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1.
Initial features of the inner dental epithelium histo-morphogenesis in the first lower molar in mouse. 总被引:1,自引:0,他引:1
H Lesot R Peterková R Schmitt J M Meyer L Viriot J L Vonesch B Senger M Peterka J V Ruch 《The International journal of developmental biology》1999,43(3):245-254
First lower molar development in the mouse was investigated from the cap to early bell stage using histology, morphometry, TEM and 3D reconstructions. This period was characterized by the histogenesis of the enamel organ (EO), folding of the epithelio-mesenchymal junction and growth of the tooth. The histogenesis of the EO and appearance of the enamel knot (EK) were initiated at the early cap stage (ED14). From ED14 to ED15, the anterior and posterior extension of the EK was very prominent whilst the length of the enamel organ did not substantially change. The EK appeared as a dynamic and transitory histological structure including dying and replacement cells. At ED16, the folding of the IDE, which extended over the anterior two thirds of the molar, was the first sign of cuspidogenesis. It was accompanied by a local remodeling of the basement membrane (BM): IDE cells involved in this folding transitorily lost contact with the BM which formed a loop in the mesenchyme. During this period, the growth of the lower M1 along the antero-posterior axis was restricted to the posterior part of the molar. Histogenesis occurred in the whole EO, whilst initial cuspidogenesis was limited to the anterior part of the tooth. Distinct cell populations were thus involved in different contemporary processes leading to changes in the cell density in the mesenchyme, in the mitotic activity, in cell-shape, and cell-matrix interactions in the IDE, and remodeling of the BM where both epithelium and mesenchyme might participate. 相似文献
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Kieffer S Peterkova R Vonesch JL Ruch JV Peterka M Lesot H 《The International journal of developmental biology》1999,43(6):531-539
The development of the lower incisor in the mouse was investigated from histological sections using computer-aided 3D reconstructions. At ED 13.0, the incisor was still at the bud stage. At ED 13.5, the initial cap was delimited by a short cervical loop, the development of which proceeded on the labial side, but was largely retarded on the medial side. This difference was maintained up to ED 15.0. From ED 16.0, the bell stage was achieved. Metaphases had a ubiquitous distribution both in the enamel organ and in the dental papilla from the bud to early bell stage. Apoptosis gradually increased in the mesenchyme posteriorly to the labial cervical loop from ED 13.5 to 14.0 and then disappeared; this apoptosis was not related to the posterior growth of the incisor. From ED 13.5, a high apoptotic activity was observed in the stalk. A focal area of apoptosis was observed at ED 13.5 in the enamel organ, approaching the epithelio-mesenchymal junction at the future tip of the incisor. There, the inner dental epithelium formed a bulbous protrusion towards dental papilla, reminiscent of the secondary enamel knot of mouse molars. This epithelial protrusion was still maintained at the bell stage. The enamel knot in the incisor demonstrated specific features, different from those characterizing the enamel knot in the molar: the concentric arrangement of epithelial cells was much less prominent and the occurrence of apoptosis was very transitory in the incisor at ED 13.5. The disappearance of the enamel knot despite a low apoptotic activity and the maintenance of the protrusion suggested a histological reorganization specific for rodent incisor. 相似文献
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Miard S Peterková R Vonesch JL Peterka M Ruch JV Lesot H 《The International journal of developmental biology》1999,43(6):517-529
The X-linked tabby (Ta) syndrome in the mouse is homologous to the hypohidrotic ectodermal dysplasia (HED) in humans. As in humans with HED, Ta mice exhibit hypohidrosis, characteristic defects of hairs and tooth abnormalities. To analyze the effects of Ta mutation on lower incisor development, histology, morphometry and computer-aided 3D reconstructions were combined. We observed that Ta mutation had major consequences for incisor development leading to abnormal tooth size and shape, change in the balance between prospective crown- and root-analog tissues and retarded cytodifferentiations. The decrease in size of Ta incisor was observed at ED13.5 and mainly involved the width of the tooth bud. At ED14.5-15.5, the incisor appeared shorter and narrower in the Ta than in the wild type (WT). Growth alterations affected the diameter to a greater extent than the length of the Ta incisor. From ED14.5, changes in the shape interfered with the medio-lateral asymmetry and alterations in the posterior growth of the cervical loop led to a loss of the labio-lingual asymmetry until ED17.0. Although the enamel organ in Ta incisors was smaller than in the WT, a larger proportion of the dental papilla was covered by preameloblasts-ameloblasts. These changes apparently resulted from reduced development of the lingual part of the enamel organ and might be correlated with a possible heterogeneity in the development of the enamel organ, as demonstrated for upper incisors. Our observations suggest independent development of the labial and lingual parts of the cervical loop. Furthermore, it appeared that the consequences of Ta mutation could not be interpreted only as a delay in tooth development. 相似文献
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Miquella G. Chavez Jimmy Hu Kerstin Seidel Chunying Li Andrew Jheon Adrien Naveau Orapin Horst Ophir D. Klein 《Journal of visualized experiments : JoVE》2014,(87)
Understanding the cellular and molecular mechanisms that underlie tooth regeneration and renewal has become a topic of great interest1-4, and the mouse incisor provides a model for these processes. This remarkable organ grows continuously throughout the animal''s life and generates all the necessary cell types from active pools of adult stem cells housed in the labial (toward the lip) and lingual (toward the tongue) cervical loop (CL) regions. Only the dental stem cells from the labial CL give rise to ameloblasts that generate enamel, the outer covering of teeth, on the labial surface. This asymmetric enamel formation allows abrasion at the incisor tip, and progenitors and stem cells in the proximal incisor ensure that the dental tissues are constantly replenished. The ability to isolate and grow these progenitor or stem cells in vitro allows their expansion and opens doors to numerous experiments not achievable in vivo, such as high throughput testing of potential stem cell regulatory factors. Here, we describe and demonstrate a reliable and consistent method to culture cells from the labial CL of the mouse incisor. 相似文献
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FGF10 maintains stem cell compartment in developing mouse incisors 总被引:27,自引:0,他引:27
Harada H Toyono T Toyoshima K Yamasaki M Itoh N Kato S Sekine K Ohuchi H 《Development (Cambridge, England)》2002,129(6):1533-1541
Mouse incisors are regenerative tissues that grow continuously throughout life. The renewal of dental epithelium-producing enamel matrix and/or induction of dentin formation by mesenchymal cells is performed by stem cells that reside in cervical loop of the incisor apex. However, little is known about the mechanisms of stem cell compartment formation. Recently, a mouse incisor was used as a model to show that fibroblast growth factor (FGF) 10 regulates mitogenesis and fate decision of adult stem cells. To further illustrate the role of FGF10 in the formation of the stem cell compartment during tooth organogenesis, we have analyzed incisor development in Fgf10-deficient mice and have examined the effects of neutralizing anti-FGF10 antibody on the developing incisors in organ cultures. The incisor germs of FGF10-null mice proceeded to cap stage normally. However, at a later stage, the cervical loop was not formed. We found that the absence of the cervical loop was due to a divergence in Fgf10 and Fgf3 expression patterns at E16. Furthermore, we estimated the growth of dental epithelium from incisor explants of FGF10-null mice by organ culture. The dental epithelium of FGF10-null mice showed limited growth, although the epithelium of wild-type mice appeared to grow normally. In other experiments, a functional disorder of FGF10, caused by a neutralizing anti-FGF10 antibody, induced apoptosis in the cervical loop of developing mouse incisor cultures. However, recombinant human FGF10 protein rescued the cervical loop from apoptosis. Taken together, these results suggest that FGF10 is a survival factor that maintains the stem cell population in developing incisor germs. 相似文献
9.
Wang XP Suomalainen M Felszeghy S Zelarayan LC Alonso MT Plikus MV Maas RL Chuong CM Schimmang T Thesleff I 《PLoS biology》2007,5(6):e159
Epithelial stem cells reside in specific niches that regulate their self-renewal and differentiation, and are responsible for the continuous regeneration of tissues such as hair, skin, and gut. Although the regenerative potential of mammalian teeth is limited, mouse incisors grow continuously throughout life and contain stem cells at their proximal ends in the cervical loops. In the labial cervical loop, the epithelial stem cells proliferate and migrate along the labial surface, differentiating into enamel-forming ameloblasts. In contrast, the lingual cervical loop contains fewer proliferating stem cells, and the lingual incisor surface lacks ameloblasts and enamel. Here we have used a combination of mouse mutant analyses, organ culture experiments, and expression studies to identify the key signaling molecules that regulate stem cell proliferation in the rodent incisor stem cell niche, and to elucidate their role in the generation of the intrinsic asymmetry of the incisors. We show that epithelial stem cell proliferation in the cervical loops is controlled by an integrated gene regulatory network consisting of Activin, bone morphogenetic protein (BMP), fibroblast growth factor (FGF), and Follistatin within the incisor stem cell niche. Mesenchymal FGF3 stimulates epithelial stem cell proliferation, and BMP4 represses Fgf3 expression. In turn, Activin, which is strongly expressed in labial mesenchyme, inhibits the repressive effect of BMP4 and restricts Fgf3 expression to labial dental mesenchyme, resulting in increased stem cell proliferation and a large, labial stem cell niche. Follistatin limits the number of lingual stem cells, further contributing to the characteristic asymmetry of mouse incisors, and on the basis of our findings, we suggest a model in which Follistatin antagonizes the activity of Activin. These results show how the spatially restricted and balanced effects of specific components of a signaling network can regulate stem cell proliferation in the niche and account for asymmetric organogenesis. Subtle variations in this or related regulatory networks may explain the different regenerative capacities of various organs and animal species. 相似文献
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Parsa S Kuremoto K Seidel K Tabatabai R Mackenzie B Yamaza T Akiyama K Branch J Koh CJ Al Alam D Klein OD Bellusci S 《Development (Cambridge, England)》2010,137(22):3743-3752
Rodent incisors regenerate throughout the lifetime of the animal owing to the presence of epithelial and mesenchymal stem cells in the proximal region of the tooth. Enamel, the hardest component of the tooth, is continuously deposited by stem cell-derived ameloblasts exclusively on the labial, or outer, surface of the tooth. The epithelial stem cells that are the ameloblast progenitors reside in structures called cervical loops at the base of the incisors. Previous studies have suggested that FGF10, acting mainly through fibroblast growth factor receptor 2b (FGFR2b), is crucial for development of the epithelial stem cell population in mouse incisors. To explore the role of FGFR2b signaling during development and adult life, we used an rtTA transactivator/tetracycline promoter approach that allows inducible and reversible attenuation of FGFR2b signaling. Downregulation of FGFR2b signaling during embryonic stages led to abnormal development of the labial cervical loop and of the inner enamel epithelial layer. In addition, postnatal attenuation of signaling resulted in impaired incisor growth, characterized by failure of enamel formation and degradation of the incisors. At a cellular level, these changes were accompanied by decreased proliferation of the transit-amplifying cells that are progenitors of the ameloblasts. Upon release of the signaling blockade, the incisors resumed growth and reformed an enamel layer, demonstrating that survival of the stem cells was not compromised by transient postnatal attenuation of FGFR2b signaling. Taken together, our results demonstrate that FGFR2b signaling regulates both the establishment of the incisor stem cell niches in the embryo and the regenerative capacity of incisors in the adult. 相似文献
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SUMMARY Root development is traditionally associated with the formation of Hertwig's epithelial root sheath (HERS), whose fragments give rise to the epithelial cell rests of Malassez (ERM). The HERS is formed by depletion of the core of stellate reticulum cells, the putative stem cells, in the cervical loop, leaving only a double layer of the basal epithelium with limited growth capacity. The continuously growing incisor of the rodent is subdivided into a crown analog half on the labial side, with a cervical loop containing a large core of stellate reticulum, and its progeny gives rise to enamel producing. The lingual side is known as the root analog and gives rise to ERM. We show that the lingual cervical loop contains a small core of stellate reticulum cells and suggest that it acts as a functional stem cell niche. Similarly we show that continuously growing roots represented by the sloth molar and K14-Eda transgenic incisor maintain a cervical loop with a small core of stellate reticulum cells around the entire circumference of the tooth and do not form a HERS, and still give rise to ERM. We propose that HERS is not a necessary structure to initiate root formation. Moreover, we conclude that crown vs. root formation, i.e. the production of enamel vs. cementum, and the differentiation of the epithelial cells into ameloblasts vs. ERM, can be regulated independently from the regulation of stem cell maintenance. This developmental flexibility may underlie the developmental and evolutionary diversity in tooth patterning. 相似文献
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A three dimensional reconstruction of the epithelial tissue at the apical end of the lower rat incisor was made from serial 1 mum thick cross sections. This tissue formed an elongated structure, called the odontogenic organ, which was composed of a bulbous and a "U"-shaped part. Both parts were joined to one another at the posterior aspect of the apical foramen. The bulbous part of the odontogenic organ was situated at the lingual side of the "U"-shaped part and protruded anteriorly over the pulp. It was formed by cells of the outer dental epithelium and stellate reticulum whose organization suggested that the bulbous part was important in the production of cells for renewal of all the epithelia of the incisor. The "U"-shaped part of the odontogenic organ was apparently derived from the bulbous part and delineated the pulp by forming the lateral, mesial and labial sidewalls around the apical foramen. It was composed of all the epithelial cell types recognizable as precursors to (a) cells of the enamel organ which form the enamel, and (b) Hertwig's epithelial root sheath, a part of the odontogenic organ which induces the formation of dentin on the lingual aspect of the incisor. 相似文献
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Cho SW Lee HA Cai J Lee MJ Kim JY Ohshima H Jung HS 《Differentiation; research in biological diversity》2007,75(5):441-451
The enamel knot (EK), which is located in the center of bud and cap stage tooth germs, is a transitory cluster of non-dividing epithelial cells. The EK acts as a signaling center that provides positional information for tooth morphogenesis and regulates the growth of tooth cusps by inducing secondary EKs. The morphological, cellular, and molecular events leading to the relationship between the primary and secondary EKs have not been described clearly. This study investigated the relationship between the primary and secondary EKs in the maxillary and mandibular first molars of mice. The location of the primary EK and secondary EKs was investigated by chasing Fgf4 expression patterns in tooth germ at some intervals of in vitro culture, and the relationship between the primary EK and secondary EK was examined by tracing the primary EK cells in the E13.5 tooth germs which were frontally half sliced to expose the primary EK. After 48 hr, the primary EK cells in the sliced tooth germs were located on the buccal secondary EKs, which correspond to the future paracone in maxilla and protoconid in mandible. The Bmp4 expression in buccal part of the dental mesenchyme might be related with the lower growth in buccal epithelium than in lingual epithelium, and the Msx2 expressing area in epithelium was overlapped with the enamel cord (or septum) and cell dense area. The enamel cord might connect the primary EK with enamel navel to fix the location of the primary EK in the buccal side during the cap to bell stages. Overall, these results suggest that primary EK cells strictly contribute to form the paracone or protoconid, which are the main cusps of the tooth in the maxilla or mandible. 相似文献
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Viriot L Lesot H Vonesch JL Ruch JV Peterka M Peterková R 《The International journal of developmental biology》2000,44(2):233-240
In the mouse embryonic maxilla, rudimentary tooth primordia have been identified, which can be mistaken for the first upper molar. In order to determine whether such a situation might exist in the lower jaw as well, tooth development was investigated in the mouse mandibular cheek region during ED 12.5-15.0. A combination of histology, morphometry and computer-aided 3D reconstructions demonstrated the existence of rudimentary dental structures, whose gradual appearance and regression was associated with the segmental progress of odontogenesis along the mesio-distal axis of the jaw: 1) At ED 12.5, the mesial segment (MS) was the most prominent part of the dental epithelial invagination. It included an asymmetrically budding dental lamina. The MS, although generally mistaken for the lower first molar (M1, primordium, regressed and did not finally participate in M1 cap formation. 2) At ED 13.5, a wide dental bud (called segment R2) appeared distally to the MS. Although the R2 segment transiently represented the predominant part of the dental epithelium at ED13.5, it participated only in the formation of the mesial end of the M1 cap. 3) The top of the R2 segment at ED13.5 was not the precursor of the enamel knot (EK), contrary to what has been assumed. 4) The central segment of the M1 cap as well as the EK developed later and distally to the R2 segment. 5) Time-space specific apoptosis correlated with the retardation in growth of the R2 segment as well as with strong regressive changes in the epithelium situated mesially to it. These highlight the need to reinterpret current molecular data on early M1 development in the mouse in order to correlate the expression of signalling molecules with specific morphogenetic events in the appropriate antemolar or molar segments of the embryonic mandible. 相似文献
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In several primate groups enamel is reduced or absent from the lingual (tongue) side of the mandibular incisor crowns akin to other placental and marsupial mammalian groups such as rodents, lagomorphs and wombats. Here we investigate the presumed adaptation of crowns with unilateral enamel to the incision of tough foods in cercopithecines, an Old World monkey subfamily, using a simulation approach. We developed and validated a finite element model of the lower central incisor of the rhesus macaque (Macaca mulatta) with labial enamel only to compute three-dimensional displacements and maximum principal stresses on the crown subjected to compressive loads varying in orientation. Moreover, we developed a model of a macaque incisor with enamel present on both labial and lingual aspects, thus resembling the ancestral condition found in the sister taxon, the leaf-eating colobines. The results showed that, concomitant with experimental results, the cercopithecine crown with unilateral enamel bends predominantly towards the inside of the mouth, while displacements decreased when both labial and lingual enamel are present. Importantly, the cercopithecine incisor crown experienced lower maximum principal stress on the lingual side compared to the incisor with enamel on the lingual and labial aspects under non-axial loads directed either towards the inside or outside of the mouth. These findings suggest that cercopithecine mandibular incisors are adapted to a wide range of ingestive behaviours compared to colobines. We conclude that the evolutionary loss of lingual enamel in cercopithecines has conferred a safeguard against crown failure under a loading regime assumed for the ingestion (peeling, scraping) of tough-skinned fruits. 相似文献
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The lingual (root analogue) and the labial (crown analogue) mouse incisor dentin promotes ameloblast differentiation 总被引:1,自引:0,他引:1
S Amar V Karcher-Djuricic J M Meyer J V Ruch 《Archives d'anatomie microscopique et de morphologie expérimentale》1986,75(4):229-239
Previous studies have suggested that mouse molar ameloblast differentiation was triggered by the predentin-dentin. Knowing that enamel is absent on the lingual surface of the mouse incisor, the aim of this study was to compare in heterotopic tissue recombinations the behavior of mouse molar inner dental epithelium associated with lingual or labial mouse incisor dentin. It was shown that root-analogue and crown-analogue incisor dentin promotes ameloblast differentiation of competent molar inner dental epithelium. 相似文献
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Frederic Michon Mark Tummers Marika Kyyrönen Mikko J. Frilander Irma Thesleff 《Developmental biology》2010,340(2):355-368
Teeth form as appendages of the ectoderm and their morphogenesis is regulated by tissue interactions mediated by networks of conserved signal pathways. Micro-RNA (miRNA) pathway has emerged as important regulator of various aspects of embryonic development, but its function in odontogenesis has not been elucidated. We show that the expression of RNAi pathway effectors is dynamic during tooth morphogenesis and differentiation of dental cells. Based on microarray profiling we selected 8 miRNAs expressed during morphogenesis and 7 miRNAs in the incisor cervical loop containing the stem cell niche. These miRNAs were mainly expressed in the dental epithelium. Conditional deletion of Dicer-1 in the epithelium (DcrK14−/−) resulted in rather mild but significant aberrations in tooth shape and enamel formation. The cusp patterns of the DcrK14−/− molar crowns resembled the patterns of both ancestral muroid rodents and mouse mutants with modulated signal pathways. In the DcrK14−/− incisors, longitudinal grooves formed on the labial surface and these were shown to result from ectopic budding of the progenitor epithelium in the cervical loop. In addition, ameloblast differentiation was impaired and resulted in deficient enamel formation in molars and incisors. To help the identification of candidate target genes of the selected tooth enriched miRNAs, we constructed a new ectodermal organ oriented database, miRTooth. The predicted targets of the selected miRNAs included several components of the main morphogenetic signal pathways regulating tooth development. Based on our findings we suggest that miRNAs modulate tooth morphogenesis largely by fine tuning conserved signaling networks and that miRNAs may have played important roles during tooth evolution. 相似文献
20.
Basement membrane attachment is dispensable for radial glial cell fate and for proliferation, but affects positioning of neuronal subtypes 总被引:5,自引:0,他引:5
Haubst N Georges-Labouesse E De Arcangelis A Mayer U Götz M 《Development (Cambridge, England)》2006,133(16):3245-3254
Radial glial cells have been shown to act as neuronal precursors in the developing cortex and to maintain their radial processes attached to the basement membrane (BM) during cell division. Here, we examined a potential role of direct signalling from the BM to radial glial cells in three mouse mutants where radial glia attachment to the BM is disrupted. This is the case if the nidogen-binding site of the laminin gamma1 chain is mutated, in the absence of alpha6 integrin or of perlecan, an essential BM component. Surprisingly, cortical radial glial cells lacking contact to the BM were not affected in their proliferation, interkinetic nuclear migration, orientation of cell division and neurogenesis. Only a small subset of precursors was located ectopically within the cortical parenchyma. Notably, however, neuronal subtype composition was severely disturbed at late developmental stages (E18) in the cortex of the laminin gamma1III4-/- mice. Thus, although BM attachment seems dispensable for precursor cells, an intact BM is required for adequate neuronal composition of the cerebral cortex. 相似文献