scholarly journals Zebrafish sp7 mutants show tooth cycling independent of attachment, eruption and poor differentiation of teeth

2018 ◽  
Author(s):  
E Kague ◽  
P.E Witten ◽  
M Soenens ◽  
CL Campos ◽  
T Lubiana ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Thin Layer ◽  
Root Formation ◽  
Tooth Development ◽  
Tooth Replacement ◽  
Stages Of Development ◽  
Odontoblast Differentiation ◽  
Osteoclast Activity ◽  
Poor Differentiation

SummaryThe capacity to fully replace teeth continuously makes zebrafish an attractive model to explore regeneration and tooth development. The requirement of attachment bone for the appearance of replacement teeth has been hypothesized but not yet investigated. The transcription factor sp7 (osterix) is known in mammals to play an important role during odontoblast differentiation and root formation. Here we study tooth replacement in the absence of attachment bone using sp7 zebrafish mutants. We analysed the pattern of tooth replacement at different stages of development and demonstrated that in zebrafish lacking sp7, attachment bone is never present, independent of the stage of tooth development or fish age, yet replacement is not interrupted. Without bone of attachment we observed abnormal orientation of teeth, and abnormal connection of pulp cavities of predecessor and replacement teeth. Mutants lacking sp7 show arrested dentinogenesis, with non-polarization of odontoblasts and only a thin layer of dentin deposited. Osteoclast activity was observed in sp7 mutants; due to the lack of bone of attachment, remodelling was diminished but nevertheless present along the pharyngeal bone. We conclude that tooth replacement is ongoing in the sp7 mutant despite poor differentiation and defective attachment. Without bone of attachment tooth orientation and pulp organization are compromised.

Wnt Production in Dental Epithelium Is Crucial for Tooth Differentiation

2019 ◽  
Vol 98 (5) ◽  
pp. 580-588 ◽  
Author(s):  
Y. Xiong ◽  
Y. Fang ◽  
Y. Qian ◽  
Y. Liu ◽  
X. Yang ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Tooth Development ◽  
Wnt Signaling Pathway ◽  
Conditional Knockout ◽  
Canonical Wnt Signaling ◽  
Odontoblast Differentiation ◽  
Wnt Ligands ◽  
Dental Epithelium ◽  
Canonical Wnt

The Wnt ligands display varied spatiotemporal expression in the epithelium and mesenchyme in the developing tooth. Thus far, the actions of these differentially expressed Wnt ligands on tooth development are not clear. Shh expression specifies the odontogenic epithelium during initiation and is consistently restricted to the dental epithelium during tooth development. In this study, we inactivate Wntless ( Wls), the key regulator for Wnt trafficking, by Shh-Cre to investigate how the Wnt ligands produced in the dental epithelium lineage act on tooth development. We find that conditional knockout of Wls by Shh-Cre leads to defective ameloblast and odontoblast differentiation. WlsShh-Cre teeth display reduced canonical Wnt signaling activity in the inner enamel epithelium and the underlying mesenchyme at the early bell stage, as exhibited by target gene expression and BAT-gal staining. The expression of Wnt5a and Wnt10b is not changed in WlsShh-Cre teeth. By contrast, Wnt10a expression is significantly increased in response to epithelial Wls deficiency. In addition, the expression of Hedgehog signaling pathway components Shh, Gli1, and Patched1 was greatly decreased in WlsShh-Cre teeth. Epithelial Wls loss of function in Shh lineage also leads to aberrant cell proliferation in dental epithelium and mesenchyme at embryonic day 16.5; however, the cell apoptosis is unaffected. Moreover, we find that Decorin and Col1a1, the key markers for odontoblast differentiation that are downregulated in WlsShh-Cre teeth, act as direct downstream targets of the canonical Wnt signaling pathway by chromatin immunoprecipitation analysis. Additionally, Decorin and Col1a1 expression can be increased by lithium chloride (LiCl) treatment in the in vitro tooth explants. Taken together, our results suggest that the spatial expression of Wnt ligands within the dental epithelial lineage regulates the differentiation of tooth structures in later stages.

scholarly journals The Effects of Premature Tooth Extraction and Damage on Replacement Timing in the Green Iguana

2020 ◽  
Vol 60 (3) ◽  
pp. 581-593
Author(s):  
Kirstin S Brink ◽  
Ping Wu ◽  
Cheng-Ming Chuong ◽  
Joy M Richman
Keyword(s):  
Tooth Extraction ◽  
Tooth Development ◽  
Tooth Wear ◽  
X Rays ◽  
Tooth Replacement ◽  
Green Iguana ◽  
Dental Tissues ◽  
Functional Tooth ◽  
Green Iguanas ◽  
Replacement Cycle

Synopsis Reptiles with continuous tooth replacement, or polyphyodonty, replace their teeth in predictable, well-timed waves in alternating tooth positions around the mouth. This process is thought to occur irrespective of tooth wear or breakage. In this study, we aimed to determine if damage to teeth and premature tooth extraction affects tooth replacement timing long-term in juvenile green iguanas (Iguana iguana). First, we examined normal tooth development histologically using a BrdU pulse-chase analysis to detect label-retaining cells in replacement teeth and dental tissues. Next, we performed tooth extraction experiments for characterization of dental tissues after functional tooth (FT) extraction, including proliferation and β-Catenin expression, for up to 12 weeks. We then compared these results to a newly analyzed historical dataset of X-rays collected up to 7 months after FT damage and extraction in the green iguana. Results show that proliferation in the dental and successional lamina (SL) does not change after extraction of the FT, and proliferation occurs in the SL only when a tooth differentiates. Damage to an FT crown does not affect the timing of the tooth replacement cycle, however, complete extraction shifts the replacement cycle ahead by 4 weeks by removing the need for resorption of the FT. These results suggest that traumatic FT loss affects the timing of the replacement cycle at that one position, which may have implications for tooth replacement patterning around the entire mouth.

Phosphohydrolase Activities in Developing and Mature Dental Tissues

1990 ◽  
Vol 45 (3-4) ◽  
pp. 280-292
Author(s):  
Edda Warth ◽  
Reinhard Jeck
Keyword(s):  
Alkaline Phosphatase ◽  
Root Formation ◽  
Specific Activity ◽  
Tooth Development ◽  
Inorganic Pyrophosphatase ◽  
Dental Tissues ◽  
Dental Hard Tissues ◽  
Hard Tissues ◽  
Enamel Epithelium ◽  
Enamel Mineralization

Abstract In the course of the odontogenesis of bovine incisors several clearly distinguishable phosphohydrolase activities are observed in the pulp and in dental hard tissues. Using various substrates and inhibitors, unspecific alkaline phosphatase, two isoenzymes of acid phosphatase, Ca2+-activated ATPase and inorganic pyrophosphatase are characterized. The enzymatic activity of alkaline phosphatase in pulp and hard tissues is significantly high at the beginning of dentine and enamel mineralization. The specific activity of this enzyme decreases quite fast with the beginning of root formation, then more slowly, until it reaches a constant final value. Histochemical studies show that during mineralization the maximum of alkaline phosphatase activity is in the subodontoblasts. Lower enzyme concentrations are found in the stratum intermedium and in the outer enamel epithelium during that process. The specific activities of ATPase, acid phosphatases and pyrophosphatase show little temporal variation during tooth development, but they also appear in a characteristic spatial pattern in the dental tissues.

scholarly journals Signaling Pathways Critical for Tooth Root Formation

2017 ◽  
Vol 96 (11) ◽  
pp. 1221-1228 ◽  
Author(s):  
J. Wang ◽  
J.Q. Feng
Keyword(s):  
Signaling Pathways ◽  
Root Formation ◽  
Root Resorption ◽  
Tooth Development ◽  
Critical Role ◽  
Future Research ◽  
Tooth Root ◽  
Short Root ◽  
Dentin Formation

Tooth is made of an enamel-covered crown and a cementum-covered root. Studies on crown dentin formation have been a major focus in tooth development for several decades. Interestingly, the population prevalence for genetic short root anomaly (SRA) with no apparent defects in crown is close to 1.3%. Furthermore, people with SRA itself are predisposed to root resorption during orthodontic treatment. The discovery of the unique role of Nfic (nuclear factor I C; a transcriptional factor) in controlling root but not crown dentin formation points to a new concept: tooth crown and root have different control mechanisms. Further genetic mechanism studies have identified more key molecules (including Osterix, β-catenin, and sonic hedgehog) that play a critical role in root formation. Extensive studies have also revealed the critical role of Hertwig’s epithelial root sheath in tooth root formation. In addition, Wnt10a has recently been found to be linked to multirooted tooth furcation formation. These exciting findings not only fill the critical gaps in our understanding about tooth root formation but will aid future research regarding the identifying factors controlling tooth root size and the generation of a whole “bio-tooth” for therapeutic purposes. This review starts with human SRA and mainly focuses on recent progress on the roles of NFIC-dependent and NFIC-independent signaling pathways in tooth root formation. Finally, this review includes a list of the various Cre transgenic mouse lines used to achieve tooth root formation–related gene deletion or overexpression, as well as strengths and limitations of each line.

Tricho-Rhino-Phalangeal Syndrome with Supernumerary Teeth

2008 ◽  
Vol 87 (11) ◽  
pp. 1027-1031 ◽  
Author(s):  
P. Kantaputra ◽  
I. Miletich ◽  
H.-J. Lüdecke ◽  
E.Y. Suzuki ◽  
V. Praphanphoj ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Amino Acid ◽  
Zinc Finger ◽  
Clinical Features ◽  
Tooth Development ◽  
Supernumerary Teeth ◽  
Gene Encoding ◽  
Gata Transcription Factor ◽  
Craniofacial Defects

Tricho-rhino-phalangeal syndromes (TRPS) are caused by mutation or deletion of TRPS1, a gene encoding a GATA transcription factor. These disorders are characterized by abnormalities of the hair, face, and selected bones. Rare cases of individuals with TRPS displaying supernumerary teeth have been reported, but none of these has been examined molecularly. We used two different approaches to investigate a possible role of TRPS1 during tooth development. We looked at the expression of Tprs1 during mouse tooth development and analyzed the craniofacial defects of Trps1 mutant mice. In parallel, we investigated whether a 17-year-old Thai boy with clinical features of TRPS and 5 supernumerary teeth had mutation in TRPS1. We report here that Trps1 is expressed during mouse tooth development, and that an individual with TRPS with supernumerary teeth has the amino acid substitution A919V in the GATA zinc finger of TRPS1. These results suggest a role for TRPS1 in tooth morphogenesis.

scholarly journals Transcription factor Sp3 is essential for post-natal survival and late tooth development

2000 ◽  
Vol 19 (4) ◽  
pp. 655-661 ◽  
Author(s):  
Peter Bouwman ◽  
Heike Göllner ◽  
Hans-Peter Elsässer ◽  
Gabriele Eckhoff ◽  
Alar Karis ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Tooth Development

Changes in the distribution of tenascin during tooth development

Development ◽  
1987 ◽  
Vol 101 (2) ◽  
pp. 289-296 ◽  
Author(s):  
I. Thesleff ◽  
E. Mackie ◽  
S. Vainio ◽  
R. Chiquet-Ehrismann
Keyword(s):  
Tooth Development ◽  
Polyclonal Antibodies ◽  
Staining Intensity ◽  
Mesenchymal Cells ◽  
Hard Tissue ◽  
Connective Tissues ◽  
Odontoblast Differentiation ◽  
Dental Papilla ◽  
Extracellular Matrix Molecule ◽  
Dental Papilla Cells

Tenascin is an extracellular matrix molecule that was earlier shown to be enriched in embryonic mesenchyme surrounding the budding epithelium in various organs including the tooth. In the present study tenascin was localized by immunohistology throughout the course of tooth development in the mouse and rat using polyclonal antibodies against chick tenascin. The results indicate that tenascin is expressed by the lineage of dental mesenchymal cells throughout tooth ontogeny. The intensity of staining with tenascin antibodies in the dental papilla mesenchyme was temporarily reduced at cap stage when the tooth grows rapidly and undergoes extensive morphogenetic changes. During the bell stage of morphogenesis, the staining intensity increased and tenascin was accumulated in the dental pulp even after completion of crown development and eruption. Tenascin was present in the dental basement membrane at the time of odontoblast differentiation. The dental papilla cells ceased to express tenascin upon differentiation into odontoblasts and tenascin was completely absent from dentin. It can be speculated that the remarkable expression of tenascin in the dental mesenchymal cells as compared to other connective tissues is associated with their capacity to differentiate into hard-tissue-forming cells.

scholarly journals Identification of the Novel Tooth-Specific Transcription Factor AmeloD

2018 ◽  
Vol 98 (2) ◽  
pp. 234-241 ◽  
Author(s):  
B. He ◽  
Y. Chiba ◽  
H. Li ◽  
S. de Vega ◽  
K. Tanaka ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Epithelial Cell ◽  
Tooth Development ◽  
Tooth Germ ◽  
Regulatory Elements ◽  
Proximal Promoter ◽  
Epithelial Cell Line ◽  
Bhlh Transcription Factor ◽  
Specific Cell ◽  
E Cadherin

Basic-helix-loop-helix (bHLH) transcription factors play an important role in various organs’ development; however, a tooth-specific bHLH factor has not been reported. In this study, we identified a novel tooth-specific bHLH transcription factor, which we named AmeloD, by screening a tooth germ complementary DNA (cDNA) library using a yeast 2-hybrid system. AmeloD was mapped onto the mouse chromosome 1q32. Phylogenetic analysis showed that AmeloD belongs to the achaete-scute complex-like ( ASCL) gene family and is a homologue of ASCL5. AmeloD was uniquely expressed in the inner enamel epithelium (IEE), but its expression was suppressed after IEE cell differentiation into ameloblasts. Furthermore, AmeloD expression showed an inverse expression pattern with the epithelial cell-specific cell–cell adhesion molecule E-cadherin in the dental epithelium. Overexpression of AmeloD in dental epithelial cell line CLDE cells resulted in E-cadherin suppression. We found that AmeloD bound to E-box cis-regulatory elements in the proximal promoter region of the E-cadherin gene. These results reveal that AmeloD functions as a suppressor of E-cadherin transcription in IEE cells. Our study demonstrated that AmeloD is a novel tooth-specific bHLH transcription factor that may regulate tooth development through the suppression of E-cadherin in IEE cells.

scholarly journals Early development of rostrum saw-teeth in a fossil ray tests classical theories of the evolution of vertebrate dentitions

2015 ◽  
Vol 282 (1816) ◽  
pp. 20151628 ◽  
Author(s):  
Moya Meredith Smith ◽  
Alex Riley ◽  
Gareth J. Fraser ◽  
Charlie Underwood ◽  
Monique Welten ◽  
...  
Keyword(s):  
Oral Cavity ◽  
Early Development ◽  
Developmental Plasticity ◽  
Tooth Development ◽  
Ct Scanning ◽  
Tooth Size ◽  
Micro Ct ◽  
Tooth Replacement ◽  
Self Renewal ◽  
Dental Lamina

In classical theory, teeth of vertebrate dentitions evolved from co-option of external skin denticles into the oral cavity. This hypothesis predicts that ordered tooth arrangement and regulated replacement in the oral dentition were also derived from skin denticles. The fossil batoid ray Schizorhiza stromeri (Chondrichthyes; Cretaceous) provides a test of this theory. Schizorhiza preserves an extended cartilaginous rostrum with closely spaced, alternating saw-teeth, different from sawfish and sawsharks today. Multiple replacement teeth reveal unique new data from micro-CT scanning, showing how the ‘cone-in-cone’ series of ordered saw-teeth sets arrange themselves developmentally, to become enclosed by the roots of pre-existing saw-teeth. At the rostrum tip, newly developing saw-teeth are present, as mineralized crown tips within a vascular, cartilaginous furrow; these reorient via two 90° rotations then relocate laterally between previously formed roots. Saw-tooth replacement slows mid-rostrum where fewer saw-teeth are regenerated. These exceptional developmental data reveal regulated order for serial self-renewal, maintaining the saw edge with ever-increasing saw-tooth size. This mimics tooth replacement in chondrichthyans, but differs in the crown reorientation and their enclosure directly between roots of predecessor saw-teeth. Schizorhiza saw-tooth development is decoupled from the jaw teeth and their replacement, dependent on a dental lamina. This highly specialized rostral saw, derived from diversification of skin denticles, is distinct from the dentition and demonstrates the potential developmental plasticity of skin denticles.

Stage- and tissue-specific effect of cyclophosphamide during tooth development

2019 ◽  
Vol 41 (5) ◽  
pp. 519-530
Author(s):  
Kohei Nakatsugawa ◽  
Hiroshi Kurosaka ◽  
Toshihiro Inubushi ◽  
Gozo Aoyama ◽  
Yukako Isogai ◽  
...  
Keyword(s):  
Root Formation ◽  
Histological Analysis ◽  
Developmental Stages ◽  
Tooth Development ◽  
Specific Effect ◽  
Tooth Agenesis ◽  
Histological Observation ◽  
Micro Computed Tomography ◽  
Tooth Germs ◽  
Morphological Phenotype

Summary Objective The aim of this study was to investigate the toxic effect of cyclophosphamide (CPA) in the development of rodent molars. Methods CPA was administered intraperitoneally in postnatal mice between Day 1 and Day 10, and the morphological phenotype was evaluated at Day 26 using micro-computed tomography and histological analysis, including cell proliferation and cell death analyses. Results M3 molars of the mice who received 100 mg/kg CPA treatment at Day 6 or M2 molars who received treatment at Day 1 resulted in tooth agenesis or marked hypoplasia. Histological observation demonstrated that CPA treatment at Day 6 resulted in shrinkage of the M3 tooth germs, with a significant reduction in the proliferation of apoptotic cells. Conversely, CPA exposure at Day 2, which occurs at around the bud stage of M3, resulted in crown and root hypoplasia, with reduced numbers of cusp and root. In addition, CPA exposure at Day 10, which is the late bell stage of M3, induced root shortening; however, it did not affect crown morphogenesis. Limitations The timing of CPA administration is limited to after birth. Therefore, its effect during the early stages of M1 and M2 could not be investigated. Conclusion Defective phenotypes were evident in both crown and roots due to the effect of CPA. Interestingly, the severity of the phenotypes was associated with the developmental stages of the tooth germs at the time of CPA administration. The cap/early bell stage is the most susceptive timing for tooth agenesis, whereas the late bell stage is predominantly affected in terms of root formation by CPA administration.

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