）来刺激破骨细胞生成；通过应用与核因子κB受体活化因子配体（RANKL）信号相关的分子（如RANKL-Fc和骨保护素（OPG）抗体）来触发破骨细胞分化；通过应用蛋白酶（如组织蛋白酶K（CTSK））来增强破骨细胞的功能。从临床角度来看，我们可以将这些分子注射到患牙的口腔黏膜中以诱导骨吸收，进而重建牙齿萌出通道。
