Rudiment incisors survive and erupt as supernumerary teeth as a result of USAG-1 abrogation

Murashima-Suginami, Akiko; Takahashi, Kazuyuki; Kawabata, T.; Sakata, Tomoko; Tsukamoto, Hiroko; Sugai, Manabu; Yanagita, Motoko; Shimizu, Akira; Sakurai, Takeshi; Slavkin, Harold C.; Bessho, Kazuhisa

doi:10.1016/j.bbrc.2007.05.148

Cited by 65 publications

(84 citation statements)

References 24 publications

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“…The supernumerary incisors reported in mutant mice have most often been located on the lingual side of the normal incisor (Danforth, 1958;Murashima-Suginami et al, 2007;Ohazama et al, 2008;Munne et al, 2009). The detailed analysis of one of these mutants (Sostdc1) showed that the supernumerary incisor developed on the lingual side of the normal one, and this tooth was considered to belong to a different tooth generation, corresponding to the revival of either the replacement incisor (Munne et al, 2009) or of a rudimentary lacteal incisor (Murashima-Suginami et al, 2007).…”

Section: The Duplicated Incisors Belong To the Same Generation And Armentioning

confidence: 99%

“…The detailed analysis of one of these mutants (Sostdc1) showed that the supernumerary incisor developed on the lingual side of the normal one, and this tooth was considered to belong to a different tooth generation, corresponding to the revival of either the replacement incisor (Munne et al, 2009) or of a rudimentary lacteal incisor (Murashima-Suginami et al, 2007). The supernumerary incisor of Lrp4-null mice has been considered as having the same origin as the supernumerary incisor of Sostdc1 mutants (Ohazama et al, 2010).…”

Section: The Duplicated Incisors Belong To the Same Generation And Armentioning

confidence: 99%

“…However, the study of incisor development in wild-type and mutant mice can potentially shed light on these evolutionary events. Mice carrying mutations in Sostdc1 (wise, ectodin) (Munne et al, 2009;Murashima-Suginami et al, 2007), Lrp4 (Ohazama et al, 2008) or Di (Danforth, 1958) have supernumerary upper or lower incisors that are located lingually to the normal incisor, in a configuration that is similar to Lagomorpha upper incisors. The detailed study of incisor development in Sostdc1 mutants indicated that the supernumerary incisor corresponded to a replacement tooth (Munne et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Regulation of tooth number by fine-tuning levels of receptor-tyrosine kinase signaling

et al. 2011

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SUMMARYMuch of our knowledge about mammalian evolution comes from examination of dental fossils, because the highly calcified enamel that covers teeth causes them to be among the best-preserved organs. As mammals entered new ecological niches, many changes in tooth number occurred, presumably as adaptations to new diets. For example, in contrast to humans, who have two incisors in each dental quadrant, rodents only have one incisor per quadrant. The rodent incisor, because of its unusual morphogenesis and remarkable stem cell-based continuous growth, presents a quandary for evolutionary biologists, as its origin in the fossil record is difficult to trace, and the genetic regulation of incisor number remains a largely open question. Here, we studied a series of mice carrying mutations in sprouty genes, the protein products of which are antagonists of receptor-tyrosine kinase signaling. In sprouty loss-of-function mutants, splitting of gene expression domains and reduced apoptosis was associated with subdivision of the incisor primordium and a multiplication of its stem cell-containing regions. Interestingly, changes in sprouty gene dosage led to a graded change in incisor number, with progressive decreases in sprouty dosage leading to increasing numbers of teeth. Moreover, the independent development of two incisors in mutants with large decreases in sprouty dosage mimicked the likely condition of rodent ancestors. Together, our findings indicate that altering genetic dosage of an antagonist can recapitulate ancestral dental characters, and that tooth number can be progressively regulated by changing levels of activity of a single signal transduction pathway.

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Section: The Duplicated Incisors Belong To the Same Generation And Armentioning

confidence: 99%

Section: The Duplicated Incisors Belong To the Same Generation And Armentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Regulation of tooth number by fine-tuning levels of receptor-tyrosine kinase signaling

et al. 2011

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“…Mice lacking functional Ectodin have a number of anomalies associated with the mandibular molar dentition, including the presence of a supernumerary molar tooth. Signifi cantly, these mice also have additional incisors in the mandible, [58][59][60] seemingly present due to a failure, in part at least, of normal Ectodin-mediated inhibition from adjacent mesenchyme. 58 Interestingly, Ectodin also has the ability to inhibit WNT signalling and it is likely that correct modulation of this pathway in dental mesencyhme is also an important determinant of tooth number.…”

Section: Bone Morphogenetic Protein Signallingmentioning

confidence: 99%

Revisiting the supernumerary: the epidemiological and molecular basis of extra teeth

et al. 2010

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“…A variety of secreted molecules including wingless-type MMTV integration site family Correspondence to : Nao Kimura E-mail : mana14009@g.nihon-u.ac.jp (WNT), sonic hedgehog (Shh), bone morphogenetic proteins(BMPs), and fibroblast growth factors(FGFs)orchestrate development to regulate tooth shape, size, and number (10). In previous studies, sclerostin domain-containing protein 1(Sostdc1)-, LDL receptor-related protein 4(Lrp4) -, CCAAT/enhancer-binding protein beta (Cebpb) -, and adenomatous polyposis coli(Apc)-deficient mice, as well as paired box 6(Pax6)-mutant rats, presented with supernumerary teeth in the incisor area (11)(12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

<b>Analysis of the Association between Mesiodens and SNP Genotyping </b>

Kimura

2018

Int J Oral-Med Sci

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A mesiodens is the most common supernumerary tooth present in the maxillary incisor area. There have been many reports regarding the prevalence and treatment for supernumerary teeth; however, the etiology of the condition is still unknown. This study aimed to identify genes associated with susceptibility to mesiodens formation. The study population comprised 24 patients with mesiodens and 24 controls. Genomic DNA was obtained from the soft tissue of extracted supernumerary teeth or saliva samples. Genotypes and allele frequencies of single nucleotide polymorphisms (SNPs) in genes associated with the initiation of odontogenesis, including TP63, PITX2, LEF1, BMP2, BMP4, FGF9, FGF20, WNT10A, WNT10B, EDA, EDAR, MSX1, MSX2, PAX9, LHX6, and RUNX2 were compared between mesiodens group and controls using chisquared tests. In addition, SNPs in genes associated with supernumerary incisor formation in rodents, including SOSTDC1, LRP4, APC, PAX6, and CEBPB were tested. No positive polymorphisms were found in the tested SNPs between the two groups. These results suggest that these SNPs might not be candidates of genetic marker for mesiodens formation.

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Rudiment incisors survive and erupt as supernumerary teeth as a result of USAG-1 abrogation

Cited by 65 publications

References 24 publications

Regulation of tooth number by fine-tuning levels of receptor-tyrosine kinase signaling

Regulation of tooth number by fine-tuning levels of receptor-tyrosine kinase signaling

Revisiting the supernumerary: the epidemiological and molecular basis of extra teeth

<b>Analysis of the Association between Mesiodens and SNP Genotyping </b>

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