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A new, nonsyndromic dentin defect, focal odontoblastic dysplasia, is described on the basis of clinical, radiographic, histologic, and scanning electron microscopic criteria. A provisional classification is proposed for this disease entity according to the nosology of Shields and associates. Four additional cases in the literature which possibly represent this new entity are presented, and a possible genetic etiology is discussed.
Dentin matrix of demineralized primary and permanent teeth with type II dentin dysplasia was studied by transmission electron microscopy. The coronal dentin of a maxillary third molar exhibited a normal structure. In the radicular dentin, tubules were few in number; the major part of the dentin was composed of thick, curvy bundles of cross-striated collagen fibers. In the most aberrant areas of the radicular dentin, coarse collagen fibers measuring up to 140 nm in thickness were observed. The dentin of the primary tooth showed a similar, but somewhat less irregular, structure.
Dentin dyslasia is a rare autosomal dominant hereditary variant of dentinogenesis imperfecta. The primary defect is mesodermal and involves the dentin. Two types (Type I and Type II) of dentin dysplasia have been described previously. The current case presents radiographic findings which include characteristics common to both types. It is proposed that either a third type (Type III) be recognized or the variability of the developmental defect precludes definitive subclassification.
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Radicular dentin dysplasia is a peculiar anomaly in which abnormal dentin resembling the plici-dentin found in certain fish and reptiles obliterates the pulp chamber. The almost complete absence of roots leads to the early loss of teeth and predisposes to paradontal infection and the formation of cysts.
Dentinal dysplasia is one of the rarest hereditary disturbances of dentin formation characterized by the teeth present with short blunt roots, considerably reduced or obliterated pulp spaces, periapical abscess or cysts without an obvious causative factor, and spontaneous exfoliated. These features were observed on a patient referred for prosthodontic assessment, and an investigation of other members of the family revealed that the father and two siblings were also affected. The report described the clinical, radiographic, histologic and scanning electron microscopic features and discussed the features which separated from dentinogenesis imperfecta.
Dentinal dysplasia (DD) Type I, is a hereditary disturbance in dentine formation. In this anomaly, teeth in both primary and secondary dentitions are affected, and radiographically show short and blunted roots with obliterated root canals and periapical pathosis. Management of patients with DD has presented dentists with problems. Extraction has been suggested as a treatment alternative for teeth with pulp necrosis and periapical abscess. Follow-up and routine conservative treatment is another choice of treatment plan in DD. Another approach for the treatment of teeth with DD has included periapical surgery and retrograde filling, which is recommended in the teeth with long roots. The purpose of this report is to present an unusual case of dentinal dysplasia Type I in a 22-year-old woman showing upper and lower teeth with obliterated root canals and periapical radiolucencies. In this case, conventional endodontic treatment was performed. Postoperative radiographs and clinical evaluation demonstrated periapical healing and successful results. Based on the results of this case report, conventional endodontic treatment for cases with pulp necrosis and periapical radiolucencies in dentinal dysplasia is highly recommended.
Dentin dysplasia is a rare developmental disturbance of dentin affecting approximately 1:100,000 people. It has been classified as an autosomal dominant disease. Two distinct forms of dentin dysplasia have been described. As more cases of dentin dysplasia were reported these categories seemed inadequate; subclassification of type I dentin dysplasia were proposed based on root length and the presence or not of a pulpal remnant. This paper presents two cases demonstrating the classic features of type I dentin dysplasia in the mixed and permanent dentitions and discusses the suggested subclassifications. The authors suggest that while differences in root length may be useful in determining treatment options, thinking of these variables as separate types of dentin dysplasia is not warranted at this time. Justification of a subcategory of type I dentin dysplasia should be based on a different disease process, different histology, significantly different symptoms, or different etiologies, and until researchers can clearly prove from a genetic or chromosomal standpoint that the subcategories are separate entities, we should accept, as we do for many other genetic disorders, that some patients are more severely affected than others.
Dentin dysplasia, type II (MIM*125420) is an autosomal dominant disorder of dentin development. Clinically the primary dentition appears opalescent, and radiographically the pulp chambers are obliterated, resembling dentinogenesis imperfecta. However, unlike dentinogenesis imperfecta, the permanent teeth in dentin dysplasia, type II are normal in color and, on radiographs, have a thistle-tube pulp chamber configuration with pulp stones. The similarity of the primary dentition phenotype suggested that the gene for dentin dysplasia, type II is allelic with the gene for dentinogenesis imperfecta, Shields type II (DGII; MIM*125490), which has been localized to chromosome 4q13-q21. Twenty-four members of a three generation family in which ten members are affected with dentin dysplasia, type II were genotyped for microsatellite alleles specific for the area of chromosome 4q linked to DGII. Linkage was assessed by using the LINKAGE computer program, assuming autosomal dominant inheritance, a disease allele frequency of 0.0001, and complete penetrance. The maximum two-point LOD score (Zmax = 4.2 at theta = 0.0) was obtained with SPPI and D4S2691. Multipoint analysis gave a maximum LOD score of 4.33. The candidate region for dentin dysplasia, type II is approximately 14.1 cM, includes SPPI, D4S2691, D4S2690, D4S451, and D4S2456, and overlaps the most likely location of the DGII locus. A candidate gene for DGII should also be considered a candidate gene for dentin dysplasia, type II.
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Dentin dysplasia type II is a rare autosomal dominant defect which affects dentin formation in both the deciduous and the permanent dentitions. The scanning electron microscopic study performed on a primary central incisor presents some findings similar to those reported in dentinogenesis imperfecta. Because of the lack of published reports on dentin dysplasia type II, it is difficult to ascertain definitive characteristics of this dentin abnormality.
Dentin dysplasia is a defect of dentin development that was classified by Shields as type I and type II. The teeth in dentin dysplasia type I are characterized by normal enamel and abnormal dentin in the crown and root. For that reason, this disorder is characterized by dental caries, early exfoliation of the teeth and, consequently, maxillomandibular bony atrophy. In this report, we present a case of a young girl affected by dentin dysplasia type I, treated with a combination of onlay bone grafting and a sinus lift technique to accomplish implant placement. This case showed that onlay autogenous grafting and a sinus lift technique are well-tested methods of bony augmentation and can be useful in patients with congenital dentin defects, such as dentin dysplasia.
Dentinal Dysplasia Type I is a rare condition affecting the deciduous and permanent dentitions, in which the teeth present with short roots and considerably reduced or obliterated pulp spaces. These features were observed on the radiographs of a patient referred for orthodontic assessment, and an investigation of other members of the family revealed that the father and two siblings were also affected. There were variations in the lengths of the roots in those affected, and thus a subclassification of the dysplasia is proposed.
A three-generation family with dentin dysplasia (DD) Type II is presented. Affected family members share common radiologic features with clinically varied expression of tooth discoloration and occlusal wear. Both the primary and the permanent dentition appear to be affected. No generalized connective tissue involvement is found. The mode of inheritance is autosomal dominant. Histologically, the findings are consistent with DD Type II. In indirect immunofluorescence, the irregular radicular dentin of an affected permanent tooth failed to stain with specific antibodies against Type III collagen and the N-terminal propeptide of Type III procollagen.
Dentinal dysplasia type I is a relatively uncommon condition and four cases are described. The radiographic features in these patients are somewhat different to those reported in other cases in that anterior teeth appeared to be less affected than posterior, and tooth loss was less prevalent. These findings support the proposal that the characteristics of dentinal dysplasia type I can be divided into two subgroups.
The literature is reviewed to determine the radiographic appearance of the reported cases of dentin dysplasia. The sometimes confusing nomenclature is rationalized. Four distinct forms of dentin dysplasia type I and one form of dentin dysplasia type II are identified. There seems to be no need to identify more than two distinct types of this relatively rare inherited defect of human dentin, but a proposed subclassification of type I dentin dysplasia could make identification of the two types easier.
Dentin dysplasia, type I, is a rare dental anomaly characterized by abnormal dentin formation affecting the roots of both primary and permanent teeth. Short, conical roots with occlusion of the pulp chamber and canal are produced. Periapical radiolucent areas are common, although no evidence of caries or trauma to the tooth may be seen. Coronal mantle dentin is unaffected, resulting in an apparently normal clinical crown. An abnormality may not be suspected until radiographs reveal pulp and root changes. Orthodontic treatment can be a successful variation of the usual treatment offered to patients, and is discussed in this case report.
A case of dentinal dysplasia type I is presented. This rare hereditary disturbance of dentine is characterized by short-rooted teeth with sharp conical apical constrictions, aberrant growth of dentine in the pulp chamber leading to reduced pulp space in permanent teeth and total pulpal obliteration in the primary dentition. Clinical, radiographic and histopathological material from a 7-year-old boy, showing the typical features of this disorder in which teeth are prematurely lost through periapical abscesses, cysts or spontaneous exfoliation, is described. A review of the theories of pathogenesis of this condition is included. Management of patients with dentinal dysplasia is difficult and a discussion of the shortcomings of various treatment strategies, including conventional endodontic therapy, periapical curettage and retrograde root filling, and a preventive regimen, are discussed. In this case, despite diagnosis being made at an early age and the provision of regular dental care, the patient is now losing teeth because of spontaneous abscess formation.