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At least 145 records · Page 8Linked to original sources
PubMed1992

Dentin phosphoprotein gene locus is not associated with dentinogenesis imperfecta types II and III.

Dentinogenesis imperfecta (DGI) is an autosomal dominant inherited dental disease which affects dentin production and mineralization. Genetic linkage studies have been performed on several multigeneration informative kindreds. These studies determined linkage between DGI type II and III and group-specific component (vitamin D-binding protein). This gene locus has been localized to the long arm of human chromosome 4 in the region 4q11-q21. Although this disease has been mapped to chromosome 4, the defective gene product is yet to be determined. Biochemical studies have suggested abnormal levels of dentin phosphoprotein (DPP) associated with DGI type II. This highly acidic protein is the major noncollagenous component of dentin, being solely expressed by the ectomesenchymal derived odontoblast cells of the tooth. The purpose of the present study was to establish whether DPP is associated with DGI types II and III, by using molecular biology techniques. The strategy was to use a synthetic degenerative DPP oligonucleotide probe to map this sequence to the long arm of human chromosome 4, 4q13-q21, by using somatic cell hybrids. Our results indicated that DPP is not localized to any region of human chromosome 4, thus suggesting that the DPP gene is not directly associated with DGI type II or DGI type III. Our data do not exclude the possibility that other proteins associated with DPP posttranslational modifications might be responsible for this genetic disease.

Adult↗
PubMed1991

[A microradiographic and histological study of a case of dentinogenesis imperfecta type I].

Four temporary teeth, extracted for periodontal infection reasons, from a 53-months-old child with osteogenesis imperfecta, have been coated in methyl metacrylate and prepared for microradiographic analysis and light microscopic study. The enamel and dentin of three teeth (51, 65 and 85) don't show any particularity, some how the cementum is remarkably thin. Pulp chambers was large and contain a great number of calcifications. Some of them present a radial striation around a radio-transparent center, and when coloured with blue of methylen, they revealed inflammatory or fibroblastic cells. The fourth tooth (55) shows a dentinogenetic overproduction which closed the major part of the pulp chamber. The dentin presents two rows of different aspect, separated with a calcified bond. The mantle dentin contains sinuous tubules with a type I arrangement of SIAR classification (1986). But, in the deepest dentin, they are very little size and joined together while approaching the center of the tooth and coast along cellular inclusions, pathognomonic sign of dentinogenesis imperfecta. The pulpal space not obliterated contains a calcification with radial and microlacunary aspect.

Child, Preschool↗
PubMed1991

[The pedodontist and dentinogenesis imperfecta].

The purpose of this article is to present a treatment of dentinogenesis imperfecta in a 3 years old child. We reviewed some of the aspects to consider in the treatments of this alteration in primary dentition.

Child, Preschool↗
PubMedDate not supplied

[Multidisciplinary focus on dentinogenesis imperfecta type II. Clinical analysis. Ultrastructural and genetic pathology].

A review of the more relevant clinical, radiological, histopathological and genetics aspects of Dentinogenesis imperfecta (DI) is presented, together with the description of a family with DI. The complete analysis of the affected and non-affected members showed that the defect can be classified as a DI type II with an autosomal dominant mode of inheritance with complete penetrance and variable expressivity. Also it is necessary to emphasize the importance of a multidisciplinary approach (Pedodontists, Oral Pathologists and geneticists) in the description, diagnosis and treatment of the individuals affected with DI.

Adult↗
PubMed1990

[Study of the fine structure of human deciduous dentin with dentinogenesis imperfecta, with special reference to the mantle dentin].

A lower deciduous incioer exhibiting dentinogenesis imperfecta (D.I) obtained from a 6-year-old boy with osteogenesis imperfecta (Shields' Type I) was examined by means of light microscopy (LM), scanning electron microscopy (SEM), and X-ray microanalysis (XMA). With LM, the dentin displayed a sparse and irregular tubular pattern near the dentino-enamel junction (DEJ) and only few or no tubular structures in the area corresponding to the circumpulpal dentin. Between these two areas, cleft-like structures were characteristically noted. Structural irregularities in the dentinal tubules were also shown with SEM observation. XMA demonstrated that the distribution of both Ca and P in the dentin of DI teeth was apparently lower than that in the normal deciduous incisor used as a control. Specifically, an area along EDJ at a distance of 25-35 microns, corresponding to the mantle dentin, revealed extremely low or no distribution of the both elements. From the present observation, it is suggested that the generic disorder mainly involved in the primary odontoblasts and consequently results in the disturbance of calcification, especially that mediated by the matrix vesicles, and shortening of the cell life. After the death of these cells, the cells originate in, from the undifferentiated pulp cells may participate in the deposition of another irregular dentin.

Calcium↗
PubMed1990

Calcium transport in dentinogenesis.

A fundamental question in biomineralization research is the metabolism of the ionic constituents of the mineral phase. Mechanisms for the transport of Ca2+ ions have been identified and characterized in detail for various types of cells. Surprisingly little is known about osteoblasts and odontoblasts in this respect. This paper reviews what is known about calcium metabolism during dentinogenesis.

Animals↗
PubMed1989

[Osteogenesis imperfecta and dentinogenesis imperfecta. Apropos of 4 cases].

Based on four personal cases of osteogenesis imperfecta and dentinogenesis imperfecta, the authors review the semiological elements constituting the syndrome, and assign each case to the Sillence (1979) classification. The author established his classification on clinical criteria and the genetic nature of the various forms of osteogenesis imperfecta, however, the most recent discoveries concerning collagen biochemistry confirm that the condition is without doubt more heterogenous than suggested clinically, thereby better explaining the wide range of mutations encountered.

Child↗
PubMed1988

Dentinogenesis imperfecta in a six-generation family. A clinical, radiographic and histologic comparison of two branches through three generations.

Dentinogenesis imperfecta type II through 2 branches of a 6-generation family was presented focusing on individual differences in clinical, radiographic and histological appearances. These differences lead to different treatment approaches emphasizing prevention of attrition in order to avoid loss of vertical height and development of periapical lesions.

Adolescent↗
PubMed1987

Dental findings in osteogenesis imperfecta: I. Occurrence and expression of type I dentinogenesis imperfecta.

Sixty-eight patients with osteogenesis imperfecta (OI) classified according to Sillence were evaluated for dentinogenesis imperfecta (DI). Orthopantomograms of 51 of the 68 were examined. Type I DI was recognized in 22 patients from 16 families. DI was observed in 4/45 patients with type I OI, in one of two patients with type III, and in 13/16 patients with type IV OI. Four of the five patients with an unidentified type of OI had DI. The expression of type I DI was variable. Discoloration and pulpal obliteration were the major manifestations. Teeth from 14 patients from 12 families were studied histologically. Eight of the 14 patients were from six families who had clinical and/or radiographic evidence of DI. Irregularity of the dentin matrix and tubular pattern in the circumpulpal dentin and normal mantle dentin were observed. Interfamilial variability was greater than intrafamilial variability. The expression of DI was mild in one family with type I OI. There was no further relation between the type of OI and the severity of DI.

Dentin↗
PubMed1985

Experimental morphological studies on the functional role of the pulpal nerves in dentinogenesis.

The role of the pulpal nerves in the dentinogenesis of the rat dentition was studied experimentally by means of a time marker of lead acetate and by electron microscope after the individual dissection of the trigeminal and cervical sympathetic nerves or both. Following trigeminectomy, the longitudinal growth of the denervated incisor decreased. Contrary to this, following cervical sympathectomy, the longitudinal growth of the denervated incisor and molar increased 10-5%, and the collagen fibers increased predominantly in the pulpal tissue. The sympathetic nerves seem to play an important part in controlling the differentiation of the odontoblasts, inhibiting the maturation of the growth center of the apical pulp in the continuously developing teeth.

Animals↗
PubMed1981

[In vitro dentinogenesis of mice fetuses tooth germs in the presence of fluoride. Morphological nad historical observations].

Observations show that fluoride alters dentinogenesis in vitro. Morphological and cellular alterations are greater when the tooth germs are young and/or when the time of incubation is longer and the dose of fluoride higher. In the predentine, the stainability of proteoglycans is partially reduced. The persistence of alcianophilic zones far from the site of secretion indicates some delay of the process of matricial maturation.

Animals↗
PubMed1984

Endocytotic activity of kitten odontoblasts in early dentinogenesis. 1. Thin section and freeze-fracture study.

The morphological features of odontoblast processes in young kitten odontoblasts were studied by thin section and freeze-fracture electron microscopy. Freeze-fracture replication revealed depressions with particles on the plasma membranes of the proximal parts of odontoblast processes. Comparison with thin sections suggested that these depressions represented sites of endocytosis. Frequent depressions with particles (corresponding to coated pits in thin sections) indicate the high absorptive activity of young odontoblasts. The results indicate that odontoblasts, especially in the proximal parts of their processes, play a significant functional role in the modification of the predentine matrix during early dentinogenesis.

Animals↗
PubMed1995

Genetic mapping of the dentinogenesis imperfecta type II locus.

Dentinogenesis imperfecta type II (DGI-II) is an autosomal dominant disorder of dentin formation, which has previously been mapped to chromosome 4q12-21. In the current study, six novel short tandem-repeat polymorphisms (STRPs) have been isolated, five of which show significant evidence of linkage to DGI-II. To determine the order of the STRPs and define the genetic distance between them, nine loci (including polymorphisms for two known genes) were mapped through the CEPH reference pedigrees. The resulting genetic map encompasses 16.3 cM on the sex-averaged map. To combine this map with a physical map of the region, all of the STRPs were mapped through a somatic cell hybrid panel. The most likely location for the DGI-II locus within the fixed marker map is in the D4S2691-D4S2692 interval of 6.6 cM. The presence of a marker that shows no recombination with the DGI-II phenotype between the flanking markers provides an important anchor point for the creation of physical continuity across the DGI-II candidate region.

Base Sequence↗
PubMedDate not supplied

Presence of dentin phosphoprotein in molars of a patient with dentinogenesis imperfecta type II.

Dentin phosphoprotein (DPP) is the major noncollagenous protein component of the dentin extracellular matrix. This highly acidic phosphorylated protein is solely expressed by the ectomesenchymal-derived odontoblast cells of the tooth organ. Several biochemical studies have suggested diminished levels of, or even the absence of, this protein, which is associated with the human genetic disease dentinogenesis imperfecta (DGI) type II. However, more recent molecular studies have established that the DPP gene locus is not localized to the region of human chromosome 4 (4q13-q21), where several previous linkage analysis studies have mapped DGI types II and III. The purpose of this study was to determine the presence or absence of DPP in the dentition of a patient affected with DGI type II using a sensitive and specific immunodetection method with a polyclonal antibody against mouse DPP. Our results indicate that a 95-kDa protein, immunologically crossreactive with the DPP antibody, was detected within the dentin extracellular matrix of molars isolated from both a proband affected with DGI-II and from an age-matched normal individual. In addition, both DGI-II and normal individuals showed comparable DPP in situ degradation associated with dentin extracellular matrix maturation. These results strongly support the hypothesis that the DPP structural gene does not produce the gene product primarily responsible for the human genetic disease DGI type II.

Adult↗
PubMedDate not supplied

Dentinogenesis Inperfecta. Report of three cases in an Indian family.

An Indian family with Type II Dentinogenesis Imperfecta is reported in which the pedigree was traced through four generations. Clinical and radiological examination was done in three individuals in the family studied, which showed variation in expression of colour and attrition. No clinical evidence of Osteogenesis Imperfecta was noted in any of the family members. Theoretical considerations regarding the development of this disorder and its clinical features are presented.

Adolescent↗
PubMed1996

Dentinogenesis imperfecta: influence of an overdenture on gingival tissues and tooth mobility.

Case report of a child demonstrating severely-worn primary dentition with dentinogenesis imperfecta is presented. Overdentures were fabricated in order to preserve clinical crowns, re-establish the clinical dimension of occlusion and provide esthetics. The patient underwent monthly recall visits for a 6-month period, during which most rapid changes concerning the gingival tissues and tooth mobility were expected.

Alveolar Bone Loss↗