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Morphological and labeling evidence supporting and extending a modern theory of tooth eruption.

As the interest in biological mechanisms of tooth eruption has recently been revived by a new eruption theory, the present study was an attempt to contribute new data to this problem. Four male Macaca fascicularis monkeys, two infant (about 13 months old) and two juvenile (about 44 months old), were labeled either by sequential fluorochrome or by single 3H-proline injections and then served for studying the bone apposition patterns around erupting premolars and molars. About 100 microns thick ground sections cut either in the mesiodistal or bucco-oral direction and the corresponding micrographs, microradiographs and autoradiographs, as well as fluorescence micrographs were used. In the multirooted teeth studied, bone apposition was most prominent and fast in the inter-radicular region, while at the fundus of the alveoli, bone apposition was slight or negligible. Around maxillary premolars and molars, bone apposition pointed in the mesial as well as in the axial direction. This was true for the intraosseous and the supraosseous phase of tooth eruption. Using these observations in addition to preliminary data calculated for the rates of bone apposition in the inter-radicular, apical and crestal regions, and for the rate of root elongation, the new eruption hypothesis could be extended. It is suggested that eruption of multirooted teeth, in the presence of corresponding coronal resorption, is entirely explained by forces generated through inter-radicular bone apposition and that their dental follicle is in a stimulating mode inter-radicularly but neutral apically at the bottom of the alveolar fundus.

Animals↗

Protein kinase A expression and its possible roles in regulating tooth eruption genes in the dental follicle.

BACKGROUND: Tooth eruption requires the chronological expression of a series of genes in the dental follicle (DF). Protein kinase A (PKA) is a major phosphorylation pathway in the cells, and may regulate the expression of tooth eruption genes. MATERIAL/METHODS: In vivo, we studied the expression of the regulatory (R) and catalytic (C) subunits of PKA in the DF of newborn rats. In vitro, dental follicle cells (DFC) were treated with a specific PKA inhibitor, and then the gene expression of monocyte chemotactic protein-1 (MCP-1), colony-stimulating factor-1 (CSF-1) and parathyroid hormone-related protein receptor (PTHrP-R) was determined. Cells also were treated with either phorbol-12-myristate-13-acetate or dibutyryl-cAMP, and the gene expression for RI alpha, RI beta, RII alpha and RII beta of PKA was examined. RESULTS: The results indicate that RI alpha of PKA is the predominant subunit in the DF with steady expression from days 1 to 11 postnatally. In contrast, expression of the RI beta, RII alpha, RII beta subunits are progressively reduced over this time period. However, there is a sharp decline of RI beta expression at postnatal day 3. The expression of the C subunits slightly decreases at days 3 and 5 with a greater decrease at day 7 postnatally. The specific PKA inhibitor reduces MCP-1 gene expression and translation, as well as moderately reducing CSF-1 and PTHrP-R expression. CONCLUSIONS: The reduction of the RI beta subunit in the rat DF at day 3 may result in an elevated PKA activity to trigger the maximal burst of gene expression of MCP-1 and CSF-1 seen at this time.

Animals↗

The basic and applied biology of tooth eruption.

The dentition and the alveolar process of each jaw develop simultaneously so that, by the time the crown is completed and eruption begins, the crown is enclosed in a crypt within alveolar bone. Thus, the eruption of a tooth to its functional position involves discretely localized, bilaterally symmetrical bone resorption to produce an eruption pathway and bone formation to fill in the space previously occupied by the crown and growing roots. Studies of crypt surfaces during eruption confirm this polarization of alveolar bone metabolism around a tooth with respect to both bone cells and mineralized surface topography. Experimental studies of tooth eruption have shown that the dental follicle, the dense connective tissue investment of the tooth, is necessary for eruption and that neither bone resorption nor bone formation occur without the adjacent part of the dental follicle. Early in eruption the coronal part of the follicle accumulates mononuclear cells which have cytochemical and ultrastructural features of osteoclasts and the apical part of the follicle, a site of intense cell proliferation, binds epidermal growth factor (EGF). The dental follicle contains a variety of proteins and the concentration of several change during eruption. Prominent among them are a reduction in matrix metalloproteinases and an increase in protoglycans as eruption proceeds. The contribution of these changes to those in cell proliferation, migration and differentiation during tooth eruption present experimental opportunities for developmental biologists. The rate-limiting factor of the earliest (intraosseous) stage of tooth eruption is bone resorption and eruption can be accelerated or retarded by the local delivery of factors which increase or decrease the activity of osteoclasts.(ABSTRACT TRUNCATED AT 250 WORDS)

Alveolar Process↗

Effect of calcium phosphate ceramic particle insertion on tooth eruption.

The effects of calcium phosphate ceramic implants on tooth eruption were investigated radiographically and histologically in 20 3-month-old dogs. Four kinds of ceramic particles were used: dense and porous hydroxyapatite particles, and dense and porous tricalcium phosphate particles. These particles were implanted in the sockets after deciduous tooth extraction. The four types of calcium phosphate ceramic particles produced similar radiographic and histologic findings. There was no delay of tooth eruption, no dysplasia, and no resorption of dental hard tissue.

Animals↗

New forensic approach to age determination in children based on tooth eruption.

The present study proposes equations for age determination both in living and dead children, obtained with the help of stepwise ascending multiple linear regression. The equations should be applied, based on the number of erupted teeth and tooth germs, which were detected on radiographs, during clinical examination and in infant skeletal remains. The proposed equations proved to be efficient just like Demirjian's method used as a reference today, and permit age estimation till 20 years of age.

Adolescent↗

Exposure to oral uranyl nitrate delays tooth eruption and development.

The risk of oral exposure to uranium potentially involves the population at large. Tooth eruption and development are ongoing processes that begin during fetal development and continue until the age of 18 y. Since one of the mechanisms involved in tooth eruption is bone formation and it is well documented that uranium inhibits bone formation, the aim of the present work was to study the effect of oral administration of uranyl nitrate (UN) on tooth eruption and development. Wistar rats aged 1 and 7 d were orally administered a single dose of 90 mg kg(-1) body weight of uranyl nitrate. Two age matched groups received an equal volume of saline and served as controls. The animals were killed at 7 and 14 d of age, respectively. Mandibles were resected and processed to obtain bucco-lingual sections oriented at the level of the mesial root of the first mandibular molar, and histomorphometric studies were performed. Results showed that an acute high dose of uranyl nitrate delays both tooth eruption and development, probably due to its effect on target cells.

Animals↗

A mechanism of noncontinuous supraosseous tooth eruption.

Numerous theories have been propounded to explain the various aspects of tooth eruption, but no general consensus exists about some of the underlying mechanisms that govern these aspects. An important unresolved issue is the source of the motive forces that displace teeth. We proposed that supraosseous eruptive forces are generated by tooth socket distortions caused by functional jaw deformations. Previous studies used basic equations of static equilibrium to demonstrate that the concomitant stretching of the oblique periodontal ligament (PDL) fibers give rise to forces that may cause supraosseous tooth eruption. For a more rigorous and expanded analysis, we applied the finite element method (FEM). Three functional loads were considered, but the FEM calculations strongly suggested that all jaw deformations contribute to tooth extrusion. It was also demonstrated that the PDL fiber disruptions that are likely to occur with increased stretching can provide a mechanism to stabilize the erupted position.

Computer Simulation↗

Delayed tooth eruption and suppressed osteoclast number in the eruption pathway of heterozygous Runx2/Cbfa1 knockout mice.

Genetic studies have recently identified a mutation of one allele of runt-related gene 2 (RUNX2/CBFA1) as the cause for an autosomal-dominant skeletal disorder, cleidocranial dysplasia (CCD), which is characterised by hypoplasia of the clavicles and calvariae and widened sutures and fontanelles. In addition, CCD is frequently affected with multiple supernumerary teeth and the impaction and delayed eruption of teeth, the causes of all these dental abnormalities are still unknown. To clarify the cellular mechanism of the delayed tooth eruption in CCD, the process of tooth eruption was examined in heterozygous Runx2/Cbfa1 (mouse homolog of RUNX2/CBFA1) knockout mice, known to mimic most of the bone abnormalities of CCD. The timing of the appearance of maxillary and mandibular teeth into the oral cavity was significantly delayed in heterozygous mutant mice compared with wild-type mice. From postnatal days 8 to 10, an active alveolar bone resorption and a marked increase of the osteoclast surfaces was observed in the eruption pathway of both genotypes, but this increase was significantly suppressed in the mutant mice. In contrast, the osteoclast surfaces did not show a significant difference between the two genotypes in the future cortical area of femora. These results suggest that haploinsufficiency of Runx2/Cbfa1 does not effect the femoral bone remodelling but is insufficient for the active alveolar bone resorption essential for the prompt timing of tooth eruption. These results also suggest the possibility that impaired recruitment of osteoclasts is one of the cellular mechanisms of delayed tooth eruption in CCD patients.

Animals↗

In vivo expression of classic PKC isoforms in the rat dental follicle as related to tooth eruption.

Activation of protein kinase C (PKC) can upregulate tooth eruption molecules such as osteoprotegerin (OPG) and vascular endothelial growth factor (VEGF). In this study, we examined the in vivo gene expression of classic isoforms of PKC in the dental follicle of postnatal rats. The expression level of PKC-alpha was significantly reduced at day 3 followed by a gradual return to day 1 level, a profile similar to OPG expression. The expression of PKC-beta was the lowest at day 1 followed by elevated levels from day 3 to day 11. Expression of PKC-beta is positively correlated with the expression of overall VEGF and VEGF120. The expression level of PKC-gamma was relatively steady in the postnatal days. Injection of a PKC activator, phorbol 12-myristate 13-acetate (PMA), at late postnatal days, slightly accelerated first mandibular molar eruption. This study suggests that PKC isoforms may be involved in the regulation of tooth eruption.

Animals↗

Effect of calcium phosphate ceramic implants on tooth eruption.

This study evaluated the effects of calcium phosphate ceramics, hydroxylapatite, and tricalcium phosphate implants on tooth eruption and development. Forty kittens, three to four months of age, had their primary right second and third mandibular premolars extracted and the sockets packed with either hydroxylapatite, tricalcium phosphate, autogenous cancellous marrow, or nothing. The results of this study indicated that the use of a nonresorbable hydroxylapatite for grafting resulted in impediment of tooth eruption and distortion of crown development. This was in contrast to the tricalcium phosphate, which had minimal effect on tooth eruption and development.

Alveolar Process↗

Collagen metabolism and tooth eruption: the effects of sodium morrhuate infusions on premolar eruption in dogs.

To test the essential contribution to tooth eruption of the known high level of collagen metabolism in the periodontal ligament, we have infused the crypts of erupting premolars in dogs with sodium morrhuate, a compound known to reduce production, hydroxyproline content and maturation of collagen. Infusions of sodium morrhuate early or later in eruption for more than half the period of eruption had no effect on the process evaluated radiographically and clinically. These data, considered together with other studies, suggest that collagen metabolism per se plays no essential role in tooth eruption.

Animals↗

Radiographic and histological analysis of tooth eruption through calcium phosphate ceramics in the cat.

The effect of implanting calcium phosphate ceramics (CPC) into metabolically active sites within kitten mandibles during permanent premolar tooth eruption was examined. Forty kittens, 3-4 months of age were used: the deciduous second and third mandibular premolars were extracted and their sockets implanted with autologous blood clot, autogenous cancellous marrow, and the calcium phosphate ceramics, non-porous beta-tricalcium phosphate or porous hydroxylapatite. Animals were killed at 1, 2, 3, 4 and 5 months after implantation and undermineralized sagittal sections were evaluated by light microscopy. Eighty percent of hydroxylapatite implanted mandibles showed delay in tooth eruption concurrent with distortion in crown development, and a dense cellular fibro-proliferative response within the follicle of unerupted teeth. This response occurred in only one specimen with tricalcium phosphate, whereas normal eruptive patterns and crown development were routinely noted. Both the tricalcium phosphate and hydroxylapatite were integrated into the surrounding alveolar bone without evidence of an inflammatory response. Thus hydroxylapatite initiated a dense cellular fibrous network within the dental follicle preventing formation of an eruptive pathway, delaying tooth eruption and causing crown deformation. This was rarely seen with tricalcium phosphate, and may be due to the resorbability of tricalcium phosphate when compared to hydroxylapatite. Hydroxylapatite should therefore be used with caution for implanting into areas containing unerupted teeth with a metabolically active dental follicle.

Animals↗

Delay of tooth eruption in null mice devoid of the type I IL-1R gene.

Interleukin-one alpha (IL-1alpha) is located in the stellate reticulum and its receptor, type I IL-1R (IL-1R), is present in the adjacent dental follicle. IL-1alpha may play a role in initiating tooth eruption because of its ability to enhance the gene expression in the dental follicle of putative tooth eruption molecules colony-stimulating factor-one (CSF-1). monocyte chemotactic protein-1 (MCP-1), and nuclear factor kappa B (NFkappa-B). To directly examine the effect of IL-1alpha and IL-1R on tooth eruption, we observed the times of tooth eruption in null mice devoid of the type I IL-1R gene. The results showed that the time of eruption in the null mice was delayed by 2 d for the first mandibular molar and 1 d for incisors as compared to wild type controls. Reverse transcription-polymerase chain reaction (RT-PCR) techniques confirmed the absence of the IL-1R gene in the null mice, but the genes for CSF-1 and NFkappaB were still expressed. Thus, a molecule(s) other than IL-1alpha also may enhance the expression of CSF- and NFkappaB in the dental follicle. Because there is a slight delay of tooth eruption in IL-1R null mice, IL-1alpha may normally play a role in eruption. However, eruption eventually can occur without the signaling from IL-1alpha.

Animals↗

Nutritional status, tooth eruption, and dental caries: a review.

Animal studies have shown that early malnutrition affects tooth structure, delays tooth eruption, and results in increased dental caries. However, epidemiologic evidence in support of these findings has been elusive. Cross-sectional surveys show that populations with a higher prevalence of caries in their deciduous teeth also show a lower prevalence of caries in their permanent teeth. However, longitudinal data from individuals show exactly the opposite. Caries development is also delayed as a consequence of a delayed tooth eruption and thus the bell-shaped curve that results from plotting deciduous caries prevalence vs age is shifted to the right in malnourished children. This effect will result in an apparently negative association between caries in deciduous and permanent teeth when cross-sectional surveys are compared. Once the effect on tooth eruption is taken into account, the contribution of malnutrition to increased caries susceptibility may be observed, as demonstrated by a recent cross-sectional study involving Peruvian children.

Adolescent↗

Collagen responsible for tooth eruption? A study of the eruption of rat incisors.

The rate of turnover of collagen in periodontal ligament (PDL) is closely associated with the process of tooth eruption and tissue adaptation allowing good anchorage of the tooth within the socket. Collagen may even be associated with orthodontic relapse. As the collagen protein seems to play a key role in tooth eruption, the investigation concentrated on the presence and maturation of collagen and its possible function in the process of tooth eruption.

Aminoacetonitrile↗

Impaired tooth eruption: a review.

Eruption is the continuous process of movement of a tooth from its developmental location inside the jaw to its functional location in the mouth. Impaired tooth eruption, where this process is disturbed, is common in dental practice. It may manifest either as delayed or complete absence of eruption. Although unerupted teeth are usually asymptomatic, they may cause cosmetic and pathologic complications. The purpose of this article is to provide a review on the pathogenesis and differential radiographic interpretation of impaired tooth eruption.

Amelogenesis Imperfecta↗

Osteoprotegerin and osteoclast differentiation factor in tooth eruption.

A critical cellular event in tooth eruption is the formation of osteoclasts that are needed for bone resorption to form an eruption pathway. To analyze molecular regulation of osteoclast formation and activation, we examined the expression of osteoprotegerin (OPG), an inhibitor of osteoclast formation. In vivo, the gene expression of OPG is reduced in the dental follicle of the first mandibular molar of the rat at day 3 post-natally and in the mouse at day 5. This correlates with the days of maximal mononuclear cell influx and osteoclast numbers in the rat and mouse. Thus, inhibition of OPG gene expression on these days might allow osteoclasts to be formed and/or activated. In vitro studies demonstrated that both colony-stimulating factor-1 and parathyroid hormone-related protein reduced OPG gene expression in follicle cells, suggesting that these are candidate molecules for the in vivo inhibition of OPG expression. Osteoclast differentiation factor (ODF) immunolocalizes to the alveolar bone stromal cells adjacent to the follicle, whereby it might act to stimulate fusion of the mononuclear cells in the follicle.

Alveolar Process↗