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The pattern and control of eruptive tooth movements.

Assumptions about eruptive tooth movements based on experience with adolescents may not be applicable to all ages. The eruptive process can be subdivided into six phases--three profunctional stages of individual tooth eruption (follicular growth, pre-emergent eruptive spurt, and postemergent eruptive spurt) and three postfunctional stages of the eruption of the entire dentition (juvenile occlusal equilibrium, circumpubertal occlusal eruptive spurt, and adult occlusal equilibrium). Differences in tooth-eruption rates in each of these phases result from variations in systemic and local factors. A series of working hypotheses which incorporate recent research into a theoretical explanation of the control of eruption during each stage is presented. Prior to emergence, the force of eruption may influence the rate of bone resorption and later of gingival remodeling, but the resorptive processes occur independently and are the rate-limiting factors in pre-emergent eruption. After emergence, intermittent occlusal loading disrupts the generative or adaptive mechanisms of the periodontal ligament so that eruption slows. The light continuous forces from resting tongue pressure also are significant influences on tooth eruption during periods of rapid facial growth. Cellular adaptation of the alveolar bone and gingiva plays an important role in the control of tooth eruption in the adult.

Adolescent↗

Nuclear matrix-intermediate filament proteins of the dental follicle/enamel epithelium and their changes during tooth eruption in dogs.

Tooth eruption activates a localized resorption and formation of alveolar bone and these activities depend upon the adjacent parts, coronal and basal, respectively, of the dental follicle-enamel epithelium. In this study the nuclear matrix-intermediate filament (NM-IF) proteins of these tissues were isolated in order to continue investigations into the molecular mechanisms underlying eruption. Dental follicles were removed from the third and fourth premolar of dogs at 13, 16 and 20 weeks (pre-, early, and mid-to-late eruption of these teeth) and NM-IF proteins were extracted from the coronal and basal halves. Most of the NM-IF protein profiles of these coronal and basal parts on one-dimensional, sodium dodecyl sulphate-polyacrylamide gel electrophoresis were remarkably constant, indicating an essentially uniform cellular composition. However, differences between these tissues were observed and some of these changed during eruption. Based on recent observations that nuclear matrix changes reflect and may even mediate cell-specific changes in gene expression, these findings suggest that changes in nuclear matrix proteins may be related to the molecular basis for some aspects of differential gene expression in the coronal and basal regions of the dental follicle and account for the ability of these tissues to activate bone resorption and formation during tooth eruption.

Alveolar Process↗

Effects of dexamethasone on tooth eruption in rats: differences in incisor and molar eruption.

A requirement for tooth eruption is the resorption of alveolar bone. Because bone resorption is stimulated by dexamethasone both in vivo and in vitro, dexamethasone 21-phosphate, a soluble form of dexamethasone, was injected into rats to determine its effect on tooth eruption. Such dexamethasone injections accelerate the time of intra-osseous eruption in rat incisors but do not accelerate the eruption time of rat molars when injected into rats. The injections of dexamethasone 21-phosphate also accelerate the time of eyelid opening in the postnatal rats, as well as retarding growth, as measured by body weight. These effects of dexamethasone 21-phosphate parallel the effects of epidermal growth factor injections, including the absence of an effect on molar eruption. This suggests that the molecular signals for the initiation of tooth eruption (i.e., onset of bone resorption) differ between rat incisors and molars. Given that rat incisors are teeth of continuous eruption whereas rat molars are teeth of limited eruption, as are human teeth, care must be taken in extrapolating results derived from rat incisors to human dentition. In vitro, dexamethasone has no effect on the gene expression of either osteoprotegerin or epidermal growth factor in dental follicle cells derived from molars. Because osteoprotegerin expression during normal tooth eruption is transitorily inhibited early postnatally in the molar dental follicle to allow osteoclast formation, the absence of inhibition of its expression by dexamethasone could explain why dexamethasone does not accelerate eruption in molars.

Animals↗

The effects of colony-stimulating factor-1 on tooth eruption in the toothless (osteopetrotic) rat in relation to the critical periods for bone resorption during tooth eruption.

The toothless (tl) rat is an osteopetrotic mutation characterized by a generalized skeletal sclerosis, reduced bone resorption, few osteoclasts and a total absence of erupted teeth. This mutation is not cured by bone marrow transplants from normal littermates. It is known that the skeletal defects in tl rats are greatly improved after treatment with colony-stimulating factor-1 (CSF-1). This investigation concerns the effects of CSF-1 on the development and eruption of the dentition of tl rats. Untreated tl rats had no erupted teeth by 56 days after birth, and the roots of incisors and molars were severely distorted by compression against bone. The apex of the mandibular incisor did not extend past the first molar and continued growth of its apical end produced odontoma-like masses consisting of distorted dentine and enamel matrices. In addition, few osteoclasts were seen on alveolar bone surfaces surrounding the developing teeth. Mutants given CSF-1 were characterized by delayed eruption of all molars and sometimes incisors. The incidence of incisor eruption was related inversely to the age at which CSF-1 treatment began. Molars of treated tl rats had well-developed roots similar to those in normal rats. Treated mutants had numerous osteoclasts in alveolar bone and well-developed haemopoietic marrow spaces in the mandible. Histochemical staining for both tartrate-resistant acid phosphatase and tartrate-resistant acid ATPase was reduced or negligible in osteoclasts of untreated tl rats, heavy in normal osteoclasts and of intermediate intensity in CSF-1-treated mutants.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[The regulation of tooth eruption].

The aim of the present publication is to provide a broad survey of the current concepts on the regulation of tooth eruption. There is increasing evidence that tooth eruption is a multifactorial process. The bone resorption occlusal to an erupting tooth is probably induced by the occlusal part of the follicle, and allows the tooth to erupt. The occlusal movement it self is likely to be regulated by a localized increase in tissue fluid pressure in the apical area. The bone deposition which is often observed apical to an erupting tooth is more likely to be a reaction to the eruption than a source of eruptive forces.

Bone Resorption↗

Concrescence of teeth: cemental union between the crown of an impacted tooth and the roots of an erupted tooth.

Concrescence of teeth is a condition showing a union of adjacent teeth by only cementum. In all the previously reported cases, the union has been observed between the roots of the affected teeth. Here, we describe the first case that showed a concrescence of the crown of an impacted tooth and the roots of the erupted tooth. In addition, we discuss how this condition, especially the deposition of acellular cementum on the crown, occurred.

Female↗

Tooth eruption depends on bone resorption: experimental evidence from osteopetrotic (ia) rats.

Resorption of alveolar bone around erupting teeth is known to be independent of tooth eruption. However, the failure of tooth eruption and reduction in bone resorption in the osteopetrotic rat mutation, incisors absent (ia), suggest that tooth eruption depends upon bone resorption. This hypothesis was tested by determining the effects of neonatal restoration of bone resorption in ia rats on eruption of first molars. Newborn ia rats were treated with irradiation and spleen cells and tooth eruption and bone resorption were examined 30 days later. In 24 treated ia rats at least two molars erupted in every rat and all four molars erupted in 14. In 24 untreated ia littermates, no molars erupted in 21, one molar erupted in two and two molars erupted in one rat. All molars erupted in 38 untreated normal littermates. Alveolar bone overlying unerupted first molars in untreated ia rats was not present in treated mutant littermates. Neonatally treated ia rats had osteoclasts with ruffled borders and no skeletal sclerosis by 30 days. Within 48 hours after treatment two types of osteoclasts could be found in treated rats. One type resembled those found in untreated ia littermates and the other those found in normal rats. These data suggest that failure of tooth eruption in ia rats is directly related to the reduction in bone resorption and that alveolar bone resorption is required for tooth eruption.

Animals↗

Cell death during tooth eruption in the rat: surrounding tissues of the crown.

We investigated the occurrence of apoptosis and other types of cell death around the crown during tooth eruption of the rat upper molar. The TdT-mediated-dUTP-biotin nick end labeling (TUNEL) method and transmission electron microscopy (TEM) were employed. Apoptosis was detected by both TUNEL and TEM in part of the reduced enamel epithelium and connective tissue in the resorbing bony crypt of the pre-erupted tooth. In TEM, a large number of cells showed condensed chromatin and membrane-bound small bodies (apoptotic bodies). Macrophages that phagocytosed apoptotic bodies could be detected. Based upon the distance between bone surface and these apoptotic cells, and the characteristics of their organelles, we suggested that the apoptotic cells might be osteocytes, bone-lining cells (osteoblasts), and macrophages. We surmised that the osteoclasts had also died. Cells which contained autophagic vacuoles and autophagosomes, and others whose cytoplasm had dissolved, were also frequently observed. No progressive cell death was found in the oral epithelium or the fibrous connective tissue over the crown. These results suggest that apoptosis gives rise to some cell death during tooth eruption, but that other types of cell death also occur in various cells.

Age Factors↗

Tooth eruption: theories and facts.

The mechanisms of tooth eruption (i.e., the answer to the question of how and why teeth erupt) has been a matter of long historical debate. This review focuses on human and other mammalian teeth with a time- and spacewise limited period of eruption and analyzes recent observations and experimental data on dogs, rats, primates, and humans in a framework of basic biological parameters to formulate a guiding theory of tooth eruption. Acknowledging basic parameters (i.e., that teeth move in three-dimensional space, erupt with varying speed, and arrive at a functional position that in inheritable) eliminates a number of previously held theories and favors those that accommodate basic parameters, such as alveolar bone remodeling in association with root elongation, with possible correction factors in the form of cementum apposition and periodontal ligament formation. We have critically analyzed, summarized, and integrated recent findings associated with preeruptive movements of developing teeth, the intraosseous stage of premolar eruption in dogs, molar eruption in rodents, and premolar and molar eruption in primates. The variable speeds of eruption are particularly important. We conclude with basic principles of tooth eruption--that is, the type of signals generated by the dental follicle proper, the conditions under which teeth are moved and the clinical understanding to be derived from this knowledge.

Animals↗

Reduction of osteoclasts in a critical embryonic period is essential for inhibition of mouse tooth eruption.

Alveolar bone resorption by osteoclasts is essential for tooth eruption. Osteoclast-deficient Csfm(op) homozygous (op/op) mice, which lack functional macrophage colony-stimulating factor (M-CSF), suffer from osteopetrosis and completely lack tooth eruption. Although osteoclasts appear, and osteopetrosis is cured with age in op/op mice, tooth eruption is never seen. This fact suggests that there is a critical period when osteoclasts are required for tooth eruption. In this study, to detect the critical period, we administered an antagonistic antibody directed against c-Fms, a receptor for M-CSF, to inbred C57BL/6 mice for various periods. Administration of this antibody decreased tartrate-resistant acid phosphatase-positive (TRAP) osteoclasts, and incisor eruption was completely inhibited by continual administration of this antibody from embryonic day 15.5 (E15.5) until postnatal day 12.5 (D12.5). A 1-day delay of this administration abolished the inhibition of incisor eruption. The number of TRAP-positive osteoclasts was significantly reduced between E16.5 and E18.5 in the mice treated with antibody from E15.5 compared with those treated from E16.5. These results indicate that this period, during which the number of osteoclasts decreases significantly, is critical for inhibiting incisor eruption in C57BL/6 mice.

Acid Phosphatase↗

A longitudinal study of Streptococcus mutans colonization in infants after tooth eruption.

We previously reported that, before tooth eruption, over one-half of infants aged 6 mos were already infected with Streptococcus mutans. The aim of this investigation was to determine the colonization of S. mutans after tooth eruption in the same cohort of 111 infants (35 pre-term, 76 full-term). Our results showed that S. mutans colonization increased with increasing age, so that by 24 mos of age, 84% harbored the bacteria (p < 0.01). The mean and median ages of S. mutans colonization in dentate infants were 15.7 mos and 16.0 mos, respectively. Factors associated with S. mutans colonization were sweetened fluids taken to bed (p < 0.01), frequent sugar exposure (p < 0.03) and snacking (p < 0.03), sharing of foods with adults (p < 0.03), and maternal S. mutans levels of > 10(5) CFU/mL (p < 0.02). In contrast, non-colonization of S. mutans was associated with toothbrushing (p < 0.03) and multiple courses of antibiotics (p < 0.001). Analysis of our data establishes the timing of S. mutans colonization in children from birth to 24 mos of age.

Age Factors↗

Delayed primary tooth eruption in premature infants: relationship to neonatal factors.

Previous studies suggest that primary tooth eruption (PTE) in preterm infants is related primarily to gestational age, but the impact of other neonatal factors has not been studied. In a prospective longitudinal study, the timing and sequence of PTE were documented by a pictorial PTE record completed by the parents and by frequent oral exams in 14 preterm infants whose first tooth erupted at < or = 10 months chronologic age (normal group) and 21 preterm infants whose first tooth erupted at > 10 months (late group). Initial eruption sequence in both groups was the same as full-term infants, with the two lower central incisors erupting first. PTE occurred significantly later in children with BW < 1000 g (t = 3.4, P < 0.01) or < or = 30 weeks (t = 2.41, P < 0.05). Factors related to nutrition appeared to be important. Age at first tooth correlated significantly with age when full enteral feedings were attained, age when oral vitamin supplementation was started, and with average weight gain per day. Five neonatal factors (duration of oral intubation, birthweight, gestational age, age when full enteral feedings were attained, and apnea of prematurity) explained 44% (R = 0.67, P < 0.05) of the variability in age at which the first tooth erupted. Of that 44%, 77% was explained by a single factor, duration of oral intubation. These results suggest that factors related to severity of neonatal illness and postnatal nutrition as well as degree of prematurity affect timing of primary tooth eruption.

Apnea↗

Three-dimensional analysis of mandibular growth and tooth eruption.

Normal and abnormal jaw growth and tooth eruption are topics of great importance for several dental and medical disciplines. Thus far, clinical studies on these topics have used two-dimensional (2D) radiographic techniques. The purpose of the present study was to analyse normal mandibular growth and tooth eruption in three dimensions based on computer tomography (CT) scans, extending the principles of mandibular growth analysis proposed by Björk in 1969 from two to three dimensions. As longitudinal CT data from normal children are not available (for ethical reasons), CT data from children with Apert syndrome were employed, because it has been shown that the mandible in Apert syndrome is unaffected by the malformation, and these children often have several craniofacial CT scans performed during childhood for planning of cranial and midface surgery and for follow-up after surgery. A total of 49 datasets from ten children with Apert syndrome were available for study. The number of datasets from each individual ranged from three to seven. The first CT scan in each of the ten series was carried out before 1 year of age, and the ages for the 49 scans ranged from 1 week to 14.5 years. The mandible and the teeth were segmented and iso-surfaces generated. Landmarks were placed on the surface of the mandible, along the mandibular canals, the inner contour of the cortical plate at the lower border of the symphysis menti, and on the teeth. Superimposition of the mandibles in the longitudinal series was performed using the symphysis menti and the mandibular canals as suggested by Björk. The study supported the findings of stability of the symphysis menti and the mandibular canals as seen in profile view previously reported by Björk & Skieller in 1983. However, the mandibular canals were, actually, relocated laterally during growth. Furthermore, the position of tooth buds remained relatively stable inside the jaw until root formation started. Eruption paths of canines and premolars were vertical, whereas molars erupted in a lingual direction. The 3D method would seem to offer new insight into jaw growth and tooth eruption, but further studies are needed.

Acrocephalosyndactylia↗

Delayed tooth eruption: pathogenesis, diagnosis, and treatment. A literature review.

Delayed tooth eruption (DTE) is the emergence of a tooth into the oral cavity at a time that deviates significantly from norms established for different races, ethnicities, and sexes. This article reviews the local and systemic conditions under which DTE has been reported to occur. The terminology related to disturbances in tooth eruption is also reviewed and clarified. A diagnostic algorithm is proposed to aid the clinician in the diagnosis and treatment planning of DTE. The sequential and timely eruption of teeth is critical to the timing of treatment and the selection of an orthodontic treatment modality. This review addresses the need for a more in-depth understanding of the underlying pathophysiology of DTE and gives the clinician a methodology to approach its diagnosis and treatment.

Chronic Disease↗

Influence of aging on tooth eruption: experimental canine mandibular allograft.

PURPOSE: Aging is clinically related to tooth eruption; however, there are no known studies that have elucidated the relationship. We examined whether tooth eruption would occur normally in a mature subject. MATERIALS AND METHODS: Using vascularized composite tissue mandibular transplantation, we extracted portions of immature mandibles including the tooth germs from young beagle dogs and placed them into unrelated immature and mature beagle dogs. We then examined eruption of the lower first molar in the grafted mandibular bone and compared the results clinically, radiographically, and histologically. RESULTS: Normal tooth eruption was observed in the transplanted mandibles in the young dogs. In the mature dogs, eruption from the gingiva was delayed, whereas that from alveolar bone occurred normally in the transplanted mandibles. Further, the whole crown was covered with a cap of gingival tissue in the mature dogs, although this cap was not gingival overgrowth. CONCLUSIONS: Tooth eruption is influenced by some unknown factors related to aging. Apparently, apoptosis did not occur in the connective tissues between the reduced enamel epithelia and oral epithelia that overlay the teeth in the mature subjects.

Aging↗

Tooth eruption: the regulation of a localized, bilaterally symmetrical metabolic event in alveolar bone.

Tooth eruption is a complicated process by which developing teeth are moved within the jaws to their functional position. The usual model chosen to study this process, the erupted rodent incisor, differs both structurally and functionally from the human dentition and conclusions drawn from these studies are not directly applicable to tooth eruption in human beings. We have studied the eruption of developing permanent premolars in dogs and present evidence by scanning electron microscopy for regional differences in metabolic activities on bone surfaces of the crypt during eruption. We review evidence that these polarization of alveolar bone metabolism are cell-mediated, dependent upon the dental follicle, independent of root formation or the tooth itself and that tooth eruption depends on coordination of these activities by the dental follicle. We conclude that tooth eruption is a localized, bilaterally symmetrical event in alveolar bone and that this is an excellent model system in which to study the regulation of alveolar bone metabolism.

Animals↗

Disturbed tooth eruption in osteopetrotic (op/op) mice: histopathogenesis of tooth malformation and odontomas.

BACKGROUND: Odontoma-like structures are formed in the jaw bone of osteopetrotic (op/op) mice, which have a congenital deficiency in osteoclastic differentiation due to the absence of functional macrophage colony-stimulating factor (M-CSF). METHODS: To clarify the histopathogenesis of tooth malformation and odontoma-like structures, a 2-year postnatal process of development of the op/op mandibular incisor was examined radiologically and histologically. At the same time, extracellular matrix (ECM) remodeling around tooth germs was analyzed immunohistochemically. RESULTS: Abnormal forms of op/op tooth germ were noticeable even at 3 days after birth on a radiogram. Histologically, op/op mice were clearly distinguished by the disappearance of dental follicular space at 3 days. With aging, bone trabeculae, which were not remodeled, penetrated into op/op tooth germs and divided them into several daughter germs, which were recognized as odontomas. In mandibular incisor bodies, the immature ECM components, such as heparan sulfate proteoglycan and tenascin, were preserved diffusely in the dental papilla/pulp, which indicates that maturation of the stroma does not take place in op/op mandibular incisors. CONCLUSION: The observation suggests that the disturbed morphogenesis of op/op tooth germs is functionally explained by the disordered immunolocalization of ECM molecules, and that the dental follicular space is essential for normal tooth development because it prevents bone penetration into the tooth germs.

Animals↗