Transposition--an unusual dental anomaly.
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Familial or X-linked hypophosphatemic rickets (XLHR) is the most common type of rickets in developed countries today. While the dental manifestations of rickets are well reported, there is little information regarding its relationship to dental development and other dental anomalies. This investigation studied the rate of dental development and associated dental anomalies in 19 XLHR subjects compared with 38 race-, age-, and sex-matched control children. The results showed that in both XLHR and control children, no significant differences existed in dental age compared with the respective chronological age, indicating that rickets did not affect the rate of dental development. Longitudinal growth curves of seven XLHR and matched control children substantiated that relationships of dental to chronological ages were comparable in both groups. Male XLHR subjects showed significantly increased tendency for dental taurodontism with mean Crown-Body (CB):Root (R) ratio of 1.1 compared with 1.0 in females and 0.8 in controls (P < 0.02). Male XLHR children also showed significantly increased prevalence (50%) of ectopic permanent canines compared with control children (8%, P < 0.01).
Resection of the odontogenic region or root transection of normal (impeded) rat lower incisors showed that eruption ceased from 1 to 13 weeks when the base of the resected teeth (87.5%) or of the distal segment of the transected ones (86%) reached the alveolar-crest region. When the operated teeth reached the crestal region, the enamel-related periodontal tissues were absent and the periodontal ligament (PDL) was the only periodontal tissue that remained. The PDL of the crestal region may be considered as mature PDL, showing a length of approx. 5-6 6 mm at the mesial face of the tooth, 4-5 mm at lingual face and 1 mm at distal face; from these limits towards the apical end of the socket the PDL becomes gradually immature. The mature PDL seems not to have a role in the process of tooth eruption. Several factors can be suggested to explain the more frequent retention, at the crestal region of the socket, of impeded rather than unimpeded incisors submitted to the same procedures. The connective tissue that develops between the base of the tooth and the bone that fills the alveolus may have more time to organize itself in impeded than in unimpeded teeth, which erupt at a faster rate; this tissue could support and retain the impeded operated teeth longer than the unimpeded ones. The decrease in the mechanical properties of the PDL in the unimpeded condition may ease the traumatic effects and lead to exfoliation. Eruption might be stopped by the increase in occlusal forces, per unit area of root surface, as the root becomes shorter; this effect is likely to be greater in impeded than unimpeded teeth.
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Experiments in vivo have established that tooth eruption fails in the absence of parathyroid hormone (PTH)-related protein (PTHrP) action in the microenvironment of the tooth because of the failure of osteoclastic bone resorption on the coronal tooth surface to form an eruption pathway. To elucidate the effects of PTHrP on osteoclast regulation in this environment, we established primary cultures of epithelial stellate reticulum cells and mesenchymal dental follicle (DF) cells surrounding the teeth. When cocultured, these cells are fully capable of supporting the formation of functional osteoclasts in the absence of added splenic osteoclast precursors, osteoblasts, or vitamin D/PTH/PTHrP. Neutralizing the effects of PTHrP resulted in a decrease in the number of osteoclasts formed, suggesting that stellate reticulum-derived PTHrP drives osteoclast formation. DF cells were found to express functional PTH/PTHrP type I receptors, and conditioned media collected from PTHrP-treated DF cells were able to induce bone resorption in the fetal-rat long-bone assay. PTHrP treatment also induced an increase in osteoclast differentiation factor expression and a concomitant decrease in osteoclastogenesis inhibitory factor expression in DF cells. The addition of osteoclastogenesis inhibitory factor resulted in a decrease in the number of osteoclasts formed in the cocultures, suggesting that osteoclast formation is mediated by osteoclast differentiation factor. Thus, PTHrP seems to regulate osteoclast formation via mediation of the DF, in a manner analogous to the osteoblast-mediated process in the peripheral skeleton. The primary coculture system of dental crypt cells also offers a system for the study of osteoclast formation and regulation.
Eleven patients with idiopathic hypoparathyroidism and pseudohypoparathyroidism were examined orally and medically. All patients had a history of tetanic and/or epileptic manifestations. Correspondingly, disturbances in the metabolism of calcium and phosphorus had been present in all. Dental anomalies were demonstrated in all patients but one. Enamel hypoplasia was observed in six cases, disturbances in tooth eruption in eight, root defects in five and hypodontia in seven. Dental anomalies were more frequent than could be expected from the literature, probably because the dental aspects of hypoparathyroid disease often have been overlooked. In the present material, the above-mentioned disturbances were most severe and frequent in the pseudohypoparathyroid group. Hypoparathyroid conditions are highly invalidating, easily accessible to treatment, but often undiagnosed for years. Therefore, the dental observation of severe disturbances in tooth formation and eruption pattern may be of crucial importance and should lead to further medical investigation.
Parathyroid hormone-related protein (PTHrP) has been implicated in regulating tooth eruption and/or development. Formation of cementum, a mineralized tissue covering the tooth root surface, is a critical biological event for tooth root development. To test the hypothesis that PTHrP targets cementoblasts (CMs) and acts to regulate cementogenesis, CM cell lines were established and their responsiveness to PTHrP stimulation was determined, in vitro. First, subclones were derived from two immortalized murine cell populations that contained CMs; SV-CM/periodontal ligament (PDL) cells were obtained from the root surface of first mandibular molars of CD-1 mice and immortalized with SV40 T-antigen (TAg), and OC-CM cell population was established from OC-TAg transgenic mice in which their cells harbor an osteocalcin (OC and/or OCN) promoter-driving immortal gene SV40 TAg. Based on our previous in situ studies, CM subclones were identified as cells expressing bone sialoprotein (BSP) and OCN transcripts, while PDL cell lines were designated as cells lacking BSP and OCN messenger RNA (mRNA). CMs exhibited a cuboidal appearance and promoted biomineralization, both in vitro and in vivo. In contrast, PDL cells (PDL subclones) displayed a spindle-shaped morphology and lacked the ability to promote mineralized nodule formation, both in vitro and in vivo. Next, using these subclones, the effect of PTHrP on cementogenesis was studied. CMs, not PDL cells, expressed PTH/PTHrP receptor mRNA and exhibited PTHrP-mediated elevation in cyclic adenosine monophosphate (cAMP) levels and c-fos gene induction. PTHrP stimulation repressed mRNA expression of BSP and OCN in CMs and blocked CM-mediated mineralization, in vitro. Collectively, these data suggest that CMs possess PTH/PTHrP receptors and, thus, are direct targets for PTHrP action during cementogenesis and that PTHrP may serve as an important regulator of cementogenesis.
The distribution of cellular retinoic acid-binding protein (CRABPI) and cellular retinol binding protein (CRBPI) was studied in a series of prenatal and early postnatal rats, covering the main stages of development and eruption of the molar teeth. CRABPI positive cells were found in the mesenchymal cells of the dental follicle from the cap stage and in the dental papilla from the early bell stage. In the dental papilla, CRABPI positive cells were situated adjacent to the enamel organ in the cervical loop region and in the subodontoblastic region. Newly formed odontoblasts were CRABPI positive for a short period of time. The enamel organ was CRBPI and CRABPI negative, except for the presence of CRABPI positive cells in the internal enamel epithelium over the tip of cusps and in parts of the stratum intermedium. During root formation, CRABPI positive cells were found in the developing periodontal ligament, in the dental papilla adjacent to the epithelial root sheath and in the subodontoblastic zone. During crown formation, CRBPI positive cells were mainly localized to the mesenchymal cells of the dental papilla during the cap stage of crown development. The periosteum of the developing mandible contained CRABPI positive cells while some osteoclasts appeared to show a weak but positive reaction to CRBPI. The findings were considered in terms of the possible significance of retinoid-binding proteins during tooth and bone development.
Dental caries, a bacterial disease of teeth characterized by destruction of enamel and dentine, is often the underlying cause of dental pain. When a carious lesion impinges on the dental pulp, pulpitis follows and, ultimately, necrosis of the pulp occurs. Untreated necrosis may lead to a localized abscess or a spreading infection into the surrounding soft tissue that results in cellulitis. Immediate treatment involves antibiotic therapy for cellulitis, perhaps with drainage of abscesses, while definitive treatment requires root canal therapy or extraction of the involved tooth. Pericoronitis is an inflammation of the soft tissue overlying a partially erupted tooth. Localized cases respond to irrigation. Secondary cellulitis can develop. Definitive treatment may require surgical extraction of the underlying tooth or excision of the gum flap. Avulsion of a permanent tooth secondary to trauma is a true dental emergency. The tooth should be reimplanted on the spot, and the patient should be seen immediately by a dentist for splinting and antibiotic prophylaxis. Most dental problems can be prevented with regular dental care and steps to minimize risks of oral trauma.
The impacted or mal-erupted tooth and its associated pathosis provide great diagnostic challenges to the dentist. The frequency of occurrence of impaction was found to be over 10,000 in 5,000 Army recruits. The type and position of impaction are summarized in tables. The incidence of impactions was higher than previously reported and may reflect some sampling bias. The incidence of impacted second and fourth molars is higher than expected. Impactions or mal-eruptions were seen to involve every permanent tooth except the mandibular incisors and first molars. Impactions can occur because of malpositioning of the tooth bud or obstruction in the path of eruption. However, the exact mechanism is still unknown. Six unusual cases of impacted permanent teeth are described to illustrate the importance of panoramic radiographs in the discovery of some anomalously located impactions.
Tooth dislocation (tilting) was recorded in 1,200 skulls from 34 museum collections. The findings of dislocation by tooth type, tooth wear, and abscess location are presented. A model for dislocation based upon the progressive loss of tooth support provides a rational explanation for the phenomenon. Physiological continuous tooth eruption was considered to account for a component of the progressive loss of tooth attachment. The process of attrition, pulp perforation, and dental abscess cavity formation resulted in further, more severe loss of tooth support. Heavy functional forces, in association with greatly reduced bone support, tilted the crown lingually and root buccally. When the tooth had tilted to such an extent that the root apices protruded from the bone and, presumably (in life) through the gingival/mucosal tissues, the infected root canals were effectively isolated from the internal environment. The tooth continued to function. The more typical consequence of severe attrition and dental abscess formation was tooth loss; it also isolated an infected tooth from living tissue, but without the benefit of retaining function.
The enamel of a natal tooth in a healthy full-term child and the enamel of a postnatally erupted tooth in a premature child have been studied with scanning electron microscopy on longitudinal and cross sections. The first case shows that following a normal development, amelogenesis was arrested. This is evident by the presence of the external aprismatic layer in spite of the narrowness of the enamel which corresponds to about a third of the normal thickness. This premature arrest of amelogenesis can be dated to about the 6th month "in utero". In the second case we observed a reversible amelogenesis disturbance as attested by the absence of the external aprismatic layer as well as by a new and fast enamel apposition that took a pseudonormal course. Happening about 10 weeks before birth, this disturbance has probably been induced by factors of maternal origin. In both cases, the eruption anomaly was associated with an enamel anomaly. These observations open new perspectives in the study of natal and neonatal teeth. By extension, such observations are likely to produce complementary informations in neonatology.
Osteoclastic bone resorption has recently been implicated in the tooth formation and eruption in alveolar bone. Cathepsin K (CK) is a cysteine proteinase expressed predominantly in osteoclasts and is believed to play a critical role in degradation of bone matrix proteins. Here we present evidence that the alveolar bone resorption is essential for the tooth formation and that eruption proceeds normally in CK-deficient (CK-/-) mice. Radiographic and histological analyses revealed that the alveolar bone from these animals had no significant abnormalities during the tooth development between 5 and 28 days after birth. The tooth crown was normally erupted through the alveolar bone layer at 28 days after birth. The number of tartrate-resistant acid phosphatase-positive multinuclear cells in the alveolar bone around the tooth germ was apparently increased in 5-day-old CK-/- mice compared with age-matched littermates. More important, however, the immunohistochemical localization of matrix metalloproteinase-9 (MMP-9) was clearly increased in the CK-/- osteoclasts. In contrast, no significant difference in the immunoreactivity for cathepsin D was observed between the CK-/- osteoclasts and the wild-type ones. These results indicate that CK-/- osteoclasts are fully differentiated and are capable of degrading the organic phase of alveolar bone during the tooth formation and eruption, which may result from the compensatory action by MMP-9 increasingly expressed in the osteoclasts.
This case report describes an unusual hypoplastic maxillary first premolar tooth that was diagnosed radiographically in a 10-year-old boy. The maxillary primary first molar had been extracted. When the tooth erupted the hypoplasia was seen to be confined to the mesial aspect of the tooth. The cause of this unusual distribution was considered to be either infection associated with the mesiobuccal root of the primary first molar or trauma during extraction of the primary tooth. The tooth was restored using dentine adhesive and posterior composite material.
Localized hypoplasia of the primary canine (LHPC) occurs in prehistoric and contemporary populations with prevalence varying from 0 to 89%. One of the highest prevalences ever reported is Upper Paleolithic infants from Europe where 70% are affected. In that LHPC is found in relatively high proportions of contemporary children with reported or suspected malnutrition, it is important to investigate the etiology of LHPC. Previous research indicates that LHPC occurs in two steps: craniofacial osteopenia results in temporary fenestration of the cortical bone overlying the primary canine crypt; secondly, minor physical trauma to the perioral region impacts on the unprotected forming tooth crown resulting in a small pit visible on the labial surface of the erupted tooth. Investigation of the prenatal diet of mothers whose children are shown later to have LHPC found mothers are significantly low in vitamin A. Hitherto an animal model for this problem has been lacking. Recently Newell and Skinner have recognized that LHPC occurs very commonly in orangutans. Recent study of infant jaws from Pongo pygmaeus (n=75) and Pan paniscus (n=39) shows all stages of fenestration and healing of the labial bone of the primary canine crypt. 85% of orangutan and 62% of bonobos show LHPC. Current research is directed at bioavailability of vitamin A to ape infants. LHPC is a marker of malnutrition; a common factor that could link orangutan and Upper Paleolithic mothers is low dietary fat intake. A minimal level of dietary fat is required for gut absorption of both vitamin A and carotenoids.