Three-dimensional evaluation of alveolar bone thickness of mandibular anterior teeth in different dentofacial types.

AIM: The aim of this randomized study was to compare the alveolar bone thickness (ABT) of the mandibular incisor teeth of dental and skeletal Class I, II, and III adult patients at labial and lingual aspects of the bone and develop recommendations for the associated movements of teeth in this region, taking vertical facial type into consideration. MATERIAL AND METHODS: : Sixty-two Class I, 74 Class II, and 63 Class III patients - aged between 20 and 45 - were assigned to three subgroups - high (H), low (L), and normal (N) growth patterns. On the axial slices of computerized tomographies, the measurements for the ABT on labial and lingual sides of the mandibular incisors were carried out at three levels. RESULTS: In Class I group, at apex region, ABT of subgroups N and L were greater than H, at labial side. In Class II, ABT of subgroups N and L were greater than H, at apex at both sides and cervical lingual region. Similarly, ABT of subgroup L of Class III group was greater than H, at labial and lingual apex, mid-root regions. In Class II, the ABT of subgroup H was greater than L, at lingual cementoenamel junction. CONCLUSIONS: ABT of mandibular incisors of Class I patients is not affected from vertical pattern except for apical region. There is not a thick bone on the lingual side of the Class II, high-angle patients. The ABT of the Class III, high-angle patients is thin as a risk factor for proclination.

Effects of PAX9 and MSX1 gene variants to hypodontia, tooth size and the type of congenitally missing teeth.

ooth agenesis, affecting up to 20% of human population, is one of the most common congenital disorder. The most frequent form of tooth agenesis is known as hypodontia, which is characterized by the absence of one to five permanent teeth excluding third molars. It was considered that hypodontia is especially related with gene mutations which play role in tooth formation. Additionally mutations in PAX9 and/or MSX1 have been identified as the defects responsible for missing permanent molars and second premolars. In some studies it was also found that PAX9 and MSX1 gene mutations may change tooth size. Therefore  in this study all of these factors were investigated. Thirty one patients and 30 controls were enrolled to the study. Information about tooth sizes and type of congenitally missing teeth were collected. MSX1 and PAX9 gene mutations were investigated by direct sequencing. Results were evaluated statistically. As a result, 22 variations were detected in PAX9 in which 18 of them are novel. In addition, 7 variations were found in MSX1 in which 5 of them are novel and one of them lead to amino acid change. Statistically significant relations were found between detected variations and tooth sizes. Any relation between mutations and type of congenitally missing teeth were not detected. In conclusion, especially new mutations which may cause hypodontia, effect tooth size and type of congenitally missing teeth, should be investigated with other researchers for clarifying the mechanism.