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Results for “TOOTH ERUPTION”

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At least 19 recordsLinked to original sources
PubMed2003

Expression of extracellular matrix molecules, MMPs and TIMPs in alveolar bone, cementum and periodontal ligaments during rat tooth eruption.

Tooth eruption involves extensive degradation and reorganization of extracellular matrix (ECM) components. It is not known how ECM-degrading enzymes are coordinated with each other or how they are regulated in the event. The present study was designed to investigate mRNA expression of inhibitors of metalloproteinases (TIMPs) in comparison with matrix metalloproteinases (MMPs) as well as ECM molecules during rat first molar eruption using in situ hybridization. We also examined how TIMPs are involved in the process of tooth eruption, root formation, cementogenesis and alveolar bone remodelling. Expressions of type-I collagen, osteocalcin, MMPs 2 and 8, and TIMPs 1, 2 and 3 were shown in osteoblasts, osteocytes, cementoblasts, cementocytes and periodontal ligament fibroblasts, and the concomitant high expressions of the ECM molecules, MMPs and TIMPs in alveolar bone, cementum and periodontal ligaments were identified in the middle of first molar eruption. The remodelling of ECM in these periodontal tissues might be regulated through balance among the production of ECM molecules, the degradation of ECM by MMPs and the inhibition of MMPs by TIMPs during tooth eruption.

Alveolar Process↗
PubMed2006

Injections of osteoprotegerin and PMA delay tooth eruption.

Tooth eruption requires alveolar bone resorption that is regulated by the dental follicle. This is reflected by the fact that failures of eruption often can be traced to either osteoclast deficiencies or to dental follicle abnormalities. To achieve maximal osteoclastogenesis and subsequent alveolar bone resorption for eruption, we have hypothesized that a reduction in gene expression of osteoprotegerin (OPG) in the follicle of the first mandibular molar of the rat at Day 3 is needed. To determine if OPG affects eruption, postnatal rats were injected with varying concentrations of OPG from Days 1-9 postnatally. Such studies indicated that the eruption time of the first mandibular molar was significantly delayed by 1 day or more as a result of OPG injection. Injection of phorbolmyristate acetate (PMA), an activator of protein kinase C (PKC) that in turn upregulates OPG expression, also delayed eruption by 1 day. PMA was only injected from Days 1-4 such that PKC-alpha would be increased and activated. Previous studies had shown that PKC-alpha gene expression is downregulated at the time (Day 3) that OPG expression is downregulated. In this study, using reverse transcription polymerase chain reaction techniques to examine OPG gene expression showed that PMA injection increased OPG gene expression in the dental follicle at Day 3 as compared to the controls. Thus, either injecting OPG or enhancing its expression in the follicle at Day 3 by injecting PMA delays the time of tooth eruption. Consequently, regulation of OPG production by the dental follicle likely affects the alveolar bone resorption needed for tooth eruption.

Animals↗
PubMed1998

Secretion of CSF-1 and its inhibition in rat dental follicle cells: implications for tooth eruption.

Tooth eruption requires the presence of a dental follicle around the unerupted tooth. Before the onset of eruption there is an influx of mononuclear cells into the follicle which, in turn, form osteoclasts that erode the alveolar bone. Eruption can be accelerated by the injection of colony-stimulating factor-one (CSF-1), a molecule that is maximally transcribed and translated in the dental follicle cells at the time of peak influx of mononuclear cells into the follicle of the rat first mandibular molar. To determine if the rat dental follicle cells secrete the CSF-1 needed for these cellular events, conditioned medium was collected from cultures of these cells. Using as a bioassay, a cell line (m-NFS 60) that is responsive to CSF-1 for growth, it was shown that conditioned medium from the follicle cells stimulated growth of the m-NFS 60 cells by almost 33% over the controls. Western blots confirmed that CSF-1 was secreted into the medium. Treating the dental follicle cells with an antisense oligodeoxynucleotide probe against CSF-1 reduced the amount of CSF-1 produced. These results demonstrate that CSF-1 is secreted by the dental follicle cells and that the production of CSF-1 can be reduced with an antisense probe. This secretion by the dental follicle might recruit mononuclear cells into the follicle to initiate tooth eruption.

Alveolar Process↗
PubMed2002

Cellular, molecular, and genetic determinants of tooth eruption.

Tooth eruption is a complex and tightly regulated process that involves cells of the tooth organ and the surrounding alveolus. Mononuclear cells (osteoclast precursors) must be recruited into the dental follicle prior to the onset of eruption. These cells, in turn, fuse to form osteoclasts that resorb alveolar bone, forming an eruption pathway for the tooth to exit its bony crypt. Some of the molecules possibly involved in the signaling cascades of eruption have been proposed in studies from null mice, osteopetrotic rodents, injections of putative eruption molecules, and cultured dental follicle cells. In particular, recruitment of the mononuclear cells to the follicle may require colony-stimulating factor-one (CSF-1) and/or monocyte chemotactic protein-1 (MCP-1). Osteoclastogenesis is needed for the bone resorption and may involve inhibition of osteoprotegerin transcription and synthesis in the follicle, as well as enhancement of receptor activator of NF kappa B ligand (RANKL), in the adjacent alveolar bone and/or in the follicle. Paracrine signaling by parathyroid-hormone-related protein and interleukin -1 alpha, produced in the stellate reticulum adjacent to the follicle, may also play a role in regulating eruption. Osteoblasts might also influence the process of eruption, the most important physiologic role likely being at the eruptive site, in the formation of osteoclasts through signaling via the RANKL/OPG pathway. Evidence thus far supports a role for an osteoblast-specific transcription factor, Cbfa1 (Runx2), in molecular events that regulate tooth eruption. Cbfa1 is also expressed at high levels by the dental follicle cells. This review concludes with a discussion of the several human conditions that result in a failure of or delay in tooth eruption.

Animals↗
PubMed1994

Dynamic variations in the expression of type I collagen and its molecular chaperone Hsp47 in cells of the mouse dental follicle during tooth eruption.

Tooth eruption is a precisely timed and sequenced event that brings the tooth from within bone into a functional position in the mouth. Every part of the developing tooth has been theoretically implicated as a primary factor in this process, but it now appears that eruption is multifactorial, with the dental follicle and type I collagen playing an important part. Immunological probes were used here to investigate in vivo and in vitro the temporal and spatial expression of type I collagen and its molecular chaperone Hsp47 in the dental follicle during eruption. Mandibles were dissected from 2-, 5-, 9- and 11-day-old neonatal mice and fixed in 95% ethanol overnight. Sections of 7 microns were obtained and reacted with antibodies directed against type I collagen. Dental follicles were isolated from 2-, 5-, 9- and 11-day-old neonates and cells were grown in culture for 8 days. Slides were then reacted with antibodies directed against type I collagen and Hsp47. The production of type I collagen and Hsp47 in the follicle varied with the stage of dental development and eruption. There was a progressive decrease of type I collagen in the coronal part of the follicle, leading to an arrest of its production in these areas. These findings support the notion that cells of the coronal portion of the dental follicle stop producing type I collagen as a prerequisite to the initiation of tooth eruption and that this phenotype persists in vitro.

Animals↗
PubMed1992

Current concepts of the biology of tooth eruption.

Tooth eruption is defined as the movement of a tooth from its site of development within the jaws to its position of function within the oral cavity. We present a critical review of evidence for the mechanisms and regulation of the intraosseous and supraosseous phases of eruption, with an emphasis upon the canine premolar model studied by the authors. Analyses at different stages of premolar eruption indicate that selective fragmentation of dental follicle protein DF-95 correlates with the presence of elevated levels of follicular collagenase and stromelysin, and with the onset of premolar movement. A dramatic decrease in these metalloproteinases followed initiation of movement. A biochemical and cell biological model for regulation of tooth eruption is proposed based upon these new and existing data.

Animals↗
PubMed1983

The physiology of tooth eruption.

Tooth eruption is a complex phenomenon that involves numerous biologic activities of the bone and the soft tissue surrounding teeth. While the exact mechanisms of eruption are not clearly understood, numerous experiments of nature, including many of the inborn errors of metabolism, should prove useful in their study. Nutritional studies may also prove useful, but will always be problematic [56]. Studies on endocrinologic changes such as puberty, pregnancy, menopause, and diseases such as diabetes, have already shown that the periodontium may not be able to accommodate to changes in the body's equilibrium [51].

Animals↗
PubMed2002

Inhibition of osteoclastogenesis by the secretion of osteoprotegerin in vitro by rat dental follicle cells and its implications for tooth eruption.

Tooth eruption requires the presence of the dental follicle, a loose connective tissue sac that surrounds each unerupted tooth. Early postnatally in the rat, the follicle secretes colony-stimulating factor-1 (CSF-1) and monocyte chemotactic protein-1 (MCP-1), chemotactic molecules that are probably responsible for the recruitment of mononuclear cells. These cells, in turn, fuse to form osteoclasts, which are required for alveolar bone resorption to form an eruption pathway. Recent studies have shown that the osteoprotegerin (OPG) gene is expressed in the dental follicle, but in the first mandibular molar of the rat, that expression is reduced at day 3, the time of maximal osteoclast numbers on the alveolar bone. Inhibition of OPG expression at this time would allow osteoclast formation/activation. To determine if the dental follicle cells do secrete OPG that inhibits osteoclastogenesis, spleen cell cultures were established and soluble osteoclast differentiation factor (ODF) and CSF-1 added to some of them to promote osteoclast formation. In other cultures, dental follicle cells were added in an insert, such that they did not touch the spleen cells. Using a quantitative, tartrate-resistant acid phosphatase (TRAP) assay, it was shown that ODF and CSF-1 promoted osteoclastogenesis in the spleen cell cultures, but the addition of the follicle cells inhibited this and returned the TRAP activities to those seen in cultures of spleen cells only. Adding anti-OPG to these cultures, however, negated the effect of the follicle cells, demonstrating that OPG was the inhibitory molecule secreted by those cells. The follicle cells also immunostained for OPG, confirming that they synthesize OPG. These findings, coupled with those of other studies which show that the periodontal ligament (a derivative of the dental follicle) also secretes OPG, indicate that, except for the period of time in tooth eruption, where osteoclast formation is needed to form an eruption pathway, secretion of OPG would be the norm, presumably to prevent resorption of alveolar bone and subsequent disruption of the periodontal ligament.

Acid Phosphatase↗
PubMed1987

Regional control by the dental follicle of alterations in alveolar bone metabolism during tooth eruption.

Tooth eruption is a localized, bilaterally symmetrical series of events which involves resorption and formation of alveolar bone on opposite sides of the tooth and requires the presence of the dental follicle. We examined the effect on eruption of selective surgical removal of parts of the follicle. Removal of either the basal or coronal halves of the follicle prevented eruption. Bone resorption and formation of an eruption pathway did not occur after removal of the coronal part of the follicle and bone formation did not occur after removal of the basal part of the follicle. Exposure and incisions of the follicle had no effect on eruption. We interpret these data to mean that the polarized resorption and formation of alveolar bone that occur around a tooth during eruption are regulated by the adjacent parts of the dental follicle.

Alveolar Process↗
PubMed1996

The mechanism of tooth eruption.

Tooth eruption is an essential process for the survival of many different species and although the movement of teeth into function has been the subject of extensive research there is no consensus as to the mechanisms involved. Recent understanding of the mechanisms of cell activation and regulation has widened the scope for further research at the molecular level. This paper reviews the evidence for an eruptive force, its direction and source. The relationships between the eruptive force and molecular mechanisms of cell activation remain to be determined.

Alveolar Process↗
PubMed1985

Ultrastructural features of the dental follicle associated with formation of the tooth eruption pathway in the dog.

The dental follicle is a loose connective tissue layer that surrounds the developing and erupting tooth. The follicle is necessary for tooth eruption in dogs and specific cellular changes occur in the follicle at the onset of tooth eruption. In particular, within the coronal region of the follicle next to areas of subsequent bone resorption there is an increase in mononuclear cells which have the ultrastructure features of monocytes and contain specific granules characteristic of preosteoclasts. The follicle has an extensive microvasculature and monocytes are often seen adjacent to capillaries and venules. Monocytes increase in number in direct proportion to the increase in osteoclasts that form the eruption pathway and decrease in number as soon as this activity is completed. It is postulated that monocytes enter the follicle from the microvasculature and then migrate to the walls of the bony crypt to participate in the formation of the eruption pathway.

Age Factors↗
PubMed1991

[Maturation of enamel and tooth eruption].

The tertiary maturation of the erupting tooth needs much more time than it is supposed in literature. Possibly the completion is in accord with the decline of the caries activity at the end of the second decade of lifetime. With the aid of polarizing microscopy, electron microprobe, microhardness testing (Vickers) and scanning electron microscopy different stages of posteruptive maturation from human and other mammalian teeth were analysed. The mineralization level in the outer surface of human enamel is completing little by little in more than 5 years after eruption. This state is in the ruminant tooth obvious never within reach in consequence of the specific physiological conditions. The maturating mineralization after our preliminary findings is fundamentally different to remineralization.

Animals↗
PubMed2005

CSF-1, RANKL and OPG regulate osteoclastogenesis during murine tooth eruption.

During tooth eruption, osteoclast-mediated bone resorption predominates in alveolar bone along the occlusal surface rather than in bone basal to the tooth. CSF-1, RANKL and OPG, regulatory molecules essential for osteoclastogenesis, are expressed during eruption. However, it is unclear if these cytokines exhibit an expression pattern that correlates with sites of osteoclastogenesis in vivo. To address this issue, mouse mandibles, isolated from 1 to 14 days postnatal, were analysed for osteoclast activity using tartrate-resistant acid phosphatase (TRAP) staining as well as colony-stimulating factor-1 (CSF-1), receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG) mRNA expression using in situ hybridisation. Results showed that CSF-1, RANKL and OPG are expressed in a distinct temporal and spatial manner. In the occlusal region, osteoclast activity was maximal at day 5 and correlated with a relative high expression of CSF-1 and RANKL compared to OPG. In basal bone at this time point, osteoclast activity decreased despite persistent CSF-1 expression and was associated with increased expression of OPG compared to RANKL. By day 8, osteoclastogenesis declined and correlated with upregulation of OPG at the occlusal and basal regions, with this effect continuing throughout eruption. These findings suggest that the spatiotemporal pattern and relative abundance of CSF-1, RANKL and OPG during eruption are key determinants of site-specific osteoclast activity in bone surrounding the tooth. Targeting these cytokines to specific regions in alveolar bone may provide a mechanism for regulating osteoclastogenesis in dental disorders associated with altered tooth eruption.

Acid Phosphatase↗
PubMed2006

Chronological gene expression of parathyroid hormone-related protein (PTHrP) in the stellate reticulum of the rat: implications for tooth eruption.

OBJECTIVE: Tooth eruption is a localized event that requires the expression of certain molecules at precise times to regulate bone resorption and bone formation. Parathyroid hormone-related protein (PTHrP) may be one of those molecules. Although PTHrP is produced in the stellate reticulum (SR) of the tooth and exerts its effect on the adjacent dental follicle, its expression pattern in the SR is unknown. Thus, it was the objectives of this study to determine the chronology of expression of PTHrP, and then to determine its effect on vascular endothelial growth factor (VEGF) expression for osteoclastogenesis and on bone morphogenetic protein-2 (BMP-2) for bone growth. DESIGN: Laser capture microdissection and RT-PCR were used to determine the chronological expression of PTHrP in vivo. In vitro, dental follicle cells were incubated with PTHrP and RT-PCR was conducted to determine its effect on VEGF and BMP-2 gene expression. RESULTS: PTHrP was maximally expressed at day 7 postnatally in the SR with the level of expression still high at day 9. In vitro, PTHrP upregulated VEGF120 and VEGF164 expression after 4h of incubation with a maximum effect at 6h. PTHrP upregulated BMP-2 gene expression with a maximal effect at 2h. CONCLUSIONS: Because the secondary burst of osteoclastogenesis needed for eruption occurs around day 10, it is possible that PTHrP is stimulating this osteoclastogenesis by upregulating VEGF. Concurrently, the upregulation of BMP-2 by PTHrP may stimulate bone growth at the base of the bony crypt to promote eruption.

Animals↗
PubMed1995

The mechanisms and mediators of tooth eruption--models for developmental biologists.

Tooth eruption is a localized process in the jaws which exhibits precise timing and bilateral symmetry. It involves resorption and formation of bone on opposite sides of the erupting tooth and these activities depend on the dental follicle, a thin connective tissue investment of the developing and erupting tooth. Biochemical studies have shown that during eruption cells, proteins and enzymes change in the dental follicle and several growth factors and proteins known to accelerate or retard eruption have been identified. This review discusses these aspects of tooth eruption and proposes testable hypotheses and strategies that can make studies of tooth eruption new experimental opportunities for developmental biologists.

Animals↗
PubMed1995

Bafilomycin A1 in bone resorption and tooth eruption in dogs.

Tooth eruption depends on bone resorption to form an eruption pathway. We have previously shown that a 2-wk local infusion of bafilomycin A1, an inhibitor of vacuolar H(+)-ATPases in osteoclasts, into the crypts of erupting mandibular premolars in dogs blocks bone resorption during this period and eruption of these teeth is delayed for 8 wk. Here we report the limits of inhibition of resorption that still permit eruption of these teeth. In 3 dogs 10(-6) M bafilomycin was delivered by osmotic minipumps early (18 wk) in eruption to the fourth premolar for 1, 3 or 4 wk. Radiographs taken at weekly intervals thereafter showed that bafilomycin delivery for 1 wk delayed eruption for 3 wk, delivery for 3 wk delayed eruption 9 wk and delivery for 4 wk prevented eruption. These data show that tooth eruption is delayed in direct proportion to the time resorption is blocked, and that this process for dog premolars cannot be blocked for more than 3 wk with 10(-6) M bafilomycin without blocking eruption itself.

Alveolar Process↗