[Contribution to the study of tooth buds in the mouse. I. Periods of induction and morphodifferentiation].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
This study was designed to determine the possible effect of one X-chromosome constitution on components of the human permanent and primary molar teeth. Enamel, dentine, pulp and crown dimensions were measured on radiographs of first and second permanent and second primary mandibular molars of 49 Finnish 45,X females (Turner syndrome), their 46 first-degree male and female relatives and 50 non-related males and females. In permanent first and second molars of the 45,X females, crown width and the dimensions of tooth components were less than those of normal females and males. Reduction in size affected first more than second molars, and in both teeth the enamel was relatively as well as absolutely thinner than in the controls. No differences were found in tooth components between normal relatives and unrelated controls. These data agree with previous studies which have demonstrated that the X chromosome promotes enamel apposition and that both X chromosomes in normal females are active in amelogenesis, while the Y chromosome influences both dentine and enamel growth. The relative reduction in "dentine" or the estimated mesiodistal width of the tooth germ in the 45,X females indicates that their tooth development is affected at an early stage of morphogenesis. Taken together with the results already reported for anterior teeth, the present results suggest that there is an inverse correlation between the duration of crown formation and the severity of size reduction.
The three-dimensional architecture of enamel prisms and their relationship to Hunter-Schreger bands were examined in the developing enamel of several dog teeth by light and electron microscopy, and computer-assisted reconstruction. Sections were prepared from a single demineralized tooth germ. Longitudinal semithin sections parallel to the meridian of the tooth showed parazones and diazones of the Hunter-Schreger bands in alternate rows at equal intervals. On sections vertical to the tooth crown through the middle region of parazone or diazone, a row of parallel prisms were angulated with the largest tilting angle being 55 degrees to the enamel-dentin junction, running in opposite directions in the respective zones. Tangential sections parallel to the enamel-dentin junction showed numerous belt-like zones arranged perpendicular to the meridian of the tooth. Each belt-like zone consisted of a group of enamel prisms oriented in the same direction, those in the neighboring zones being oriented in an opposite direction. The densely stained boundaries between the adjacent belt-like zones corresponded to the interface between parazone and diazone. Computer-reconstructed enamel prisms in the adjacent two zones were oriented in the opposite sidewards direction with occasional confluence and divergence. Scanning electron-microscopic observation of the developing enamel surface exposed by dissolution of the enamel organ revealed band-like arrangements of groups of pits encasing the Tomes' processes of secretory ameloblasts. The secretory faces of the pits inclined uniformly in the same sidewards direction, with those in the neighboring groups, in the opposite direction.
The study was done in 1982/83 as an oral health baseline for a comprehensive health project involving primary school children in rural areas of Tanzania. A number of 399 standard two pupils with a mean age of 10.9 yr were dentally examined and interviewed using closed questions. Interexaminer reproducibility for caries was 99%, inter-interviewer reliabilities for population correspondence were between 81% and 100%. DMFS + defs was 1.1 for the 92% brushing their teeth daily and 1.9 for children brushing once a week or less. The amount of plaque, calculus, and gingivitis showed no relation to brushing, if it was performed more than once a week. The effect of using chewing sticks or plastic toothbrushes was identical. Children eating cakes, biscuits and/or sweets at least three times a day seemed to have more caries than the rest, DMFS + defs being 1.5 and 1.1, respectively. Consumption of sugar cane did not show any relation to the caries amount. In one of five districts traditional removal of primary tooth germs had caused a mean loss (or deformity) of 1.0 permanent tooth, thereby being the most injurious dental condition. The study confirms the need of educational interventions. It does not indicate any justification for prompting children in general to brush more than once a day or restricting sweet snacks to less than once a day.
The 'problem' of the (neo)natal tooth is discussed in conjunction with a report of two cases and a review of the literature. The estimated incidence is between 1:700 and 1:3500 births. Girls are more often affected than boys. It usually concerns the two lower central deciduous incisors. The cause is most likely to be a superficial position of the tooth-germ, in which a hereditary component is a positive factor. The tooth is often deficient and very mobile, which may require treatment. In these cases extraction is the best therapy, if necessary after administration of vitamin K.
Teeth have been missing from birds (Aves) for at least 60 million years. However, in the chick oral cavity a rudiment forms that resembles the lamina stage of the mammalian molar tooth germ. We have addressed the molecular basis for this secondary loss of tooth formation in Aves by analyzing in chick embryos the status of molecular pathways known to regulate mouse tooth development. Similar to the mouse dental lamina, expression of Fgf8, Pitx2, Barx1, and Pax9 defines a potential chick odontogenic region. However, the expression of three molecules involved in tooth initiation, Bmp4, Msx1, and Msx2, are absent from the presumptive chick dental lamina. In chick mandibles, exogenous bone morphogenetic protein (BMP) induces Msx expression and together with fibroblast growth factor promotes the development of Sonic hedgehog expressing epithelial structures. Distinct epithelial appendages also were induced when chick mandibular epithelium was recombined with a tissue source of BMPs and fibroblast growth factors, chick skin mesenchyme. These results show that, although latent, the early signaling pathways involved in odontogenesis remain inducible in Aves and suggest that loss of odontogenic Bmp4 expression may be responsible for the early arrest of tooth development in living birds.
The aim of this study was to investigate the enamel microhardness and the histological features of eight enamel pearls of various size. The microhardness of the pearl enamel ranged from 272.4 to 407.2 Vickers microhardness values (VMV) and resembled that of the enamel of the carrier teeth (277.1-424.3). A histological resemblance between the tissues of the enamel pearls and those of the carrier teeth was also found. The resemblance was more pronounced in larger pearls, which showed a variability of the enamel microhardness and structure in the occlusal-cervical direction typical of the tooth crown. Large pearls also exhibited a root and a pulp. Some histological features of the enamel pearls were probably caused by pressures exerted on the developing pearl by its surroundings. It is suggested that the histogenesis of small and large pearls is based on the ability of the developing root of the carrier tooth to behave in part as a new tooth germ.
The paired-related homeobox gene, prx-1, is expressed in the postmigratory cranial mesenchyme of all facial prominences and is required for the formation of proximal first arch derivatives. We introduced lacZ into the prx-1 locus to study the developmental fate of cells destined to express prx-1 in the prx-1 mutant background. lacZ was normally expressed in prx-1(neo); prx-1(lacZ )mutant craniofacial mesenchyme up until 11.5 d.p.c. At later time points, lacZ expression was lost from structures that are defective in the prx-1(neo) mutant mice. A related gene, prx-2, demonstrated overlapping expression with prx-1. To test the idea that prx-1 and prx-2 perform redundant functions, we generated prx-1(neo;)prx-2 compound mutant mice. Double mutant mice had novel phenotypes in which the rostral aspect of the mandible was defective, the mandibular incisor arrested as a single, bud-stage tooth germ and Meckel's cartilage was absent. Expression of two markers for tooth development, pax9 and patched, were downregulated. Using a transgene that marks a subset of prx-1-expressing cells in the craniofacial mesenchyme, we showed that cells within the hyoid arch take on the properties of the first branchial arch. These data suggest that prx-1 and prx-2 coordinately regulate gene expression in cells that contribute to the distal aspects of the mandibular arch mesenchyme and that prx-1 and prx-2 play a role in the maintenance of cell fate within the craniofacial mesenchyme.
Horseradish peroxidase-wheat germ agglutinin (HRP-WGA) applied to proximal stumps of tooth pulp primary afferent neurons in rats was taken up and transported transneuronally to neurons in the ipsilateral trigeminal brainstem nuclear complex. The results of this study suggest that HRP-WGA transport may be a novel means of labeling both primary and higher order neurons that transmit tooth pulp sensory information in the rat and may be used to investigate the fine structure and synaptic contacts of central nervous system neurons that receive tooth pulp afferent input.
Tooth migration into jaw segments where granular hydroxy apatite had been implanted was studied in rats. To prevent premature contact with the ceramic granules, tooth germs were completely removed in the animals at the age of 10 days. Tooth root contact with the ceramo-osseous complex as a result of physiological tooth migration had deleterious effects. In the light of these findings the implantation of granular hydroxy apatite in the vicinity of tooth roots is not advisable.
We have investigated fibroblast growth factor (FGF) signaling during the development of the zebrafish pharyngeal dentition with the goal of uncovering novel roles for FGFs in tooth development as well as phylogenetic and topographic diversity in the tooth developmental pathway. We found that the tooth-related expression of several zebrafish genes is similar to that of their mouse orthologs, including both epithelial and mesenchymal markers. Additionally, significant differences in gene expression between zebrafish and mouse teeth are indicated by the apparent lack of fgf8 and pax9 expression in zebrafish tooth germs. FGF receptor inhibition with SU5402 at 32 h blocked dental epithelial morphogenesis and tooth mineralization. While the pharyngeal epithelium remained intact as judged by normal pitx2 expression, not only was the mesenchymal expression of lhx6 and lhx7 eliminated as expected from mouse studies, but the epithelial expression of dlx2a, dlx2b, fgf3, and fgf4 was as well. This latter result provides novel evidence that the dental epithelium is a target of FGF signaling. However, the failure of SU5402 to block localized expression of pitx2 suggests that the earliest steps of tooth initiation are FGF-independent. Investigations of specific FGF ligands with morpholino antisense oligonucleotides revealed only a mild tooth shape phenotype following fgf4 knockdown, while fgf8 inhibition revealed only a subtle down-regulation of dental dlx2b expression with no apparent effect on tooth morphology. Our results suggest redundant FGF signals target the dental epithelium and together are required for dental morphogenesis. Further work will be required to elucidate the nature of these signals, particularly with respect to their origins and whether they act through the mesenchyme.
Our research concerns the immunohistochemical localization of EGF and IGF-I receptors in the tooth germ, using monoclonal antibodies. The results show that in the early phases of human tooth development EGF and IGF-I receptors are present. At bud stage both receptors are localized at dental laminae level, in some epithelial cells of the tooth bud and in some mesenchymal cells. At cap stage the receptors are present in the outer and inner enamel epithelium, and in some cells of stellate reticulum. As far as concerns the mesenchymal cells, some cells of dental papilla in contact with enamel organ, are intensely positive. The immunopositivity is present also in some mesenchymal cells at follicular level. At late cap stage and at early bell stage receptors are not present at inner enamel epithelium level but they can be detectable in the mesenchyma of dental papilla and in some cells of the follicle. On the basis of these results it may be hypothesized that EGF and IGF-I can act as growth factors in the modulation of cellular proliferation and differentiation during the human tooth morphogenesis. Moreover, it is possible that these substances can play a role in the mesenchymal-epithelial interaction in the developing human tooth.
A case of delayed differentiation and/or calcification, that is, development, followed by accelerated growth of the maxillary second premolars is presented. This condition was accompanied by the congenital absence of mandibular second premolars even though maxillary and mandibular third molar germs were present. The case was followed over a five-year period. It seems that agenesis of any tooth might be found in conjunction with delay in development of any other tooth. Moreover, full development of a tooth germ (followed by an accelerated growth) as well as pathological changes may occur, despite an initial marked delay in tooth development.
In this study the inductive influence of hydroxyapatite ceramic (HAC) granules on preodontoblast differentiation was investigated. Dental papilla cells harvested from upper molar tooth germs were implanted intramuscularly in a pouch created for this purpose. Six months after surgery tooth-root-like bodies had developed with pulp-like cavities in the specimens in which dental papilla cells had been implanted with and without HAC. These bodies consisted of regular tubular dentine in the central part, fibrodentine peripherally and sometimes osteodentine. HAC was haphazardly enclosed in these root-like bodies, whereas the implantation of HAC alone had no effect.
Glial cell line-derived neurotrophic factor (GDNF) is a recently identified survival factor for several populations of neurons in the central and peripheral nervous system that also regulates kidney development. To study the roles of GDNF in the regulation of tooth innervation and formation, we analyzed by in situ hybridization the expression patterns of GDNF and its receptors Ret, GDNF family receptor alpha-1 (GFRalpha-1), and GFRalpha-2 from the initiation of first molar formation to the completion of crown morphogenesis. At the time of trigeminal axon ingrowth, GDNF mRNAs were expressed in the mesenchyme around the tooth germ (i.e., target field of the dental innervation), suggesting that it is involved in the regulation of the embryonic tooth innervation. This hypothesis was supported by the ability of GDNF to induce neurite outgrowth from embryonic day 12 (E12) to E15 trigeminal ganglia. This timing correlated with the appearance of Ret in the subset of cells in the trigeminal ganglion at E12, whereas GFRalpha-1 and GFRalpha-2 receptors were constantly expressed in trigeminal ganglion during E11-E15. After birth, GDNF expression showed apparent correlation with the ingrowth and presence of trigeminal nerve fibers in the tooth, suggesting that GDNF is involved in the regulation of innervation of the dental papilla and dentin postnatally. Ret, GFRalpha-1, and GFRalpha-2 mRNAs were expressed in the dental epithelial and mesenchymal cells at stages when epithelial-mesenchymal signalling regulates critical steps of tooth morphogenesis. Ret and GFRalpha-2 were colocalized in the dental mesenchyme during bud and cap stages. Expression of GFRalpha-1 associated with the formation of the epithelial enamel knot, which is a putative embryonic signalling center regulating tooth shape. During postnatal development, GDNF and its receptors were expressed in dental papilla mesenchyme. In addition, GDNF and GFRalpha-1 transcripts were seen in the preodontoblasts and odontoblasts, suggesting that they may be involved in differentiation and maintenance of functional properties of the odontoblasts. Taken together, these results suggest that GDNF acts as a target-derived neurotrophic factor during tooth innervation. In addition, GDNF and its receptors may have nonneuronal organogenetic functions during tooth morphogenesis.
We have carried out comparative in situ hybridisation analysis of six Wnt genes Wnts-3, -4, -5a, -6, -7b, and 10b together with Wnt receptor MFz6 and receptor agonist/antagonists MFrzb1 and Mfrp2 during murine odontogenesis from the earliest formation of the epithelial thickening to the early bell stage. Expression of Wnt-4, Wnt-6, and one Wnt receptor MFz6 was observed in the facial, oral and dental epithelium. Wnt10b was localised specifically to the presumptive dental epithelium. Wnts-3 and -7b were expressed in oral epithelium but showed no expression in the presumptive dental epithelium. Wnt-3 also showed no expression in the epithelial cells of the molar bud stage tooth germs, but showed restricted expression in the enamel knots which are signalling centres believed to be involved in regulating tooth shape. Wnts -6, -10b and MFz6 were also detected in the primary and secondary enamel knots. Wnt-5a and agonist/antagonists MFrzb1 and Mfrp2 were expressed in a graded proximo-distal (P-D) manner in mesenchymal cells during the early stages of tooth development with no overlying expression in the oral or dental epithelium. Wnt-5a and MFrzb1 show strong expression in the dental papilla mesenchyme.
Classical transplantation experiments with various amphibian tissues have shown that tooth development requires not only oral ectoderm and neural crest but also foregut endoderm. In addition, histological observation of oral membrane showed that the tooth germs are initiated in some ectodermal cells and neural crest cells adjacent to foregut endoderm. These studies suggest that tooth initiation requires the presence and cooperation of these three components. In mammals, however, there is no direct evidence that tooth formation is involved in the region of oral ectoderm adjacent to foregut endoderm. In order to elucidate the contribution of foregut endoderm to tooth formation, we established a new type of endodermal cell tracing system with a recombinant adenovirus called Adex-lacZ, and performed endodermal cell tracing in a long-term culture system. Cells labelled with Adex-lacZ were seen next to non-labelled thickening epithelium, presumptive incisor epithelium. These findings show the first direct evidence in mammals that tooth formation takes place in the specified part of oral ectoderm adjacent to foregut endoderm, suggesting that foregut endoderm plays a role in tooth initiation.
In the late seventies of the previous century the culture conditions to grow rodent tooth germs in vitro in order to investigate de novo formation and mineralization of dentine and enamel, were improved. This tooth model was then used for basic studies of mineralization processes in enamel and dentine. A review on experiments aimed at elucidating the function of osteocalcin, the predominant non-collagenous protein found in all mineralising type I connective tissues, in dentine formation is presented. Studies with tooth organ cultures and analysis of osteocalcin-deficient mouse dentin failed to disclose a function of osteocalcin in dentin formation.