Complication After Extraction of Natal Teeth with Continued Growth of a Dental Papilla.

The purposes of this case report were to describe a growing two-cm gingival mass that developed after natal teeth were extracted in a four-month-old female patient, present a review of the literature on the growth of a gingival mass after the extraction of natal teeth, and illustrate the clinical and histological features that differentiate this condition from other types of gingival masses in infants. Histological examination of the excised mass revealed that it contained tooth-like hard tissue (regular and irregular dentin) that intermingled with bone, dental pulp, and fibrous tissue. We found eight cases from 1962 to 2009 in which a soft-tissue mass with dentin-like hard tissue or a tooth-like structure had developed after the extraction of natal teeth. Based on clinical and histological findings, we deduced that the mass was the result of abnormal growth of a residual dental papilla, including mesenchymal stem cells. Consequently, dentists, obstetricians, gynecologists, and pediatricians should be aware of this potential complication and observe caution before they extract natal teeth.

[Dens invaginatus--a challenge in endodontics]. / Dens invaginatus--un défi en endodontie.

Dens invaginatus is a malformation of teeth probably due to infolding of the dental papilla during tooth development. A wide range of morphologic variations have been described. Both coronal and radicular invaginations have been demonstrated. Typical characteristics associated with the coronal invagination are the complex anatomy and the early pulp necrosis. The etiology, epidemiology, classification and therapeutic considerations are reviewed.

[Effect of the Tabby mutation on the dentition of mice]. / Effets de la mutation Tabby sur la dentition chez la souris.

The X-linked hypohidrotic ectodermal dysplasia in man leads to dental defects and is homologous to the Tabby (Ta) mutation in mouse. We currently investigate the effects of the Ta mutation on odontogenesis. The incisor germ of Ta showed an abnormal size and shape, a change in the balance between prospective crown- and root-analogue tissues and retarded cytodifferentiation. Although the enamel organ in Ta incisors was smaller, a larger proportion of the dental papilla was covered by preameloblasts-ameloblasts. The independent development of the labial and lingual parts of the enamel organ in rodent lower incisor might reflect their heterogeneous origin, as demonstrated for the upper incisor. The mandibular cheek dentition in Ta mice exhibits large variations classified in five morphotypes, based on the tooth number, shape, size and position. In Ta embryos, the mesio-distal extent of the dental epithelium was similar to that in WT, but its segmentation was altered. These morphotypes could be explained by a tentative model suggesting that 1) the positions of tooth boundaries differ in Ta and WT molars and among the Ta morphotypes; 2) the tooth patterns are determined by the distal boundary of the most mesial tooth primordium while the distal teeth take advantage of the remaining dental epithelium; 3) one tooth primordium in Ta mice might derive from adjacent parts of two primordia in WT.

Msx1 deficient mice exhibit cleft palate and abnormalities of craniofacial and tooth development.

The Msx1 homeobox gene is expressed at diverse sites of epithelial-mesenchymal interaction during vertebrate embryogenesis, and has been implicated in signalling processes between tissue layers. To determine the phenotypic consequences of its deficiency, we prepared mice lacking Msx1 function. All Msx1- homozygotes manifest a cleft secondary palate, a deficiency of alveolar mandible and maxilla and a failure of tooth development. These mice also exhibit abnormalities of the nasal, frontal and parietal bones, and of the malleus in the middle ear. Msx1 thus has a critical role in mediating epithelial-mesenchymal interactions during craniofacial bone and tooth development. The Msx1-/Msx1- phenotype is similar to human cleft palate, and provides a genetic model for cleft palate and oligodontia in which the defective gene is known.

Dental lesions in tumoral calcinosis.

Tumoral calcinosis (TC) is a rare inherited autosomal dominant metabolic disease manifested by elevated serum phosphorus and 1,25 dihydroxyvitamin D levels and periarticular cystic and solid tumorous calcifications. The dental findings in a large family have been critical in determining the genetic transmission of the condition. Radiographically the teeth have short bulbous roots, pulp stones and partial obliteration of the pulp cavity. Histologically, coronal dentin and a variable amount of radicular dentin appears to be deposited regularly. At nonspecific points the developing radicular dentin appears to encounter a mass of calcified material and proceed to grow around it. This mass has a unique histologic pattern with ovoid spaces surrounded by amorphous calcification. At levels of further root development the radicular dentin has an irregular bending tubule arrangement. The dental lesion of TC appears to be different from that of radicular dentin dysplasia in histologic structure and in the method of initiation of the dentin defect. These data suggest that the specific dental lesion is a new phenotypic marker for TC.