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At least 1,675 records · Page 93Linked to original sources
PubMed2005

Runx2 (Cbfa1) inhibits Shh signaling in the lower but not upper molars of mouse embryos and prevents the budding of putative successional teeth.

Heterozygous mutations in the RUNX2 (CBFA1) gene cause cleidocranial dysplasia, characterized by multiple supernumerary teeth. This suggests that Runx2 inhibits successional tooth formation. However, in Runx2 knockout mice, molar development arrests at the late bud stage, and lower molars are more severely affected than upper ones. We have proposed that compensation by Runx3 may be involved. We compared the molar phenotypes of Runx2/Runx3 double-knockouts with those of Runx2 knockouts, but found no indication of such compensation. Shh and its mediators Ptc1, Ptc2, and Gli1 were down-regulated only in the lower but not the upper molars of Runx2 and Runx2/Runx3 knockouts. Interestingly, in front of the mutant upper molar, a prominent epithelial bud protruded lingually with active Shh signaling. Similar buds were also present in Runx2 heterozygotes, and they may represent the extension of dental lamina for successional teeth. The results suggest that Runx2 prevents the formation of Shh-expressing buds for successional teeth.

Animals↗
PubMed2004

Labial talon cusp on permanent central incisor: a case report.

Talon cusp is a supernumerary crown structure, a developmental disturbance in the shape of teeth that causes various diagnostic, functional and esthetic problems. Some synonyms for talon cusp are dens evaginatus of anterior teeth, interstitial cusp, tuberculated tooth, odontoma of the axial core type, evaginated odontoma, enamel pearl, supernumerary cusp etc. The lingual location on incisors, which frequently affects occlusion, is pathognomonic of the talon cusp. This report describes a rare odontogenic, isolated anomaly rather than an integral part of any disorder, a case of talon shaped cusp projecting from the labial surface of a maxillary permanent central incisor.

Child↗
PubMedDate not supplied

Supernumerary roots.

Supernumerary roots are one of the development anomalies pertaining to the tooth root morphology. It is generally well known that the deciduous and permanent anterior teeth have a single root. Maxillary molars have three roots and mandibular molars have two roots. Pertaining to the premolars, except for the maxillary first premolars all other premolars have a single roots. These supernumerary roots may be due to the disturbances of the Hertwig's epithelial root sheath forming the root. Cases have been reported where in both the deciduous and permanent dentition exhibiting supernumerary roots. Here with we are presenting cases of supernumerary roots in permanent teeth involving maxillary third molars, mandibular first, second molars and mandibular second premolars.

Adolescent↗
PubMed2004

Phenotypic changes in dentition of Runx2 homozygote-null mutant mice.

Genetic and molecular studies in humans and mice indicate that Runx2 (Cbfa1) is a critical transcriptional regulator of bone and tooth formation. Heterozygous mutations in Runx2 cause cleidocranial dysplasia (CCD), an inherited disorder in humans and mice characterized by skeletal defects, supernumerary teeth, and delayed eruption. Mice lacking the Runx2 gene die at birth and lack bone and tooth development. Our extended phenotypic studies of Runx2 mutants showed that developing teeth fail to advance beyond the bud stage and that mandibular molar organs were more severely affected than maxillary molar organs. Runx2 (-/-) tooth organs, when transplanted beneath the kidney capsules of nude mice, failed to progress in development. Tooth epithelial-mesenchymal recombinations using Runx2 (+/+) and (-/-) tissues indicate that the defect in mesenchyme cannot be rescued by normal dental epithelium. Finally, our molecular analyses showed differential effects of the absence of Runx2 on tooth extracellular matrix (ECM) gene expression. These data support the hypothesis that Runx2 is one of the key mesenchymal factors that influences tooth morphogenesis and the subsequent differentiation of ameloblasts and odontoblasts.

Animals↗
PubMed1995

Genetic mapping of cleidocranial dysplasia and evidence of a microdeletion in one family.

Cleidocranial dysplasia (CCD) is an autosomal, dominantly inherited disorder of high penetrance affecting skeletal ossification and tooth development. Typically, affected individuals have hypoplastic/aplastic clavicles, patent fontanelles and sutures, supernumerary teeth, and short stature. We have used a candidate locus approach to map the responsible gene in two families with typical features of CCD. Linkage was established between CCD and four loci (D6S426, D6S451, D6S459, TCTE1) that span a region of 10 cM on chromosome 6p. A maximum lod score, Zmax, of 4.1 at a recombination fraction of zero was obtained at D6S451. One highly polymorphic microsatellite from this region (D6S459) showed allelic loss in all affected members of one family with two different sets of primers. The presence of a deletion in this area was confirmed by Southern blot analysis using a probe derived from the amplification product of the D6S459 marker. The data assign a gene for CCD to chromosome 6p21 and suggest that a microdeletion within an area of tight linkage to the CCD-phenotype has been identified.

Base Sequence↗
PubMed2004

The activation level of the TNF family receptor, Edar, determines cusp number and tooth number during tooth development.

Mutations in members of the ectodysplasin (TNF-related) signalling pathway, EDA, EDAR, and EDARADD in mice and humans produce an ectodermal dysplasia phenotype that includes missing teeth and smaller teeth with reduced cusps. Using the keratin 14 promoter to target expression of an activated form of Edar in transgenic mice, we show that expression of this transgene is able to rescue the tooth phenotype in Tabby (Eda) and Sleek (Edar) mutant mice. High levels of expression of the transgene in wild-type mice result in molar teeth with extra cusps, and in some cases supernumerary teeth, the opposite of the mutant phenotype. The level of activation of Edar thus determines cusp number and tooth number during tooth development.

Animals↗
PubMed1989

Accessory root formation on a lower medial incisor.

Accessory root formation on a lower medial incisor dating from the eighth century was observed. The accessory root consisted structurally of dentin (corresponding to the root of the tooth) covered with cement but had no radicular canal. It is therefore not a real supernumerary root. Postmortem deformation was excluded by examination of the alveolar bone. It must have been formed at the time of root development, through a lesion of Hertwig's sheath, as a result of a trauma.

Dentin↗