Malposition of unerupted mandibular second premolar in children with palatally displaced canines.

OBJECTIVE: To test the hypotheses that (1) the distal angulation of unerupted mandibular premolar (MnP2) is significantly greater in children with palatally displaced canines (PDC) than in those in a control sample; and (2) delayed tooth formation is significantly more frequent in children with both malposed MnP2 and PDC than in children with PDC only. MATERIALS AND METHODS: We examined retrospectively panoramic radiographs from 43 patients with PDC who had no previous orthodontics. A control sample consisted of age- and sex-matched patients. The distal angle formed between the long axis of MnP2 and the tangent to the inferior border was measured. Dental age was evaluated using the Koch classification. RESULTS: A significant difference was observed between the mean inclination of the right side MnP2 in the PDC group (75.4 degrees) and that of the control group (85.8 degrees). This difference was highly statistically significant (P < .0001). The same evaluation was carried out for the left side, with similar results. The average dental age was found to be delayed in patients who showed both abnormalities (malposed MnP2 and PDC) compared with patients who showed the PDC anomaly only. CONCLUSION: Both hypotheses are retained. Statistically, PDC and MnP2 malposition are significantly associated suggesting a common genetic etiology, despite taking place on opposite jaws. While the presence of PDC or MnP2 anomaly has been associated with a delay in tooth formation, we find the presence of both anomalies to show a more profound delay. Our findings suggest a delay in tooth formation as a possible common genetic mechanism for these 2 malposition anomalies.

Tooth development included in the multifocal jaw lesions of Langerhans cell histiocytosis.

Many cases demonstrating the oral manifestations of Langerhans cell histiocytosis (LCH) have been reported; however, tooth development in jaw lesions has rarely been mentioned. This paper reports the case of a 3-year-old Japanese girl with LCH suffering from multiple osteolytic lesions of the skull and jaw bones. She was referred to our paediatric clinic because of swelling of the mucogingival folds in the upper and lower primary molar regions. The patient responded well to steroid therapy and the osteolytic lesions resolved. There was an accompanying development of permanent tooth germs included in the lesions. Langerhans cell histiocytosis in children usually has a long-term clinical course and paediatric dentists should be involved with oral health care for affected patients.

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.

Reduced growth hormone receptor immunoreactivity in osteoclasts adjacent to the erupting molar in the incisor-absent (osteopetrotic) rat.

First molars fail to erupt in the incisor-absent (ia/ia) rat because of a defect in osteoclast function. Growth factors that regulate local bone metabolism include growth hormone (GH), insulin-like growth factor-I (IGF-I), epidermal growth factor (EGF) and interleukin-1 alpha (IL-1alpha). Since osteoclast function may be affected by these factors, the aim of this study was to determine the distribution of GH receptor (GHr), IGF-I, EGF and IL-1alpha, in osteoclasts located occlusal to the erupting first molar, in the 'eruption pathway', in normal and ia/ia rats. Sagittal sections of the first molar and adjacent bone from 3- and 9-d-old animals were examined. Osteoclasts were identified using tartrate-resistant acid phosphatase (TRAP). The TRAP-positive osteoclast cell numbers were higher in ia/ia animals at 3 and 9 days-of-age. In the ia/ia group, fewer osteoclasts were GHr- and IGF-I-positive at 3 d of age, and at 9 d of age fewer osteoclasts were GHr-positive. In the ia/ia rat, defective osteoclast function failed to resorb bone to provide an eruption pathway for the lower first molar. The expression of GHr, and to some degree IGF-I, by these osteoclasts was reduced, which may be related to their ability to differentiate and function.

Amelogenin protein exhibits a modular design: implications for form and function.

The most abundant protein of forming enamel is amelogenin, a protein capable of self-assembly to form nanospheres. Naturally occurring mutations in the human amelogenin gene are responsible for at least some of the disease entities known collectively as amelogenesis imperfecta (AI), although it is clear that the AI phenotype may be caused by alteration to other genes responsible for the biogenesis of the enamel extracellular matrix. Mutations that create changes in the functional domains of the amelogenin protein do adversely affect enamel biomineralization. Protein engineering of amelogenin that phenocopies several of the known AI mutations exhibits defects in self-assembly. Amino acid alterations that occur within a domain of amelogenin appear to cause "mineral defects," that is to say hypocalcification of the enamel, whereas mutations that occur elsewhere in another domain of the amelogenin molecule result in "hypoplastic defects," a decrease in thickness of the enamel. However, not all patients with AI phenotypes segregate precisely into these arbitrary designations. Nonetheless, correlating the domain of the amelogenin protein that contains a specific mutation with the type of enamel structural alteration suggests a modular design for amelogenin that is corroborated by protein engineering using recombinant DNA techniques and transgenic animal studies.

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.

No developmental failure of cultured tooth germs from osteopetrotic (op/op) mice.

BACKGROUND: Incisor tooth germs of osteopetrotic (op/op) mice are known to fail to erupt, but form odontomas in their root apices instead, due to invasion of alveolar bone trabeculae into the tooth germs. The purpose of this study is to determine if the tooth developmental failures in op/op mice are intrinsic or secondarily arise as a result of the defective bone metabolism due to lack of macrophage colony-stimulating factor (M-CSF). METHODS: We isolated mandibular first molar tooth germs from normal and op/op mice and cultured them under conditions with or without bone tissues which had been formed around tooth germs. RESULTS: Tooth germs from normal mice, cultured for a week, showed almost the same developmental features as those of mice with the corresponding age. They were surrounded with dental follicular tissues and were never invaded by bone trabeculae. On the other hand, op/op tooth germs cultured in the presence of bone components were invaded by alveolar bone trabeculae around tooth germs in the same manner as shown in vivo. When cultured without bone, they developed without any interruptions. CONCLUSIONS: These findings indicated that op/op tooth germs had potential for normal development and that their abnormal development was a secondary phenomenon caused by lack of bone remodeling in the early phase of odontogenesis.

The fate of developing teeth in mandibular lengthening by distraction: an experimental study.

PURPOSE: The purpose of this study was to observe developing teeth in a lengthened mandible after distraction. MATERIAL: Ten mongrel dogs with deciduous dentitions were used. METHODS: A corticotomy was carefully made around a tooth bud and the external distractor (Orthofix M-100) was connected. After a 5-day latent period, distraction was started at a rate of 0.75 mm per day for 10 consecutive days. Then, the lower jaw was stabilized by an external fixation to allow ossification. While the operation was performed on the left side (Distraction group), the contralateral side was studied for comparison (Control). In addition, a corticotomy, artificial fracture and external fixation were carried out to confirm the influence of the operation (Fracture group). Then macroscopic, radiographic and histological evaluations were carried out. RESULTS: In the Distraction group, the space between the wall of the dental follicle and the crown expanded as distraction began. The end of the calcified root became wider and irregular during the distraction period, and finally, the apex closed. In the Fracture group, the teeth erupted although slight alterations of the root shape were observed in association with the operation period. CONCLUSION: The root became irregular, but the teeth erupted within the distraction area.

Denudación patológica radicular en los dientes temporales / Pathologic root denudation in primary teeth

Esta entidad patológica de la cavidad oral del niño es una alteración poco conocida en el ámbito odontológico, no obstante haber sido descripta hace más de treinta años por el odontólogo guatemalteco Dr. O Menéndez, el cual la observó en niños nativos de su país. Pocos años después, el Dr. Serrano reportó muchos casos de esta afección bucal visto en niños aborígenes ecuatorianos

Intrusion injuries of primary incisors. Part I: Review and management.

Intrusion injuries commonly occur in the primary dentition. They can be described as luxation injuries resulting from an axially directed impact, which drives the tooth deeper into the alveolar socket. The impact results in compression of and damage to the periodontal ligament as well as injury to the pulp of the intruded incisor. In addition to rendering treatment to the intruded primary tooth, the dentist must also be aware of the possibility of an injury to the developing permanent teeth germs located in close proximity to the roots of the injured primary teeth. This review will discuss the characteristics, implications, and management of intrusion injuries of primary incisors.

Intrusion injuries of primary incisors. Part II: Sequelae affecting the intruded primary incisors.

Luxation injuries to incisors, including intrusive displacement, occur with a high frequency in the primary dentition. Intrusion injuries are associated with damage to the pulpal and periodontal structures and possible fracture of the alveolar bone. The pulpal tissue of the intruded tooth sustains a severe shock during displacement, which may be reflected later by sequelae ranging from mild discoloration to pulpal necrosis and infection. Disintegration of pulpal tissue may result in periapical tissue inflammation, which in turn may induce developmental disturbances in the germ of the permanent successor tooth. Additionally, severe injury to the periodontal ligament during intrusion may lead to ankylosis of the primary incisor and consequently to delayed or ectopic eruption of its permanent successor. This article will review the possible sequelae affecting primary incisors following their intrusion.

Intrusion injuries of primary incisors. Part III: Effects on the permanent successors.

Intrusion injuries of the primary dentition are highly associated with developmental disturbances of their successor teeth. The age of the child at the time of injury, the direction and severity of the intrusion, and the presence of alveolar bone fracture are important variables influencing the effect of primary tooth intrusion on the developing permanent germ. The developmental defects of the permanent successor tooth range from mild alteration in enamel mineralization to severe sequestration of the developing germ. This article will review the developmental anomalies of the permanent incisors induced by intrusion injuries of their predecessors.

Effects of removing inferior alveolar neurovascular structures on mandibular growth and the eruption of permanent dentition in puppies.

Investigation was performed on the effects of removing the inferior alveolar neurovascular structures on the permanent dentition and mandibular growth. Five puppies with erupted deciduous teeth had the inferior alveolar neurovascular structures removed unilaterally. When the test animals were 28 weeks old, examination revealed that the deciduous teeth on the side operated had exfoliated but permanent teeth did not replace them. On the other hand, the permanent teeth on the side not operated on replaced the exfoliated deciduous teeth. After a second period of 28 weeks, the germs of the permanent teeth on the side operated on were still buried in the mandibular bone, and the permanent teeth on the side not operated on erupted normally. Mandibular measurements demonstrated that translative and transformative growth and developmental processes were normal in both the sides operated on and the sides not operated on.

Effects of bone marrow transplantation on impacted dental germs in osteopetrotic op/op rats.

The osteopetrotic op/op rats suffered from a complete failure of tooth eruption in association with a reduced bone resorption. An unresorbed occlusal bone overlaid the germs which remained embedded in bone. The process of prefunctional eruption in limited growing teeth depends on the resorption of the alveolar bone covering the germs. The aim of this study was to investigate the effects of hematopoïetic grafts in newborn op/op rats on the process of prefunctional eruption. Fifteen op/op treated rats were used for radiographic, microradiographic and histologic examinations. After transfusion of bone marrow cells, we observed the restoration of bone resorption and a delayed eruption of the molars. The incisors never erupted. They developed odontome-like tumors near their apices. These results confirm the dependence of tooth eruption on bone resorption.

Histopathology of the interactions between alveolar bone and impacted dental germs in osteopetrotic op/op rats.

Osteopetrosis, a general increase in bone density, is well-known as an autosomal recessive disease in several mammalian species. Compared with normal littermates, the osteopetrotic rats suffered from a complete failure of tooth eruption. Histologic and microradiographic studies show that the molars and the incisors developed a progressive ankylosis, the bone invades the germs and finally dissociates them. As early as the first days after birth, the incisors and the first molars are affected by the osteopetrotic process while the second and the third molars remain untouched. The periodontal membrane of the incisors is rapidly invaded by the osteopetrotic bone trabeculae. After the eleventh day, the process reached all molars. The germs were overlaid by an occlusal unresorbed bone. The formation of the gebernacular canal appeared to be independent of the prefunctional eruption.