Tooth agenesis, belonging to the abnormal tooth development, is a common disease in clinic. The disease not only affects the person's chewing function, but also influences the pronunciation, appearance and mental health. In the past, genetic linkage and molecular biology research have made clear of part of the genetic mutations' sites of the syndromic and non-syndromic tooth agenesis. Although the mechanism was not clear yet, but the important mutations are now known to be involved in many factors. Thesyndromic and non-syndromic tooth agenesis related gene are reviewed in this paper.
Anodontia ; Humans ; Mutation ; Odontogenesis ; Tooth

Adenomatoid odontogenic tumor (AOT) which accounts for only about 3% of all odontogenic tumors is characterized by the duct-like structures of epithelial components at the lesion. There are three variants of AOT; 1) follicular, a central lesion associated with an embedded tooth; 2) extrafollicular, a central lesion without connection to a tooth; and 3) peripheral. AOT slowly grows with few or no symptom. The central variants account for 97.2%, 73.0% of which are follicular variants. AOTs occur most commonly in the second and third of life and have a distinct predilection for the anterior maxilla of young female. The pathogenesis of this odontogenic tumor appears to involve persistent remnants of the dental lamina, especially after odontogenesis of the successional and accessional laminae. Conservative surgical excision is the treatment of choice.
Female ; Humans ; Maxilla ; Odontogenesis ; Odontogenic Tumors* ; Tooth

In this report, we present the case of a girl with delayed odontogenesis of a lower second premolar for which she was followed up for 8.5 years. Congenital absence of permanent mandibular second premolars was observed at the initial radiographic examination at 8 years and 1 month. One year later, during the treatment period, an unexpected odontogenesis of a right second premolar was diagnosed on follow-up radiography. The original treatment plan was revised and a new plan was successfully implemented. Th is unusual case showed that the orthodontist's clinical philosophy must be flexible because unexpected situations can arise, especially when treating growing patients.
Bicuspid ; Follow-Up Studies ; Humans ; Odontogenesis ; Pediatric Dentistry ; Philosophy

OBJECTIVETo determine the expression and possible function of CIC-5 during the rat tooth germ development.

METHODSIsolated total mRNA and protein from the rat tooth germs which were at different stages of development. RT-PCR and Western blot were used to investigate the mRNA and protein expression of the CIC-5 in the rat tooth germ.

RESULTSThe mRNA and protein of CIC-5 expressed in the late bell stage, but undetected inThe mRNA and protein of CIC-5 expressed in the late bell stage, but undetected in the early or middle bell stage.

CONCLUSIONThese results showed the spatial temporal distribution of expression of CIC-5 during the different stages of the rat tooth germ development and suggested that it might contribute to the rat tooth germ development.

OBJECTIVEThe Sonic hedgehog signalling peptide has been demonstrated to play important roles in the growth and patterning of the tooth development. This study aims on whether the antagonist beta-transduction repeat containing protein of Sonic hedgehog signal transduction expressed in tooth germs ameloblast and odontoblast or not.

METHODSThe mouse embryo heads of different developmental stages of E10.5, E13.5, E14.5, E16.5, E18.5 and P0, P3, P6 after birth were acquired fixed with 4% paraformaldehyde for 48 hours, embeded with Paraffin and examined using LsAB (labelled streptavidin-biotin) method to observe the beta-TrCP expression pattern in tooth germs, ameloblast and odontoblast.

RESULTSIt was demonstrated that beta-TrCP expressed in oral epithelium, tooth bud, mesenchymal cell cytoplasm of ameloblast and odontoblast of different stage of tooth development.

CONCLUSIONbeta-TrCP expressed from early stage to later stage of murine tooth development. And these findings provide the evidence of antagonist regulatory pathways for shh in teeth development.

OBJECTIVEDeveloping mouse molar was used as a model for the study of Syndecan-1, a transmembrane heparan sulfate proteoglycans, in order to approach the possible mechanism and function of this macromolecule during tooth development.

METHODSMouse embryos were removed at different days of gestation. The frozen sections of the first lower molar were made from the embryonic mouse heads and then indirect immunofluorescence was performed on these sections. The altered distribution pattern of Syndecan-1 in embryonic mouse first lower molars at different stages of development from the bud to the late bell stage was observed under a conventional fluorescence microscope.

RESULTSThere was a ubiquitous staining in the dental tissues at bud stage: Both the epithelium and mesenchyme were weakly positive for Syndecan-1. From the bud to the cap stage, there was a strong decrease of the staining for Syndecan-1 in the epithelial compartment, while an intense staining in dental mesenchyme was observed at cap stage. At bell stage, Syndecan-1 was again detected in dental epithelium including the stratum intermedium and the outer enamel epithelium, and it was found having some intense signal in the stratum intermedium. However, the staining for Syndecan-1 in dental mesenchyme of this stage became weaker and finally disappeared. Furthermore, a positive expression for Syndecan-1 was also found at the top of pre-ameloblasts as well as odontoblasts.

CONCLUSIONThese changes in the patterning of Syndecan-1 during tooth development might be related with cell proliferation during morphogenesis and later be involved in the differentiation of ameloblast and odontoblast.

Tooth root morphogenesis involves two biological processes, root elongation and dentinogenesis, which are guaranteed by downgrowth of Hertwig's epithelial root sheath (HERS) and normal odontoblast differentiation. Ubiquitin-dependent protein degradation has been reported to precisely regulate various physiological processes, while its role in tooth development is still elusive. Here we show ubiquitin-specific protease 34 (USP34) plays a pivotal role in root formation. Deletion of Usp34 in dental mesenchymal cells leads to short root anomaly, characterized by truncated roots and thin root dentin. The USP34-deficient dental pulp cells (DPCs) exhibit decreased odontogenic differentiation with downregulation of nuclear factor I/C (NFIC). Overexpression of NFIC partially restores the impaired odontogenic potential of DPCs. These findings indicate that USP34-dependent deubiquitination is critical for root morphogenesis by stabilizing NFIC.
Cell Differentiation ; Female ; Morphogenesis ; NFI Transcription Factors ; Odontogenesis ; Tooth Root

OBJECTIVES: A study was conducted to explore the expression pattern and function of ferritin heavy polypeptide gene (fth1b) in zebrafish pharyngeal teeth development and lay the foundation for subsequent research on teeth development and mineralization. METHODS: The zebrafish embryos were harvested at 56, 72, 96, and 120 h after fertilization. The expression of fth1b in zebrafish pharyngeal teeth development was detected by whole embryo RESULTS: The expression pattern of fth1b gene was very similar to that of the known zebrafish pharyngeal teeth marker dlx2b and was specifically expressed in the zebrafish pharyngeal teeth during development. After the specific knockout of the gene fth1b, the earliest gene that can be detect in zebrafish pharyngeal teeth-pitx2 was expressed normally during early development. The dlx2b expression was not significantly different from that of wild type zebrafish, but the mineralization of pharyngeal teeth in the mutant was weaker than that of wild type zebrafish. CONCLUSIONS The gene fth1b is specifically expressed in zebrafish pharyngeal teeth and acts on their early mineralization.
Animals ; In Situ Hybridization ; Odontogenesis ; Pharynx ; Tooth ; Zebrafish/genetics*

OBJECTIVE: This study aims to study the expression patterns of ectodysplasin (EDA) and ectodysplasin receptor (EDAR) during the early development of zebrafish and provide a foundation for further research of the Eda signaling pathway in tooth development. METHODS: Total RNA was extracted from zebrafish embryos at 48 hours postfertilization (hpf) and then reverse transcribed for cDNA library generation. The corresponding RNA polymerase was selected for the synthesis of the digoxin-labeled antisense mRNA probe of zebrafish pharyngeal tooth specific marker dlx2b and Eda signaling-associated genes eda and edar in vitro. The three sequences were ligated into a pGEMT vector with a TA cloning kit, and polymerase chain reaction (PCR) was applied to linearize the plasmid. The resultant PCR sequences were used as templates for synthesizing Dig-labeled mRNA probe dlx2b, eda, and edar. Zebrafish embryos were collected at 36, 48, 56, 60, 72, and 84 hpf, then whole mount in situ hybridization was performed for the detection of eda and edar expression patterns. Then, their expression patterns at 72 hpf were compared with the expression pattern of dlx2b. RESULTS: The mRNA antisense probes of dlx2b, eda, and edar were successfully obtained. The positive signals of eda and edar were observed in zebrafish pharyngeal tooth region at 48-72 hpf and thus conform to the signals of dlx2b in the positive regions. CONCLUSIONS The ligand eda and edar, which are associated with the Eda signaling pathway, are strongly expressed only at the pharyngeal tooth region in zebrafish from tooth initiation to the morphogenesis stage. Thus, the Eda signaling pathway may be involved in the regulation of the early development of zebrafish pharyngeal teeth.
Animals ; Ectodysplasins ; Edar Receptor ; Odontogenesis ; Receptors, Ectodysplasin ; Zebrafish

Tooth number abnormality is one of the most common dental developmental diseases, which includes both tooth agenesis and supernumerary teeth. Tooth development is regulated by numerous developmental signals, such as the well-known Wnt, BMP, FGF, Shh and Eda pathways, which mediate the ongoing complex interactions between epithelium and mesenchyme. Abnormal expression of these crutial signalling during this process may eventually lead to the development of anomalies in tooth number; however, the underlying mechanisms remain elusive. In this review, we summarized the major process of tooth development, the latest progress of mechanism studies and newly reported clinical investigations of tooth number abnormality. In addition, potential treatment approaches for tooth number abnormality based on developmental biology are also discussed. This review not only provides a reference for the diagnosis and treatment of tooth number abnormality in clinical practice but also facilitates the translation of basic research to the clinical application.
Gene Expression Regulation, Developmental ; Odontogenesis ; Signal Transduction ; Tooth/metabolism* ; Humans