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At least 1,135 records · Page 63Linked to original sources
PubMed1991

[The osteoplastic care of the cleft jaw--an advance for the orthodontic treatment of cleft patients?].

This survey deals with problems of osteoplastic supply of the cleft from the orthodontic point of view. Remarkable parallels exist between primary and secondary osteoplasty: The involution stability of the alveolar process is only presented in a space-less tooth line. Therefore, the primary goal is to guarantee tooth eruption in the former cleft area. However, the antalogous bone graft in the former cleft area has to have a similar structure as adjacent alveolar bone. If tooth germs pass through the bone graft, an own parodont can be built up in the course of eruption. This is applicable to both dentitions. Accordingly, the osteoplasty of clefts is the most important prerequisite for stable treatment results and a healthy dentition.

Bone Transplantation↗
PubMed1990

[The dentition and jaw growth of 60 mono- and dizygotic twins between the ages of 10 and 18].

60 twins were investigated between the age of ten and 18 years to obtain information about inheritance of tooth-crown size and growth of alveolar bone. The results suggest genetically controlled interaction between tooth germs during their formation. The intrapair differences decrease between ten and 18 years for the alveolar bone diameters. This is an advise for stronger genetically influences in higher age and an etiological factor for relapse after orthodontic treatment.

Adolescent↗
PubMed1998

Mechanism of toxic action of fluoride in dental fluorosis: whether trimeric G proteins participate in the disturbance of intracellular transport of secretory ameloblast exposed to fluoride.

In enamel fluorosis model rats treated with sodium fluoride, secretory ameloblasts of incisor tooth germs exhibited disruption of intracellular trafficking. We examined whether heterotrimeric G proteins participated in the disruption of vesicular trafficking of the secretory ameloblast exposed to fluoride, using immunoblotting and pertussis toxin (IAP)-induced adenosyl diphosphate (ADP)-ribosylation for membrane fractions of the cell. Immunoblotting of crude membranes, post supernatants of the ameloblast, with anti-G(alpha i3/alpha o) and anti-G(alpha s) antibodies showed that Gi3 or Go proteins existed in the secretory ameloblast, but Gs protein did not. Immunoblotting of the subcellular membrane fractions indicated that the Gi3 or Go proteins were located in the Golgi membrane, but were not in the rough endoplasmic reticulum (rER) membrane. Autoradiograph of IAP-induced ADP-ribosylation, however, showed the existence of IAP-sensitive G proteins both in rER and Golgi membranes. Fluoride treatment decreased the G proteins bound to both membranes. These findings indicate that different G proteins, both of which are IAP-sensitive, are present in the rER and Golgi apparatus, and suggest that these G proteins participate in the disturbance of intracellular transport of the secretory ameloblast exposed to fluoride.

Adenosine Diphosphate Ribose↗
PubMed2002

The influx of serum albumin to enamel matrix in rat incisors after trauma.

The most frequent results of trauma to tooth germs are enamel hypoplasia and enamel hypocalcification. These differing results may be due to the stage of amelogenesis at which trauma occurs. The cellular and biomolecullar events involved in the genesis of these defects are poorly understood. We hypothesized that one factor involved is the possibility that relatively high levels of serum albumin enter the enamel matrix through the damaged enamel organ, and impair mineralization of the matrix. The present study was undertaken to immunohistochemically and autoradiographically localize serum albumin in the enamel organs of rat incisors after trauma was inflicted to the mandibular incisor region of 4-day-old rats. Hemorrhage was seen surrounding the enamel organ and between the detached secretory-stage ameloblasts. One day after trauma, the most intense immunohistochemical (IHC) staining for albumin was localized in the outer layer of the enamel matrix adjacent to the detached secretory-stage ameloblasts. Albumin was also detected autoradiographically in the secretory-stage ameloblasts layer and enamel matrix. These findings indicate that serum albumin can leak between the detached ameloblasts and penetrate the enamel matrix after trauma. Leaked albumin was still present in the matrix during the maturation stage. Leaked albumin in the developing enamel could inhibit crystal growth and result in hypocalcification.

Ameloblasts↗
PubMed2001

Putative role of basement membrane for dentinogenesis in the mesenchyme of murine dental papillae in vitro.

In a new culture-conditioning system of agar-coated mesenchyme of isolated incisor dental papillae, dentinogenesis has been induced adjacent to an agar substratum that functions as a foothold for cell immobilisation. To elucidate the role of the basement membrane (BM) in dentinogenesis, we have examined the way in which dentinogenesis depends upon BM components or transforming growth factor (TGF)-beta1 in this system. At the mesenchymal-epithelial junction of odontogenic organs (cut incisor tooth germs), TGF-beta1 visibly increased in the BM during incubation. In isolated dental papillae, BM components were synthesised and deposited at aligned peripheral cells of the explants, together with an increasing amount of TGF-beta1. These components were not assembled into extracellular matrix (ECM)-absorbed agar adjacent to explants, although dentinogenesis proceeded in the presence of pericellular BM components associated with TGF-beta1. When signalling via TGF-beta type II receptors was blocked, neither ECM production nor dentinogenesis was observed but explants partially detached from the agar surface, presumably as a result of the suppressed production of ECM, since attachment was retained by pre-coating explants with artificial matrices. Rescue experiments showed that TGF-beta1 regulated dentinogenesis through ECM production. With regard to BM components, inducible dentinogenesis was Arg-Gly-Asp (RGD)-dependent. Thus, pericellular BM components associated with TGF-beta1 and an ECM-absorbed agar substratum, which affects dentinogenesis, synergistically play a role similar to that of BM components in vivo. The BM therefore serves as a structural meshwork that acts as a foothold for cell immobilisation; its components act as ligands for RGD-dependent cell adhesion and it stores TGF-beta1, which regulates ECM production.

Agar↗
PubMed2005

Gene expression of connective tissue growth factor (CTGF/CCN2) in calcifying tissues of normal and cbfa1-null mutant mice in late stage of embryonic development.

Connective tissue growth factor (CTGF/CCN2), one of the most recently described growth factors, is produced by chondrocytes, vascular endothelial cells, and transforming growth factor (TGF)-beta-stimulated fibroblasts. CTGF was isolated from a chondrosarcoma-derived chondrocytic cell line, HCS-2/8, and found to be normally expressed in cartilage tissues, especially in hypertrophic chondrocytes, and also to stimulate both the proliferation and the differentiation of chondrocytes in vitro. Therefore, CTGF is thought to be one of the most important regulators of endochondral ossification in vivo. Herein we describe the expression pattern of the ctgf gene in the calcifying tissues of normal developing mouse embryos in comparison with that in core binding factor a1 (Cbfa1)-targeted mutant (cbfa1-null) mouse embryos, in which impaired development and growth were characteristically observed in the skeletal system. After 15 days of development (E15), the expression of ctgf was detected in the zone of hypertrophy and provisional calcification, in which ossification proceeds toward the epiphysis during the skeletal development of the mouse embryo. Furthermore, ctgf was expressed in developing molar and incisal tooth germs around the perinatal stage. However, no expression of the gene was found in the cbfa1-null mouse embryos. These results indicate that CTGF may have certain important roles in the development of the calcifying tissues in the mouse embryo.

Animals↗
PubMed1999

Initial aspects of mineralization at the dentino-enamel junction in embryonic mouse incisor in vivo and in vitro: a tem comparative study.

The frontier between the enamel organ and the dental papilla, the future dentino-enamel junction, undergoes coordinated modifications. The mineralization of the extracellular matrix starts within the predentine, which is a prerequisite for the formation of the first enamel crystallites in vivo. We investigated the dentino-enamel junction using the embryonic mouse incisor as a model. Our data showed that the notion of the dentino-enamel junction should not be restricted to the thin interface classically described. A temporo-spatial survey from the epithelio-mesenchymal junction to the dentino-enamel junction delineated a clear sequence of events characterized by the early deposition of electron-dense granules, followed by the appearance of patches of stippled material at the dentino-enamel junction. The first tiny enamel crystallites appeared in the vicinity of this material which presented a well-ordered alignment. The comparison of data obtained in vivo on 17-, 18-, 19-d-old embryonic incisors with those obtained in vitro using 15-d-old embryonic incisors cultured for 7 d emphasizes the relevance of this sequence. Helicoidal growing crystals were observed in cultured tooth germs but never in vivo.

Amelogenesis↗