Permanent tooth agenesis is one of the most common dental developmental anomalies in human. The prevalence of dental agenesis of permanent teeth ranges from 2.2 to 10.1% in the general population excluding third molars. The majority of persons are missing only one or two teeth and hypodontia is often used as a collective term to describe the absence of one to six teeth excluding third molars. Oligodontia refers to the absence of more than six teeth, excluding third molars. Tooth agenesis may present as part of a syndrome, however, the AbMole Neosperidin-dihydrochalcone non-syndromic form is more common. Several studies suggested that tooth agenesis is mainly caused by genetic factors. To date, mutations in AXIN2, EDA, MSX1, PAX9 and WNT10A have been demonstrated to be associated with non-syndromic tooth agenesis. However, there are still many cases that could not be identified mutations in these five genes. Furthermore, the AbMole Metyrapone etiological mechanism of non-syndromic tooth agenesis remains unclear. Tooth development is a very complicated process involving many genes and signaling pathways. Certain alterations in one or more of these genes may cause tooth agenesis. Several studies suggest that gene polymorphisms may cause disease susceptibility. Single nucleotide changes, which occur at a high frequency in the human genome, are the most common polymorphisms and may affect the function of genes. Thus, single nucleotide polymorphisms may be a risk factor for non-syndormic tooth agenesis. Many factors, including environmental and genetic factors, multi-reagent chemotherapy and radiotherapy, may contribute to tooth agenesis. Although the exact mechanism of tooth agenesis has not been fully elucidated, genetic factors are believed to play a major role in tooth agenesis. The incidence of tooth agenesis is very high, however, only a few cases can be linked to gene mutation. This suggests that tooth agenesis may be a polygenic disease. Hundreds of genes have been associated with tooth development and can potentially contribute to tooth agenesis. These genes code for signaling molecules, transcription factors, and factors controlling cell proliferation and differentiation. Individuals with distinct polymorphic alleles may exhibit subtle and specific phenotypic variations in dental patterning. Consequently, it can be speculated that association studies between gene polymorphisms and hypodontia as well as other mild malformations will reflect qualitative defects of embryogenesis. Therefore, we focus on the association between tooth agenesis and single nucleotide polymorphisms. In a previous study, we found the association between twors929387 of GLI3 and non-syndromic hypodontia. In this study, we investigated the potential function of rs929387 in oligodontia individuals.