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A case of an unusual foreign body (a tip fragment from a plastic chopstick) embedded in one of two unerupted supernumerary teeth in the premaxillary region of a 12-year-old Japanese boy is presented.
Dentigerous cysts appear to be reasonably common near the mandibular incisors of sheep in New Zealand. Their aetiology, true prevalence, and, therefore, their economic significance, are not known at present. They appear as solitary swellings, grow slowly, and are lined by stratified squamous epithelium. Each example usually contains a single, unerupted tooth; however, the anatomical relationship of this tooth to the cyst wall differs from that in dentigerous cysts in humans. Moreover, as some do not contain an unerupted tooth, the term dentigerous is not entirely appropriate but is supported by common usage. Work is in progress to study these lesions further and to clarify their aetiology. There is no practical treatment.
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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.
The adenomatoid odontogenic tumour most commonly presents as a 1.5-3 cm radiolucency in the anterior maxilla, and often associated with an unerupted tooth. It is very unusual for these tumours to occur behind the premolar region and the few reports of much bigger lesions have been in black African patients. This article describes an unusually large example of this tumour associated with an unerupted maxillary third molar tooth in a white female.
A case report of aneurysmal bone cyst of the mandible in a seven-year-old boy which caused the destruction and loss of the bony crypt around the tooth germ and displacement of the unerupted tooth is presented. This unusual dental findings have not been previously reported in the dental literature.
A case of ankylosis of the maxillary right first permanent molar has been described. For 19 months, no change had been observed clinically or radiographically in the development of the tooth. A diagnosis of ankylosis of the unerupted tooth was made. Instead of extracting the tooth, the ankylosed tooth was rocked in the bone to break the point of ankylosis. The tooth subsequently erupted and satisfactory functional results were obtained. It is suggested that this procedure should be attempted in other cases of ankylosis of permanent teeth.
BACKGROUND: The surgical approach to cystic lesions of the jaws is either marsupialisation or enucleation. The treatment of choice is dependent on the size of the lesion, the bony integrity of the cyst and its proximity to anatomical structures. OBJECTIVES: To assess large (>2.0 cm) cystic lesions of the jaws using plain film radiography (PFR), CT, multiplanar reconstruction program (MPR) and three-dimensional CT (3D-CT). PATIENTS AND METHODS: Twelve children aged 7-14 years. RESULTS: The classic radiological feature was a unilocular radiolucent area surrounded by a well-defined radio-opaque margin adjacent to the root of a non-viable tooth or associated with the crown of an unerupted tooth. Malposition of teeth and root resorption were more common in dentigerous cysts. The features seen on CT were clear and more precise than those seen on PFR. MPR, by the three-dimensional visualisation of the jaw (axial, panoramic, and bucco-lingual), provided useful information for determining the outline of the cyst and its proximity to adjacent anatomical structures, such as teeth, nerves or maxillary sinus. 3-D CT further and more clearly demonstrated discontinuity in the buccal or palatal/lingual cortices of the jaw bone. PFR was very accurate in determining root resorption. CONCLUSIONS: CT with MPR and, ideally, 3-D CT should be used for the comprehensive diagnostic work-up and meticulous surgical management of large cystic lesions of the jaws in children.
BACKGROUND: Treatment of asymptomatic impacted maxillary canines in adults is inevitable when primary canine becomes lost through extraction or exfoliation or when the impacted tooth becomes symptomatic. Treatment alternatives include an orthodontic procedure to bring the unerupted tooth to the dental arch or prosthetic replacement of the missing tooth. The authors describe an alternative treatment that involves immediate placement of implants into extraction sockets of the teeth. CASE DESCRIPTION: A patient with bilateral palatally impacted upper canines chose to have the unerupted teeth removed and replaced with implants and crowns. Two hydroxyapatite cylindrical implants were inserted through the alveolar ridge into the extraction sites. The unfilled areas in the extraction sites, around the dental implants, were packed and covered with demineralized freeze-dried bone allograft in conjunction with a collagen membrane barrier. Six months after implantation, computed tomography revealed complete osseous fill of the extraction defects and no bone loss around the implants. The implants were uncovered, and porcelain-fused-to-metal restorations were fabricated and placed. CLINICAL IMPLICATIONS: This treatment modality avoids the need for conventional preparation of teeth as part of prosthetic reconstruction or prolonged orthodontic treatment aimed at bringing the impacted canine to the dental arch. Combining the implantation with bone augmentation preserved the alveolar bone and shortened the treatment period.
Maxillary crowding may cause failure of eruption of the canine. The teeth so displaced are directed buccally or palatally. In both cases, surgical intervention is indicated after space has been made in the arch. Palatally displaced canines are treated by surgical excision of palatal mucosa to promote eruption. Wide excision is indicated to prevent the healing process from covering the exposed tooth crown. Because of the anatomy of the buccal mucosa, however, surgical excision of the crowns of buccally displaced canine frequently results in periodontal problems. An alternative technique is therefore presented; this involves the surgical exposure of the crowns of buccally displaced teeth to allow the attachment of a wire traction hook. The crown is then recovered. The traction hook provides a point of attachment, so that orthodontic forces may be applied to the unerupted tooth to guide its eruption. The preservation of the mucosal flap ensures a normal epithelial attachment develops on the buccal surface of the tooth, and the normal gingival anatomy of the buccal mucosa is maintained. The procedure may also be used in cases where upper incisors have been prevented from erupting because of the presence of supernumerary teeth. Even after surgical removal of the supernumerary teeth, the permanent incisors often fail to erupt. In such cases, the placement of traction hooks will enable the orthodontist to bring the unerupted teeth into their correct positions in the arch.
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.
Tooth eruption requires the presence of the dental follicle, a loose connective tissue sac that surrounds each unerupted tooth. The follicle appears to regulate many of the cellular and molecular events of eruption, including the formation of osteoclasts needed to resorb alveolar bone to form an eruption pathway. To that end, the expression of the tumour necrosis factor-alpha (TNF-alpha) gene was examined in the dental follicle as a possible regulator of osteoclastogenesis. TNF-alpha was expressed slightly in the dental follicle of the first mandibular molar of the rat beginning at day 3 postnatally, but maximal expression was seen at day 9, a time that correlates with a slight burst of osteoclast formation seen at day 10 postnatally. In vitro, TNF-alpha was not expressed constitutively in the follicle cells but incubating them with interleukin 1alpha resulted in a strong expression of TNF-alpha after only 0.5h. TNF-alpha itself enhanced monocyte chemotactic protein 1 (MCP-1) and vascular endothelial growth factor (VEGF) gene expression. It also slightly decreased the expression of osteoprotegerin after 3-h incubation but this returned to the control level at 6h. MCP-1 and VEGF could aid in recruiting mononuclear cells (osteoclast precursors) to the dental follicle. In addition to the potential role of TNF-alpha in tooth eruption, this study suggests that the periodontal ligament derived from the dental follicle might have the capacity to synthesize TNF-alpha, and thereby contribute to the destructive events of periodontitis.
Cystic changes can arise in relation with unerupted lower third molars. This case report describes a large odontogenic keratocyst (OKC) which developed rapidly and aggressively over a short period of 2 years and presented with acute symptoms. The development of a large OKC over the mandible is evidenced by radiographs taken 2 years apart. The OKC was enucleated and the residual cavity was treated with Carnoy's solution and packed with bismuth iodoform paraffin paste dressing. The impacted third molar and second molar associated with the lesion were also extracted. This case illustrates how rapidly a cyst can develop in association with a previously asymptomatic, unerupted tooth and how quickly a radiographic diagnosis can become out of date. As such, the authors recommend the use of repeated radiographs for monitoring unerupted teeth at a tighter time frame of 6 to 12 months.
Epithelia differ regionally in their patterns of phenotypic expression. The junctional epithelium (JE) that attaches the oral mucosa to the teeth is a unique tissue that shows a pattern of differentiation unlike other oral epithelia and forms basal lamina against the non-vital tooth surface. The mechanisms that establish this unusual phenotype and the developmental origin of this epithelium are both uncertain. The formation of JE by downgrowth of the oral gingival epithelium (OGE) during tooth eruption has been suggested but morphological studies indicate that it may be derived from the reduced enamel epithelium (REE) that covers the crown of the unerupted tooth. These epithelia of potential origin differ in their developmental histories: intrinsic differences between them could thus significantly influence the phenotype of an epithelium formed from them. The patterns of phenotypic expression of specimens of dissected JE, OGE and REE, and of cell cultures of these epithelia grown under standardized conditions, were examined (1) by immunocytochemistry using monoclonal antibodies with specificity for individual cytokeratins, vimentin and ICAM-1, and (2) by two-dimensional SDS-PAGE and immunoblotting. The results indicated that, in vivo, OGE expressed keratin markers typical of differentiating mucosal epithelium; JE and REE, in contrast, lacked expression of most such markers but expressed keratins typical of simple epithelia together with some undefined keratin peptides. All epithelia showed changes in vitro but OGE remained different from JE and REE. OGE lost expression of the differentiation markers K1, K10 and K13; it acquired some expression of K19, but less than JE and REE. Cultures of JE and REE retained some expression of ICAM-1 and K8 and K18, and consistently acquired high levels of vimentin expression. These findings indicate that differences persist in standardized culture conditions and that these are apparently of an intrinsic nature. They support a concept of the origins of JE from REE and suggest that the unusual in vivo phenotype of JE results partly from intrinsic differences acquired during its development.
The pathogenesis of the three common forms of odontogenic cyst is discussed. It is concluded that the dental cyst arises from proliferation of the epithelial rests of Malassez in a focus of inflammation stimulated by pulpal necrosis of the associated tooth. It enlarges by unicentric expansion from the hydrostatis pressure of its contents. The dentigerous cyst arises from pooling of inflammatory exudate, which is derived from the obstructed follicular veins of an unerupted tooth and accumulates between the reduced enamel epithelium and the crown of the tooth. It enlarges by unicentric expansion from the hydrostatic pressure of its contents. The odontogenic keratocyst arises by proliferation of the residues of the dental lamina, possibly as a hamartomatous abnormality. It enlarges by both multicentric expansion due to the proliferation of localized groups of epithelial cells in the lining and by unicentric expansion from the hydrostatic pressure of its contents.
A six-year-old boy presented with extraoral eruption of a mandibular permanent canine and a loosely attached lateral incisor in the labial vestibule, 3 months following trauma to the chin. The trauma not only caused displacement of the permanent tooth buds, but also resulted in transposition of the lateral incisor and canine with subsequent ectopic eruption. The case is presented to demonstrate one of the infrequent complications of trauma involving the unerupted tooth buds of permanent teeth and its unusual clinical presentation.