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H Lesot

Publications and source records attributed to H Lesot.

84 records · Page 5Linked to original sources

[Basement membranes: general aspects, role in odontogenesis].

Basement membranes are interposed between epithelial and mesenchymal cells and surround muscles. This particular extracellular matrix was first considered as a static structure, assuming cohesiveness of adjacent tissues. However during the last ten years, basement membranes were shown to be continuously renewed and to present compositional and structural modifications. During development changing basement membranes play important roles during histomorphogenesis and cytodifferentiation and are involved in normal and pathological behavior of adult tissues.

Animals↗

Facts and hypotheses concerning the control of odontoblast differentiation.

Numerous studies using amphibians have demonstrated that preodontoblasts emerging from the dental papilla are derived from cranial neural crest cells [4, 12, 46, 64]. However this has not been established for mammals. The history of odonotogenesis begins during the early stages of cranial-facial development when the maxillary and mandibular processes processes develop. Continuous epithelio-mesenchymal interactions condition the histogenesis and morphogenesis of the teeth [24-26, 43, 44, 49, 51, 58] as well as the terminal differentiation of odontoblasts and ameloblasts [23, 47, 52, 54, 59, 61, 67]. During recent years a considerable amount of experimental data relating to differentiation of odontoblasts has been published. We summarize these data and attempt to integrate them in deductive hypothesis concerning the control of odontoblast differentiation.

Adenylyl Cyclases↗

Immunofluorescent localization of vimentin, prekeratin and actin during odontoblast and ameloblast differentiation.

The localization of constitutive proteins of different types of cytoskeletal components (prekeratin, vimentin, and actin) was examined in embryonic mouse molars using specific antibodies and immunofluorescence microscopy on frozen sections. Prekeratin and actin were found in the enamel organ. Preameloblasts demonstrated uniform staining, whereas ameloblasts demonstrated an apical accumulation of both prekeratin and actin. Vimentin and actin were observed in the dental papilla. A redistribution of vimentin accompanied the polarization of odontoblasts. A possible transmembranous control of cytoskeletal activities by the extracellular matrix is discussed.

Actins↗

Synthesis of collagen type I, type I trimer and type III by embryonic mouse dental epithelial and mesenchymal cells in vitro.

Epithelial and mesenchymal dental cells were grown in primary monolayer culture and the ability of both cell types to synthesize interstitial collagens was investigated. Pepsin-solubilized collagens were analyzed by CM-cellulose chromatography and both cell types were found to synthesize collagen type I, type III and type I trimer. The collagen phenotype of mesenchymal cells (type I: 82.4%, type III: 8.5%, type I trimer: 9.1%) was different from that of epithelial cells (type I: 71.8%, type III: 9.5%, type I trimer: 18.7%). The radioactivity incorporated into collagen molecules by mesenchymal cells was 34-times greater than the radioactivity incorporated by epithelial cells. This result agreed with previous observations obtained from tissue culture experiments (Lesot, H. and Ruch, J.V. (1979) Biol. Cell. 34, 23--37) which indicated a low synthesis of interstitial collagens by isolated dental epithelia when compared to isolated dental mesenchymes.

Animals↗

Collagen type I trimer synthesis by cultured embryonic mouse molars.

Embryonic mouse tooth germs were cultured in vitro and the collagens type I, type III and type I trimer were purified and biochemically characterized. Collagen type I trimer has been identified by means of CM-cellulose chromatography, CNBr peptide analysis, pepsin resistance and molecular sieve chromatography. Already before the odontoblasts were functional, this molecule was found to be a constituent of the dental extracellular matrix. However, the synthesis of collagen type I trimer was considerably increased when odontoblasts polarized and became functional. the incorporation of 5-bromodeoxyuridine into the dental cells inhibited the polarization of odontoblasts as well as the amplification of collagen type I and type I trimer synthesis.

Animals↗

Action of 5-bromodeoxyuridine on tooth germs "in vitro." I. - Effects on cytodifferentiation.

Sixteen or eighteen day old mouse embryonic first lower molars were treated with 5-bromodeoxyuridine (BrdU) in vitro. --In 16-day old tooth germs cytodifferentiation of both odontoblasts and ameloblasts was inhibited. This inhibition was reversible. --In 18-day old tooth germs, the odontoblasts localized at the top of the principal cusps (post-mitotic cells) differentiated normally and secreted predentin. In these conditions ameloblasts localized in front of functional odontoblasts differentiated, although they were able to incorporate BrdU. --In others experiments, control and BrdU-treated tooth germs were dissociated into enamel organs and pulps. Cultivated associations between either control or BrdU treated pulps with either control or BrdU treated enamel organs were analyzed. It appeared that the primary effect of BrdU might result in its incorporation in the preameloblasts which were no longer able to interact normally with the preodontoblasts.

Ameloblasts↗

Action of 5-bromodeoxyuridine on tooth germs "in vitro". II. - Effects on collagen synthesis.

The first lower molar tooth germs removed from 16-day-old mouse embryos were cultured for 2 days on a standard medium and then for 24 hours on the same medium containing BrdU (treated tooth germs) or not (controls). We attempted to study the effects of 5-Bromodeoxyuridine on the type I and type III collagen synthesis 24 (stage 16 + 4) and 72 (stage 16 + 6) hours after the incorporation of this thymidine analogue. At stage 16 + 4, type I and type III collagen were synthesized both in control and BrdU-treated tooth germs. However BrdU induced quantitative modifications in the type I collagen synthesis which might be explained by modifications in the turnover of this type of collagen. At stage 16 + 6, the BrdU treatment resulted in the inhibition of the terminal differentiation of odontoblasts. Consequently, the normal amplification of collagen type I synthesis could not occur. However, both control and BrdU-treated tooth germs synthesized type I and type III collagen. Quantitatively, the synthesis of type III collagen was slightly affected by BrdU treatment.

Animals↗

Position and growth of upper and lower tooth primordia in prenatal mouse--3D study.

The secondary palate formation in mouse has been associated with the period of fast growth of the mandible from embryonic days (ED) 13.0 to 16.0. During that time, the incisors and first molars develop from the bud to the bell stage. We investigated the position and growth of the tooth during prenatal elongation of the lower and upper jaws, and searched for the developmental stage when alignment of opposing teeth was achieved. Computer-aided 3D representations allowed us to represent the position of incisors and molars in the embryonic head from ED 13.5 to 18.0 on the basis of data obtained from histological sections. The atlas-hypophysis connection exhibited minimum change in length and orientation during the prenatal period, and thus was used as a reference line. The length of the teeth was calculated from 3D data. The upper first and second molars were longer than the lower ones. When viewed from the upper side, the upper and lower molar primordia were parallel from ED 13.5 to 15.0. During this period, the upper molars had a more lateral position than the lower ones. This situation was maintained in the anterior extremity of the first molars at later stages, while the posterior part of the upper and lower molar epithelia reached opposition in the medio-lateral direction from ED 16.0. The lower incisors exhibited an apparently backward position when compared to the upper incisors at earlier stages. However, the distance between the prospective anterior tips of the opposing incisors gradually decreased. The part of Meckel's cartilage associated with the lower dental quadrant elongated more than 3-fold from ED 13.5 to 18.0, and the lower jaw grew faster than the upper one. This difference resulted from the fast growth of the lower diastema from ED 14.0 to 18.0. The different growth speeds of the upper and lower jaws did not change the relative antero-posterior adjustment of the upper and lower molars, but contributed to achieving the opposition of the gnawing ends of the incisors.

Animals↗

Dentition development and budding morphogenesis.

The development of functional teeth in the mouse has been widely used as a model to study general mechanisms of organogenesis. Compared with other mammals, in which three incisors, one canine, four premolars, and three molars may occur even in each dental quadrant, the mouse functional dentition is strongly reduced. It comprises only one incisor separated from three molars by a toothless gap diastema at the location of the missing teeth. However, mouse embryos also develop transient vestigial dental primordia between the incisor and molar germs in both the upper and lower jaws. These rudimental structures regress, and epithelial apoptosis is involved in this process. The existence of the vestigial dental structures allowed a better assessment of the periodicity in the mouse dentition, which extends opportunities for the interpretation of molecular data on tooth development. We compared the dentition development with tentative models of budding morphogenesis in other epithelial appendages lungs and feathers. We suggested how developmental control by signaling molecules, including bone morphogenetic protein (Bmp), sonic hedgehog (Shh), and fibroblast growth factor (Fgf), can be similarly involved during budding morphogenesis of dentition and other epithelial appendages. We propose that epithelial apoptosis plays an important role in achieving specific features of dentition, whose development involves both budding and its more complex variant branching. The failure of segregation of the originating buds supports the participation of the concrescence of several tooth primordia in the evolutionary differentiation of mammalian teeth.

Animals↗

[Effect of the Tabby mutation on the dentition of mice].

The X-linked hypohidrotic ectodermal dysplasia in man leads to dental defects and is homologous to the Tabby (Ta) mutation in mouse. We currently investigate the effects of the Ta mutation on odontogenesis. The incisor germ of Ta showed an abnormal size and shape, a change in the balance between prospective crown- and root-analogue tissues and retarded cytodifferentiation. Although the enamel organ in Ta incisors was smaller, a larger proportion of the dental papilla was covered by preameloblasts-ameloblasts. The independent development of the labial and lingual parts of the enamel organ in rodent lower incisor might reflect their heterogeneous origin, as demonstrated for the upper incisor. The mandibular cheek dentition in Ta mice exhibits large variations classified in five morphotypes, based on the tooth number, shape, size and position. In Ta embryos, the mesio-distal extent of the dental epithelium was similar to that in WT, but its segmentation was altered. These morphotypes could be explained by a tentative model suggesting that 1) the positions of tooth boundaries differ in Ta and WT molars and among the Ta morphotypes; 2) the tooth patterns are determined by the distal boundary of the most mesial tooth primordium while the distal teeth take advantage of the remaining dental epithelium; 3) one tooth primordium in Ta mice might derive from adjacent parts of two primordia in WT.

Ameloblasts↗