Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “TOOTH ABNORMALITIES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1981

[Ichthyosis vulgaris, growth retardation, hair dysplasia, tooth abnormalities, immunologic deficiencies, psychomotor retardation and resorption disorders. Case report of 2 siblings].

Two siblings (4 and 10 years old) with ichthyosis vulgaris, growth and mental retardation, hair dysplasia, teeth abnormalities, recurrent infections and malabsorption are presented. The elder sister of the children as well as the rest of the family are unremarkable. The complex of symptoms does not fit into one of the known Ichthyosis syndromes. Microscopically the dystrophic hairs show changes in diameters, nodules, lack of the medulla, rough cuticle and splits vertical to the axis, sometimes resembling trichorrhexis nodosa. In the scanning electron-microscope there is a clear difference to Netherton's syndrome. The plasma concentrations of the vitamines A, B12 as well as of beta-carotines are low in spite of normal nutrition. During parenteral therapy with vitamin A and B12 symptoms ameliorate slightly.

Abnormalities, Multiple↗
PubMed2004

Accelerated bone formation and increased osteoblast number contribute to the abnormal tooth germ development in parathyroid hormone-related protein knockout mice.

Our previous study showed that tooth germs at late embryonic stage [later than embryonic day 17.5 (E17.5)] and neonatal homozygous parathyroid hormone-related protein (PTHrP)-knockout mice are compressed or penetrated by the surrounding alveolar bone tissue. In vivo and in vitro studies have shown that the development of the tooth germ proper is not disturbed, but insufficient alveolar bone resorption, due to the decreased number and hypofunction of osteoclasts, is the main cause of this abnormality. In addition to the insufficient alveolar bone resorption, progressive bone formation toward tooth germs was observed in homozygous mice, suggesting that accelerated bone formation also contributes to this abnormality. To further investigate this, homozygous mice at E14.0 and E15.5, when alveolar bone is forming, were used for histochemical and bone histomorphometric analyses. In contrast to the late embryonic stage, the alveolar bone did not yet compress developing tooth germs in homozygous mice on E14.0, but a larger amount of bone tissue was seen compared to wild-type littermates. Histomorphometric analysis of bone at E14.0 revealed that the osteoblast numbers and surfaces in the mandibles and in the bone collar of femora of homozygous mice were significantly higher than those of wild-type mice. However, unlike our previous study showing the osteoclast surface on E18.5 in homozygous mice to be significantly lower than that of wild-type mice, this study at E14.0 showed no significant difference between the two genotypes. To evaluate the amount of calcification around tooth germs, 3D images of mandibles were reconstructed from the calcein-labeled sections of the wild-type and mutant mice. Labeling was performed at E14.0, and the mice were sacrificed 1 h after the calcein injection to minimize the effect of bone resorption. Comparison of the 3D images revealed that the labeled surface was larger around developing tooth germs in homozygous mouse than in wild-type mouse. On day E15.5, osteoblasts approached the enamel organ of homozygous mice but this was not observed in wild-type mice. In this study, we report a systemic increase in osteoblast number and accelerated bone formation in homozygous PTHrP-knockout mice, both of which contribute to the abnormal tooth development.

Acid Phosphatase↗
PubMed1976

Abnormal tooth tissue in human odontodysplasia.

The affected teeth in this case of odontodysplasia exhibited abnormal hypoplastic enamel, abnormal dentin containing extensive interglobular regions and completely lacking a peritubular matrix, and an abnormal irregular tissue consisting of highly calcified and partially fused granules located within the dentin of the tooth tips. Electron micrographs of the irregular tissue showed that the granules consisted of crystallites densely and radically packed in a noncollagenous amorphous matrix. Granules were surrounded by a slightly calcified, irregularly arranged, collagenous matrix. The irregular tissue formed in the pulp of the tooth tip befofe and independently of the dentin. It was at least partially formed by pulpal calcification. Abnormal dentin matrix was formed by odontoblasts which were less differentiated than normal. Odontodysplastic teeth showed abnormal differentiation of odontoblasts and ameloblasts resulting in defective enamel and dentin and, in extreme cases, in extensive pulpal calcification.

Child↗
PubMed1981

Osteomatous changes and tooth abnormalities found in the jaw of patients with adenomatosis coli.

Oral findings on the panoramic tomograms of fifty-two patients with adenomatosis coli (AC) are presented. Osteomatous lesions, embedded teeth, and supernumerary teeth were found more frequently in AC patients than in a normal population. The osteomatous lesions were found in more than 80 percent of the AC patients, and the average number of such lesions per patient was 4.7. In a normal population, 15 percent had the osteomatous lesions, and the average number per patient was 1.1. The panoramic tomograms of twelve AC patients who had more than six osteomatous lesions showed very characteristic images. The possibility of early detection of AC through oral radiographic findings is suggested.

Adenoma↗
PubMed2006

Functional consequences of interactions between Pax9 and Msx1 genes in normal and abnormal tooth development.

Pax9 and Msx1 encode transcription factors that are known to be essential for the switch in odontogenic potential from the epithelium to the mesenchyme. Multiple lines of evidence suggest that these molecules play an important role in the maintenance of mesenchymal Bmp4 expression, which ultimately drives morphogenesis of the dental organ. Here we demonstrate that Pax9 is able to directly regulate Msx1 expression and interact with Msx1 at the protein level to enhance its ability to transactivate Msx1 and Bmp4 expression during tooth development. In addition, we tested how a missense mutation (T62C) in the paired domain of PAX9 that is responsible for human tooth agenesis (1) affects its functions. Our data indicate that although the mutant Pax9 protein (L21P) can bind to the Msx1 protein, it fails to transactivate the Msx1 and Bmp4 promoter, presumably because of its inability to bind cognate paired domain recognition sequences. In addition, synergistic transcriptional activation of the Bmp4 promoter was lost with coexpression of mutant Pax9 and wild-type Msx1. This suggests that Pax9 is critical for the regulation of Bmp4 expression through its paired domain rather than Msx1. Our findings demonstrate the partnership of Pax9 and Msx1 in a signaling pathway that involves Bmp4. Furthermore, the regulation of Bmp4 expression by the interaction of Pax9 with Msx1 at the level of transcription and through formation of a protein complex determines the fate of the transition from bud to cap stage during tooth development.

Animals↗
PubMed1999

Alterations in the incisor development in the Tabby mouse.

The X-linked tabby (Ta) syndrome in the mouse is homologous to the hypohidrotic ectodermal dysplasia (HED) in humans. As in humans with HED, Ta mice exhibit hypohidrosis, characteristic defects of hairs and tooth abnormalities. To analyze the effects of Ta mutation on lower incisor development, histology, morphometry and computer-aided 3D reconstructions were combined. We observed that Ta mutation had major consequences for incisor development leading to abnormal tooth size and shape, change in the balance between prospective crown- and root-analog tissues and retarded cytodifferentiations. The decrease in size of Ta incisor was observed at ED13.5 and mainly involved the width of the tooth bud. At ED14.5-15.5, the incisor appeared shorter and narrower in the Ta than in the wild type (WT). Growth alterations affected the diameter to a greater extent than the length of the Ta incisor. From ED14.5, changes in the shape interfered with the medio-lateral asymmetry and alterations in the posterior growth of the cervical loop led to a loss of the labio-lingual asymmetry until ED17.0. Although the enamel organ in Ta incisors was smaller than in the WT, a larger proportion of the dental papilla was covered by preameloblasts-ameloblasts. These changes apparently resulted from reduced development of the lingual part of the enamel organ and might be correlated with a possible heterogeneity in the development of the enamel organ, as demonstrated for upper incisors. Our observations suggest independent development of the labial and lingual parts of the cervical loop. Furthermore, it appeared that the consequences of Ta mutation could not be interpreted only as a delay in tooth development.

Animals↗
PubMed2005

Ectodermal dysplasia--an unusual dental presentation.

Ectodermal dysplasia (ED) is a rare group of disorders affecting the hair, teeth, nails and sweat glands to a variable degree. There is a wide range of clinical presentation of ED. Missing teeth or abnormal tooth form may be the first indicator of the presence of the disorder. There is typically hypodontia with microdontia. We present an unusual case of ED with severe hypodontia and macrodontia affecting all first permanent molar teeth. We also consider the classification and presentation of this disorder.

Anodontia↗