Trigger osteoclast formation and activation: molecular treatment strategy of delayed tooth eruption.

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.