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PubMed1999

Evaluation of oral problems in an osteogenesis imperfecta population.

OBJECTIVE: The incidence of craniofacial and dental anomalies in children with the more severe nonlethal forms of osteogenesis imperfecta was evaluated. STUDY DESIGN: The study evaluated 40 children (age range, 1-17.5 years) with types III and IV osteogenesis imperfecta. In each case, the dentition was evaluated for the presence of dentinogenesis imperfecta, attrition, and caries, as well as for radiographic appearance, dental development, and malocclusion. RESULTS: The incidence of dentinogenesis imperfecta was greater than 80% in the primary dentition. Clinically, the color of the dentition was of predictive value in appropriate management of the primary dentition. Tooth discoloration and attrition did not occur to the same extent in the permanent dentition as in the primary dentition in either group. Class III dental malocclusion occurred in 70% to 80% of this osteogenesis imperfecta population, with a high incidence of anterior and posterior cross bites and open bites. A delay in dental development was observed in 21% of patients type III osteogenesis imperfecta, whereas accelerated development was noted in 23% of the patients with type IV. In addition, ectopic eruption occurred in 13 patients. CONCLUSIONS: In addition to dentinogenesis imperfecta, significant oral problems occur in types III and IV osteogenesis imperfecta. Other features that impact the dental management of this population are highlighted.

Adolescent↗
PubMed1996

Effect of xylitol on dentin formation in molars of adult rats.

A xylitol-induced reduction in dentin formation has been observed in molars of post-weanling rats, but the effect in older animals with a slower rate of secondary dentinogenesis has not been investigated. We examined the effects of different concentrations of dietary xylitol on dentinogenesis in molars of young adult rats. The control group received a commercial basal diet, while for the other 3 groups, the same diet was supplemented with 5, 10 and 20% of xylitol. After 8 weeks, dentin thickness beneath the main fissures in the mandibular 1st and 2nd molars was measured. The final body weights did not differ between the groups. Dentin formation in the 1st molars of the 10 and 20% xylitol groups was significantly lower as compared to the controls, whereas no difference was found between these 2 groups. In conclusion, dietary xylitol reduces dentin formation in young adult rats in spite of the slow rate of dentinogenesis.

Animals↗
PubMedDate not supplied

Dentin dysplasia, type II linkage to chromosome 4q.

Dentin dysplasia, type II (MIM*125420) is an autosomal dominant disorder of dentin development. Clinically the primary dentition appears opalescent, and radiographically the pulp chambers are obliterated, resembling dentinogenesis imperfecta. However, unlike dentinogenesis imperfecta, the permanent teeth in dentin dysplasia, type II are normal in color and, on radiographs, have a thistle-tube pulp chamber configuration with pulp stones. The similarity of the primary dentition phenotype suggested that the gene for dentin dysplasia, type II is allelic with the gene for dentinogenesis imperfecta, Shields type II (DGII; MIM*125490), which has been localized to chromosome 4q13-q21. Twenty-four members of a three generation family in which ten members are affected with dentin dysplasia, type II were genotyped for microsatellite alleles specific for the area of chromosome 4q linked to DGII. Linkage was assessed by using the LINKAGE computer program, assuming autosomal dominant inheritance, a disease allele frequency of 0.0001, and complete penetrance. The maximum two-point LOD score (Zmax = 4.2 at theta = 0.0) was obtained with SPPI and D4S2691. Multipoint analysis gave a maximum LOD score of 4.33. The candidate region for dentin dysplasia, type II is approximately 14.1 cM, includes SPPI, D4S2691, D4S2690, D4S451, and D4S2456, and overlaps the most likely location of the DGII locus. A candidate gene for DGII should also be considered a candidate gene for dentin dysplasia, type II.

Alleles↗
PubMed2000

The reducing effects of a calcium-deficient diet and high sucrose diet on dentin apposition of rat molars.

A high sucrose diet reduces dentin apposition of growing rats. The mechanisms of reduction are unclear, but disturbances in calcium balance or in mineralization of predentin may explain them. In this experiment, 29 Sprague-Dawley rats, 21 days old, were weaned and randomized into calcium-deficient, high-sucrose or standard-diet groups for 3 weeks. They were given food and water ad libitum. During the experiment, animals were individually housed in metabolic cages where urine samples were collected. At ages of 21 and 40 days mineralizing dentin was marked using I.P. injections of oxytetracycline hydrochloride. At 42 days of age, the animals were anesthetized and their blood was collected by cardiac puncture. Right hemimandibles were sectioned sagittally and left hemimandibles were fixed, decalcified, and cut into histological sections. Dentin appositions were measured planimetrically, predentin width, from histological sections. Ca, K, and Na levels of serum and urine were measured flame photimetrically and P levels were measured by the UV method. Statistical analyses were done using one-way analysis of variation (ANOVA) Tuckey's HSD t test. In the calcium-deficient group, hypocalcemia, reduced dentin apposition, and increased predentin width were noticed when compared with the control group (P<0.05). Also, the increase in predentin width, caused by calcium deficiency, was significant compared with sucrose-fed animals (P<0.05). Sucrose diet reduced dentinogenesis, increased Ca excretion to urine, but also reduced urinary levels of P, K, and Na, and the differences were significant for the controls (P<0.05). In conclusion, despite the same kind of reduced dentinogenesis in calcium-deficient and high-sucrose groups, calcium imbalance or reduced mineralization of predentin does not explain reduced dentinogenesis in sucrose-fed animals.

Animals↗
PubMed2000

Immunohistochemical expression of neural tissue markers (neuron-specific enolase, glial fibrillary acidic protein, S100 protein) in ameloblastic fibrodentinoma: a comparative study with ameloblastic fibroma.

Formalin-fixed paraffin-embedded sections of three cases of ameloblastic fibrodentinoma (AFD) were studied by the avidin-biotin-peroxidase complex method using antibodies against neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP) and S100 protein and the results were compared with those in ameloblastic fibroma (AF). A striking histopathological characteristic of AFD was the formation of abortive dentin with various degrees of maturation at the epithelial-mesenchymal tissue interface. Central cells of enamel organ-like epithelia with various stages of abortive dentin induction in AFD were generally positive for NSE. Dental lamina-like epithelial cells also showed positive staining in some areas. No cells were positive for NSE in AF. Positive staining for GFAP was observed in the juxta-epithelial mesenchymal tissue of the formation stage of immature dentin with various numbers of entrapped cells in AFD, but GFAP staining was negative in other mesenchymal and epithelial tissues at other stages. In AF, no GFAP-positive cells were found. There were a few S100 protein-positive cells found in the foci of epithelial components in both AFD and AF. Mesenchymal cells showing a dendritic or spindle shape were positive for S100 protein in some areas of AFD and AF. Although such cells in the mesenchymal component of pigmented AFD were more numerous than in non-pigmented AFD and AF, their distribution pattern in the former condition was basically similar to that in the latter. Although the present results, obtained from conventional immunohistochemical procedures, do not directly reflect the expression of neural crest-derived cells in the dentinogenesis of AFD, such results do not disprove the possibility of the expression of neural proteins probably related to neural crest-derived cells in dentinogenesis under certain pathologic conditions in odontogenic mixed tumors. Such a phenomenon may also occur during dentinogenesis in other odontogenic mixed tumors and in normal tooth differentiation, but at an undetectable level.

Adult↗
PubMed2000

Reduced expression of dentin sialophosphoprotein is associated with dysplastic dentin in mice overexpressing transforming growth factor-beta 1 in teeth.

Transforming growth factor (TGF)-beta1 is expressed in developing tooth from the initiation stage through adulthood. Odontoblast-specific expression of TGF-beta1 in the tooth continues throughout life; however, the precise biological functions of this growth factor in the odontoblasts are not clearly understood. Herein, we describe the generation of transgenic mice that overexpress active TGF-beta1 predominantly in the odontoblasts. Teeth of these mice show a significant reduction in the tooth mineralization, defective dentin formation, and a relatively high branching of dentinal tubules. Dentin extracellular matrix components such as type I and III collagens are increased and deposited abnormally in the dental pulp, similar to the hereditary human tooth disorders such as dentin dysplasia and dentinogenesis imperfecta. Calcium, one of the crucial inorganic components of mineralization, is also apparently increased in the transgenic mouse teeth. Most importantly, the expression of dentin sialophosphoprotein (dspp), a candidate gene implicated in dentinogenesis imperfecta II (MIM 125420), is significantly down-regulated in the transgenic teeth. Our results provide in vivo evidence suggesting that TGF-beta1 mediated expression of dspp is crucial for dentin mineralization. These findings also provide for the first time a direct experimental evidence indicating that decreased dspp gene expression along with the other cellular changes in odontoblasts may result in human hereditary dental disorders like dentinogenesis imperfecta II (MIM 125420) and dentin dysplasia (MIM 125400 and 125420).

Animals↗
PubMedDate not supplied

The future role of a molecular approach to pulp-dentinal regeneration.

The ultimate goal of a regenerative pulp treatment strategy is to reconstitute normal tissue continuum at the pulp-dentin border, regulating tissue-specific processes of tertiary dentinogenesis. Experimental investigations in mature teeth have shown that a network of extracellular matrix molecules and growth factors signal tertiary dentinogenesis. Application of dentin matrix components or growth factors in deep dentinal cavities stimulated up-regulation of biosynthetic activity of primary odontoblasts (reactionary dentin formation). Pulp-capping studies with a broad spectrum of biological agents, including growth factors and extracellular matrix molecules, showed formation of osteodentin and/or tertiary dentinogenesis (reparative dentin formation). Promising biologically active substances should be subjected to careful evaluation in well-designed preclinical investigations as well as in long-term clinical trials before their introduction in clinical practice.

Animals↗
PubMed1995

Focal c-fos expression in developing rat molars: correlations with subsequent intradental and epithelial sensory innervation.

The purpose of this study was to analyze the temporal and spatial patterns of expression of the inducible transcription protein Fos and the Fos-related antigens (Fra) in developing rat teeth. Immunoreactivity (IR) for Fos/Fra was analyzed at postnatal age 1-35 days. A transient gradient of Fos/Fra-IR was found in all the molars in the coronal odontoblasts along sites of dentinogenesis, with numerous cells and intense staining near the pulp horn tip, and fewer cells and less staining in mid-crown and cervical pulp. This gradient was well established in first molars of the one day old rats; it was first seen in second molars in the 2 day old rats; and it was found in third molars at 10 days. The Fos/Fra-IR was transient and faded after a few days. Rat molars have a tilted orientation so that maxillary molar crown cusps point in a posterior direction and mandibular crowns in the anterior direction. In each set of molars dentinogenesis was initiated along the side of each pulp horn closest to the gingival surface, i.e. anterior for maxillary crowns and posterior for mandibular crowns; and the Fos/Fra-IR first appeared next to those asymmetric sites. As the wave of dentinogenesis spread around the crown, it was accompanied by odontoblastic expression of Fos/Fra-IR that had decreasing intensity in mid- and cervical crown. Molar root pulp lacked Fos/Fra-IR, and incisor teeth only had odontoblastic and ameloblastic immunoreactivity in the 1 day old rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMedDate not supplied

A radiographic survey of dental anomalies in Black pediatric patients.

During seemingly routine check-ups, the dental practitioner must be ever aware of "quiescent" abnormalities or irregularities. Knowledge of special problems occurring within a certain patient population is of great value to the practitioner when evaluating the individual patient. Numerous studies have been conducted evaluating the pediatric Caucasian population; however, no comparable studies for the Black pediatric population have been done. This study sought to establish prevalence rates for the Black pediatric population with regards to the following anomalies: congenitally missing teeth, supernumerary teeth, dens in dente, odontomas, dentinogenesis imperfecta, gemination, fusion and concrescence. The radiographs (panographs mandatory), history forms and treatment progress records of 2,267 children (1,136 males and 1,131 females) were analyzed. Radiographs of poor quality were eliminated and attempts were made to include only children of Black American heritage. Prevalence rates established for a predominantly Black pediatric population were: 4.4%, congenitally missing teeth; 1.49%, supernumerary teeth; 0.26%, dentinogenesis imperfecta (Brandywine type); 0.44%, odontomas; 0.22%, gemination; and 0.12%, fusion. Evidence of dens in dente was found in only one erupted supernumerary maxillary paralateral, and the detection of only one case of concrescence occurred; both have prevalence rates of 0.04%. No other study has produced such a high rate of dentinogenesis imperfecta (.26%), except that conducted within the tri-racial group itself. In addition, if assumptions are to be made from this investigation for the general population, supernumeraries and odontomas may be present significantly more often in the Black than Caucasian pediatric population.

Adolescent↗
PubMed1992

The role of osteonectin in human tooth development: an immunohistological study.

We investigated immunohistologically 160 teeth and dental germs in various stages of tooth development taken from human individuals (13th week of pregnancy to the 24th year of life) to study the osteonectin expression in dental hard tissue. In the course of dentinogenesis, the predentin, the odontoblasts, and their cell processes show a positive osteonectin staining reaction. During cementogenesis, osteonectin is synthesized by cement-producing fibroblasts, cementoblasts, and cementocytes. The expression of osteonectin during dentinogenesis and cementogenesis is closely related to the development of the respective calcified tissue. All cells of the inner and outer enamel epithelium, the cells of the stratum reticulare and stratum intermedium, the ameloblasts, and the enamel substance are osteonectin negative, just as dentin and cement are. The results of this study indicate one important physiological role of osteonectin as a protein associated with the formation of collagen containing mineralizing tissues like human bone, as well as human dentin and cement.

Adolescent↗
PubMed1982

Proteolytic activity of developing dentine of rat tooth germs revealed by the gelatin-film substrate technique.

The ability of tooth germs to breakdown gelatin was investigated by incubating unfixed cryostat sections of 3-8 day rat molar tooth germs on processed photographic plates. Breakdown of gelatin occurred exclusively in regions which were overlain by developing dentine and bone, suggesting that these tissues contain proteolytic enzymes. As the proteolytic activity occurred at a pH closer to that of the extracellular fluid, i.e. closer to neutrality, it is proposed that neutral proteases, presumably released by odontoblasts, breakdown components of the organic matrix during dentinogenesis. The products of breakdown may, in turn, be taken up by odontoblasts to be further degraded in their extensive lysosomal-vacuolar system. Breakdown and resorption of matrix components may reflect the normal turnover of matrix materials, or may be a mechanism concerned with the regulation of either the amount of materials present in the matrix or its chemical composition during dentinogenesis.

Animals↗
PubMed1992

Short-term dentinogenic response of dog dental pulp tissue after its induction by demineralized or native dentine, or predentine.

The events initiating the expression of odontoblastic potential by pulpal ectomesenchymal cells were investigated by exposing the pulp to demineralized, native and unmineralized autogenous dentine. The pulp responses to implants were histologically evaluated 3, 7 and 10 days postoperatively, while the surface structure of the newly mineralized matrices was examined 12 and 28 days after implantation. Differentiation of odontoblast-like cells in close proximity to the implanted matrix was consistently demonstrated after exposure to predentine. Scattered columnal cells undergoing polarization, characterized ultrastructurally by the orientation of their rough endoplasmic reticulum, were also found in direct contact with the demineralized dentine. However, in response to demineralized implants, groups of differentiated odontoblast-like cells were clearly seen only in association with a zone of matrix secreted in a polar, predentine-like pattern, indicating an asynchronous inductive influence of this type of implant on pulp cells. Further, the response of pulp cells to native dentine was characterized by the elaboration of a two-layered matrix (a fibrous and a polarly deposited matrix) before initiation of secondary dentinogenesis. Scanning electron microscopy of the newly deposited matrices revealed differences between the indirect matrix synthesis, observed in short-term response to implants of demineralized or native dentine, and the specific, dentinogenic function of the odontoblast-like cells. These observations indicate that the dentine-induced dentinogenesis is initiated by two mechanisms--direct induction of odontoblast-like cells as well as indirect matrix synthesis, which further controls cell polarization. Immobilization of the cells on implanted matrix seems to be the critical requirement for direct expression of the odontoblastic phenotype.

Animals↗
PubMed1992

Effects of epidermal growth factor and transforming growth factor-beta on insulin-induced differentiation in rat dental pulp cells.

An established pulp cell line (RPC-C2A) was used to study the regulatory effect of insulin on dentinogenesis. Insulin increased alkaline phosphatase activity and the incorporation of [2,3-3H]-proline into collagenase-digestible protein, whereas [3H]-thymidine incorporation by the cells was inhibited by insulin. The enhancing effect of insulin on alkaline phosphatase activity was inhibited by epidermal growth factor (EGF) or transforming growth factor-beta (TGF-beta). The stimulatory effect of insulin on collagen synthesis was also inhibited when insulin was combined with EGF, but was accelerated by the addition of TGF-beta. Inhibitory effects of insulin on the [3H]-thymidine incorporation were potentiated by EGF, though EGF alone strongly increased the effect; whereas the addition of TGF-beta had no significant effect on the insulin action. These findings suggest that insulin may be concerned with the differentiation of pulp cells in dentinogenesis and that EGF or TGF-beta regulate the insulin effects.

Alkaline Phosphatase↗
PubMed1993

Developmental pattern and subcellular localization of parvalbumin in the rat tooth germ.

The EF-hand calcium-binding protein parvalbumin has been extensively studied in nerve and muscle cells. Its possible role in biomineralization during tooth development was here investigated by determining its subcellular localization by immunogold cytochemistry. The developmental sequences of amelogenesis and dentinogenesis were studied in rat molars, and in continuously growing rat incisors. The findings confirm that parvalbumin is a nuclear and a cytosolic protein, not associated with any particular intracellular organelle. Epithelial and mesenchymal undifferentiated cells contained no specific parvalbumin immunolabelling. In differentiated ameloblasts, secretory-pole (Tomes' process) formation was associated with a proximal-distal gradient of parvalbumin labelling. But after the Tomes' process had formed, parvalbumin was evenly distributed throughout the cell. The parvalbumin contents of ruffle-ended and smooth-ended ameloblasts appeared to be very different. Differentiated odontoblasts were less heavily labelled than ameloblasts, and the label was restricted to the cell body during the whole of dentinogenesis. These data suggest that parvalbumin could contribute to membrane plasticity during differentiation, as shown during dendritic growth in the nervous cells. Moreover, as may occur in excitable cells, parvalbumin could buffer calcium specifically in the cells producing mineralized enamel and dentine during the later stages of tooth development.

Ameloblasts↗
PubMed1994

A confocal laser scanning microscopic study of the immunofluorescent localization of fibronectin in the odontoblast layer of human teeth.

The distribution of fibronectin in dental pulp was studied in developing and developed human teeth by indirect immunofluorescence using a confocal laser scanning microscope. In the apical region of developing teeth, intense fluorescence was found along the basement membrane facing the mesenchyme of Hertwig's epithelial sheath and first-formed (mantle) predentine. With further elongation of odontoblasts, fibronectin was observed between the cells, appearing as corkscrew fibres passing from the pulp into predentine parallel to the long axis of the odontoblasts. In the coronal region of developing and developed teeth a similar distribution of fibronectin was observed in the odontoblast layer. At the border zone between odontoblasts and predentine the reaction was intense, but was weak in the predentine itself. In the calcified dentinal matrix it had disappeared completely, except for the area along the dentinal tubules. The results demonstrate that fibronectin is present in the odontoblast layer during all stages of dentinogenesis. Fibronectin-positive fibrous structures between odontoblasts probably correspond to von Korff fibres, and are closely related to odontoblast differentiation and dentinogenesis.

Adult↗
PubMed1985

An unusual presentation of opalescent dentin and Brandywine isolate hereditary opalescent dentin in an Ashkenazic Jewish family.

Two children of Austrian Ashkenazic Jewish background, related as second cousins, have a variant of opalescent dentin in their deciduous teeth. This has been classified by Witkop as Brandywine isolate hereditary opalescent dentin and by Shields as dentinogenesis imperfecta type III. One of the children also has dysmorphic facial features, seizures, and severe mental retardation. Her mother has dysmorphic facial features and mild mental retardation. The mothers of both children and several other family members have classic opalescent dentin (dentinogenesis imperfecta type II). Radiographs of the deciduous and permanent dentitions of one mother showed obliterated pulp chambers. Confirmation of obliterated pulp chambers in the deciduous teeth of the mother of a child with Brandywine isolate hereditary opalescent dentin makes it unlikely that classic opalescent dentin and Brandywine isolate hereditary opalescent dentin are separate genetic disorders. Evidence from this family supports the hypothesis that Brandywine isolate hereditary opalescent dentin is a variant of opalescent dentin.

Adult↗
PubMed1993

Multiple idiopathic mandibular bone cysts in a patient with osteogenesis imperfecta.

Although the most common oral manifestation of osteogenesis imperfecta is dentinogenesis imperfecta, several authors have described jaw fractures and radiolucent bone lesions associated with this disease. We report a case of a 23-year-old white woman with osteogenesis imperfecta and dentinogenesis imperfecta who developed multiple unilocular, bilateral, radiolucent lesions of the mandible 5 years after presenting with a condylar fracture. This is the first documentation by surgical and histopathologic examination that the radiolucent lesions in this particular case represent multiple idiopathic bone cysts.

Adult↗
PubMed2005

Effects of maternal ethanol intake on immunoexpression of epidermal growth factor in developing rat mandibular molar.

OBJECTIVE: A polyclonal antibody was used to investigate the effects of ethanol ingestion before and during pregnancy, in the expression of EGF on dentinogenesis and amelogenesis of rat mandibular first molar. DESIGN: Ethanol was administered to drinking water (treated group) starting at concentrations of 1% and increasing weekly to 5, 10, 15, 20 and 25% (v/v). During week 7, these rats were mated and continued to receive the 25% alcoholic solution, up to delivery. The control group received tap water. On postnatal days 0, 4 and 9, two offspring of each litter were killed, their hemimandibles removed and prepared for paraffin processing and immunohistochemistry. RESULTS: At postnatal day 0 the EGF immunoreactivity of the inner enamel epithelium and presecretory ameloblasts was weak when compared to controls. At postnatal day 4 EGF immunoreactivity of the secretory ameloblasts and odontoblasts was only moderate compared to controls. At postnatal day 9 EGF staining of the ameloblasts was weak when compared to controls. CONCLUSIONS: These results suggest that, maternal alcoholism interferes with EGF expression during initial dentinogenesis and amelogenesis and in the secretion and maturation of the dentin and enamel, therefore, which may cause a reduction of dentin and enamel formation.

Amelogenesis↗