The Runx2 gene is a master transcription factor of bone and plays a role in all stages of bone formation. It is essential for the initial commitment of mesenchymal cells to the osteoblastic lineage and also controls the proliferation, differentiation, and maintenance of these cells. Control is complex, with involvement of a multitude of factors, thereby regulating the expression and activity of this gene both temporally and spatially. The use of multiple promoters and alternative splicing of exons further extends its diversity of actions. RUNX2 is also essential for the later stages of tooth formation, is intimately involved in the development of calcified tooth tissue, and exerts an influence on proliferation of the dental lamina. Furthermore, RUNX2 regulates the alveolar remodelling process essential for tooth eruption and may play a role in the maintenance of the periodontal ligament. In this article, the structure of Runx2 is described. The control and function of the gene and its product are discussed, with special reference to developing tooth tissues, in an attempt to elucidate the role of this gene in the development of the teeth and supporting structures.

The aims of the study were to analyse the records of 26 subjects (18 females, eight males) with maxillary canine-first premolar transposition (Mx.C.P1) together with 160 subjects with a palatally displaced canine (PDC) to determine the pattern of tooth agenesis in these cases and to compare them with similar samples reported in the literature. A strong association between Mx.C.P1, lateral incisor and lower second premolar agenesis was found, with a 20 per cent prevalence of lateral incisor agenesis and a 24 per cent prevalence of lower second premolar agenesis. There was a lesser association with third molar (M.3) agenesis, with a prevalence of 52.2 per cent. Weaker associations were found for a PDC, with a prevalence of 5 per cent for lateral incisor agenesis. The prevalence of lower second premolar (5 per cent) and M.3 (27.5 per cent) agenesis approached reference values. Evidence for the implication of the MSX1 or PAX9 genes in the aetiology of PDC was weak.

No abstract

No abstract

The etiology of ectopic canines is controversial, with opinion divided as to a genetic or environmental mechanism. This study addressed the hypothesis that genetic factors play a role in the etiology of ectopic maxillary canines. Sixty-three probands were identified, and information on the dental status of 395 relatives was determined. Pedigrees were constructed and the Relative Risk calculated. Complex segregation analysis was carried out by means of the Pedigree Analysis Package. The best mathematical model obtained was a single dominant gene with autosomal transmission, incomplete penetrance, and highly variable expression. Only two of seven pairs of monozygotic twins were concordant for ectopic canines. This is consistent with environmental or epigenetic variables affecting the phenotype. The low concordance rate is consistent with the low penetrance determined by the segregation analysis and further supports the existence of environmental factors.