Surface failure of commercial and experimental restorative resins.

A single-pass test was used to study the surface failure of commercial and experimental restorative resins and composites. The surface failure observed for unfilled diacrylate resins was more severe than that seen for an unfilled acrylic resin. Addition of nonsilanated filler to the diacrylate resins increased the resistance to penetration but did not dramatically change the mode of surface failure. The surface failure of the commercial composite resins, which contain silanated filler, was ductile in mode and the resistance to penetration of the diamond slider was the highest of the materials studied. The wear of restorative resins and composites is determined, therefore, by resistance to penetration as well as mode of deformation during sliding.     

Human ameloblastoma tumors express the amelogenin gene.

Instructive signals are responsible for the regulation of the expression of gene products characteristic of many cell lineages during normal development and potentially during neoplasia. The odontogenic origin of ameloblastomas is based largely on the similarity in histologic appearance between the tumor and the developing tooth organ. A pathognomonic pattern for odontogenic tissue-specific gene expression in ameloblastomas has not been previously shown. In these studies, the gene expression parameters for human ameloblastomas have been characterized with the techniques of messenger RNA phenotyping in combination with Northern and in situ hybridization analysis of messenger RNA. The results of these studies confirm that amelogenin, a gene transcribed solely by differentiated ameloblasts, was expressed by epithelial cells from human ameloblastomas. This observation suggests that the instructive signals required for ameloblast differentiation are shared during normal development and tumorigenesis of odontogenic epithelium.     

Immunocytochemical localization of growth hormone receptor in rat maxillary teeth.

To address the question of what role growth hormone may have in stimulating tooth formation, the distribution of its receptor/binding protein in developing rat incisors and molars was studied immunocytochemically using well-characterized monoclonal antibodies. Ten female 45-day-old Wistar rats were perfused with 4% paraformaldehyde. Five-microns paraffin sections of the growing end of maxillary incisors and molars were cut, deparaffinized and incubated with mouse anti-growth hormone receptor antibodies or control antibodies. A three-layer streptavidin peroxidase technique was used to detect bound antibody. Immunoreaction product was associated primarily with the cytoplasm of cells at certain stages of differentiation. Dividing cells, differentiating preameloblasts and preodontoblasts, secretory ameloblasts and odontoblasts showed immunoreactivity. Undifferentiated dental epithelium cells, stellate reticulum, external dental epithelial cells, mature odontoblasts, and most of cells in the dental papilla were non-reactive. However, at certain stages of tooth development, the stratum intermedium and the external dental epithelium also stained positively. The presence of growth hormone receptor/binding protein in tooth cells at different stages of their development indicates that growth hormone may influence cell proliferation, differentiation and differentiated functions of ameloblasts, odontoblasts and cementoblasts independent of a systemic mediator, and thus may be involved in stimulating odontogenesis directly.     

Secondary retention of permanent molars. II. Therapy

The efficacy of 5 treatment modalities for secondary retention of permanent molars was evaluated in 62 patients with 92 affected molars. The results showed that a prosthetic build up is a proper treatment if secondary retention develops late in or after the growth spurt. In these cases the extent of infraocclusion is slight and relatively stable. If secondary retention starts before the growth spurt, immediate removal of the retained molar followed by orthodontic treatment to close the diastema gives maximal success. When secondary retention develops during the growth spurt, the tooth affected has to be observed at six monthly intervals. In such cases, no active treatment is indicated if the extent of infraocclusion is minor and stable. In all other cases the affected molar should be removed, followed by orthodontic closure of the diastema.     

Regulation of glycosaminoglycan synthesis by parathyroid hormone and prostaglandin E2 in cultured dental pulp cells.

The effects of parathyroid hormone (PTH) and prostaglandin E2 (PGE2) on glycosaminoglycan (GAG) synthesis in bovine dental pulp cells were studied. Dibutyryl cyclic adenosine 3',5'-monophosphate and isobutyl methylxanthine were used to assess whether their effects were mediated by intracellular cAMP. Glycosaminoglycan synthesis was assayed by measuring [35S]sulfate incorporation into the GAG fraction of dental pulp cells. Glycosaminoglycan synthesis was increased 1.3-fold by PTH (4 units per ml) alone, 1.6-fold by PTH in the presence of isobutyl methylxanthine, 1.2-fold by PGE2 (100 ng per ml) alone, and 1.5-fold by PGE2 in the presence of isobutyl methylxanthine. Dibutyryl cyclic adenosine 3',5'-monophosphate enhanced GAG synthesis in a concentration-dependent manner and mimicked the effects of PTH and PGE2. The effects of these hormones on pulp and gingival cells were compared; addition of PTH, PGE2, and dibutyryl cAMP had no effect on gingival cell GAG synthesis, whereas their addition induced significant increases of GAG in pulp cells. These results indicate that PTH and PGE2 are involved in the differentiation of dental pulp cells and that these effects are mediated by cAMP.     

Trends in caries prevalence in 5-, 7- and 11-year-old schoolchildren in The Hague between 1969 and 1989.

Starting in 1969, periodic cross-sectional examinations of schoolchildren have been carried out in the city of The Hague. In 1989 the periodic examinations were continued and, in general, caries prevalence was found to be very low; D3MFS values ranged between 1.5 and 2.2 at age 11.8 years. Compared to 1984, 5-year-old-children of low and medium socio-economic levels (SES) in 1989 had significantly higher d3mfs values (p less than 0.01), mainly due to a marked increase in decayed surfaces per child; a significant increase in caries experience of the deciduous dentition amongst 7-year-olds of low social level was found (p less than 0.01). A further reduction of D3MFS values for 7-year-old children of low and medium SES could be observed in 1989 compared to 1984. Between 1978 and 1989 a marked D3MFS reductions amongst 11-year-olds in the three social levels was found. Possible explanations for the observed differences in caries experience between 1984 and 1989 are discussed.