Tissue Interactions Regulating Tooth Development and Renewal

Balic, Anamaria; Thesleff, Irma

doi:10.1016/bs.ctdb.2015.07.006

Cited by 237 publications

(263 citation statements)

References 100 publications

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“…64,65 Studies of the functions and regulation of SEMA3A have unraveled novel developmental regulatory mechanisms regarding tooth innervation. The developing tooth germ controls its own innervation by local epithelial-mesenchymal tissue interactions, with the regulation of SEMA3A achieved via different conserved signaling effector families.…”

Section: Discussionmentioning

confidence: 99%

Integration of tooth morphogenesis and innervation by local tissue interactions, signaling networks, and semaphorin 3A

Luukko

Kettunen

2016

Cell Adhesion & Migration

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The tooth, like many other organs, develops from both epithelial and mesenchymal tissues, and has proven to be a valuable tool with which to investigate organ formation and peripheral innervation. Tooth formation is regulated by local epithelial-mesenchymal tissue interactions, and is closely integrated with stereotypic dental nerve navigation and patterning. Recent analyses of the function and regulation of semaphorin 3A (SEMA3A) have shed light on the regulatory mechanisms that coordinate organogenesis and innervation at the tissue and molecular levels. In the tooth, SEM3A acts as a developmentally regulated secretory chemo-repellent, that controls tooth innervation during embryonic and postnatal development. The tooth germ governs its own innervation by a combination of local tissue interactions and SEMA3A expression. SEMA3A signaling, in turn, is controlled by a number of conserved signaling effectors, including TGF-b superfamily members, FGF, and WNT; all function in embryo and organ development, and are essential for tooth histo-morphogenesis. Thus, SEMA3A driven axon guidance is integrated into key odontogenic signaling networks, establishing this protein as a critical molecular tether between 2 distinct developmental processes (morphogenesis and sensory innervation), both of which are required to obtain a functional tooth.

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Section: Discussionmentioning

confidence: 99%

Integration of tooth morphogenesis and innervation by local tissue interactions, signaling networks, and semaphorin 3A

Luukko

Kettunen

2016

Cell Adhesion & Migration

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“…Collagen type I(encoded by Col1)is involved in dentin and dental pulp development in the pre-secretory and secretory stages of odontoblast development (30). Sonic hedgehog(SHH)is essential in tooth development (28). The different steps of tooth development result from reciprocality maturation of ectodermal and mesenchymal cells.…”

Section: Discussionmentioning

confidence: 99%

Enamel Defects in the Alpl- /- murine Model of Infantile Hypophosphatasia

Yokoi

Yamamoto-Nemoto

2017

Int J Oral-Med Sci

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Hypophosphatasia(HPP)is caused by mutations in the gene encoding tissue-nonspecific alkaline phosphatase (ALPL). HPP patients develop deficient calcification of bones and teeth including defects in cementum, dentin, and enamel and the characteristic premature loss of primary teeth. Here, we investigated the enamel defects of knockout(Alpl -/-)mice compared with that of control wild type(Alpl +/+ )mice.No alkaline phosphatase (ALP) activity was detected by specific staining in the first molar germ of Alpl -/-mice on postnatal day 5. Hematoxylin and eosin staining revealed that the enamel layer in Alpl -/-mice was thin, undulated, and rugged. Furthermore, Alpl Our study suggests that ALP may have involvement in EMPs and enamel defects in Alpl -/-mice is caused by ameloblasts disorder. Furthermore, our study advances elucidation of the mechanisms that underlie enamel development, and will support establish the causes of enamel defects of HPP patients.

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“…These genes are responsible for the acquisition of odontogenic potential in the mesenchyme and are critical for early tooth development, as demonstrated in the knockout mice (20,23). Genetic mutations in MSX1 (28) and PAX9 (29) cause tooth agenesis, and mutations in RUNX2 are associated with cleidocranial dysplasia, that is characterized by multiple supernumerary teeth, including those in the upper incisor region(5).…”

Section: Discussionmentioning

confidence: 99%

Analysis of the Association between Mesiodens and SNP Genotyping

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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Tissue Interactions Regulating Tooth Development and Renewal

Cited by 237 publications

References 100 publications

Integration of tooth morphogenesis and innervation by local tissue interactions, signaling networks, and semaphorin 3A

Integration of tooth morphogenesis and innervation by local tissue interactions, signaling networks, and semaphorin 3A

<b>Enamel Defects in the </b><b><i>Alpl</i></b><b><sup>- /- </sup></b><b>murine Model of Infantile Hypophosphatasia </b>

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

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