Rootless teeth: Dentin dysplasia type I

Fulari, Sangamesh; Tambake, Deepti

doi:10.4103/0976-237x.123063

Cited by 12 publications

(14 citation statements)

References 7 publications

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“…We observed narrowed dental pulp cavities, increased dentin thickness, and abnormal tooth attrition in both Ssuh2 +/− and Ssuh2 −/− mice by μCT (Fig. b,A), consistent with the clinical characteristics of DDI patients [Toomarian et al., ; Fulari et al., ; de et al., ]. In addition, similar levels of tooth attrition occurred in MT TG mice with a normal diet and those with a soft diet.…”

Section: Resultssupporting

confidence: 84%

“…We identified a large Chinese family with autosomal‐dominant DDI according to clinical and radiographic diagnostic features (Toomarian et al., ; Fulari et al., ; de et al., ).The family had 14 affected members in a six‐generation pedigree (Fig. ), and affected individuals appeared in good general health and exhibited no abnormalities upon extraoral examination (Supp.…”

Section: Resultsmentioning

confidence: 99%

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Mutation inSSUH2Causes Autosomal-Dominant Dentin Dysplasia Type I

Xiong

Liu

et al. 2016

Human Mutation

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Dentin dysplasia type I (DDI) is an autosomal-dominant genetic disorder resulting from dentin defects. The molecular basis of DDI remains unclear. DDI exhibits unique characteristics with phenotypes featuring obliteration of pulp chambers and diminutive root, thus providing a useful model for understanding the genetics of tooth formation. Using a large Chinese family with 14 DDI patients, we mapped the gene locus responsible for DDI to 3p26.1-3p24.3 and further identified a missense mutation, c.353C>A (p.P118Q) in the SSUH2 gene on 3p26.1, which co-segregated with DDI. We showed that SSUH2 (p.P118Q) perturbed the structure and significantly reduced levels of mutant (MT) protein and mRNA compared with wild-type SSUH2. Furthermore, MT P141Q knock-in mice (+/- and -/-) had a unique partial obliteration of the pulp cavity and upregulation or downregulation of six major genes involved in odontogenesis: Dspp, Dmp1, Runx2, Pax9, Bmp2, and Dlx2. The phenotype of missing teeth was determined in zebrafish with morpholino gene knockdowns and rescued by injection of normal human mRNA. Taken together, our observations demonstrate that SSUH2 disrupts dental formation and that this novel gene, together with other odontogenesis genes, is involved in tooth development.

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Section: Resultssupporting

confidence: 84%

Section: Resultsmentioning

confidence: 99%

Mutation inSSUH2Causes Autosomal-Dominant Dentin Dysplasia Type I

Xiong

Liu

et al. 2016

Human Mutation

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“…In many cases, like in the case described above, the endodontic treatment is not possible, which is why it is so important to prevent pulp complications [5]. It is frequently possible to suppress the inflammation around root apexes by curettage procedures with the application of medicines into gingival pockets [9,19,21].…”

Section: Discussionmentioning

confidence: 99%

Dentin dysplasia type I

Kobus

Świsłocka²,

Kierklo

et al. 2019

Folia Morphol

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This paper describes a rare case of genetically determined dentin dysplasia type I in 26-year-old male patient. The paper highlights anatomical and radiological aspects of dental abnormalities and emphasizes the significance of the education of both general practitioners and paediatricians as regards referring patients with diagnosed dentin dysplasia for a multi-specialty therapy. (Folia Morphol 2019; 78, 3: 637-642)

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“…1,2 The first case reported with this condition was in 1920 termed as "rootless teeth", and in 1939, Rushton termed this condition as DD. 3 Dentinal dysplasia is classified into radicular dentin dysplasia (DDI) and coronal dysplasia (DDII). Both types include generalized/ multiple involvements of the primary and permanent dentitions.…”

Section: Introductionmentioning

confidence: 99%

Dentin Dysplasia Type I: Report of Two Cases

Azimi¹,

Jafari²,

Farzanegan³

et al. 2017

International Journal of Experimental Dental Science

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Objectives:In this article, we report two cases of type I dentin dysplasia (DD): the first case is subtype "d" DD and second case is severe form of DD type I, which presents all of four subtypes and describes characteristics and the management of this type of teeth anomalies. Materials and methods:Dentin dysplasia is a rare abnormality of dentin that involves both primary and permanent dentition. The normal shape of crown, short roots or its total absence, pulp chamber obliteration, crescent-shaped pulp, pulp stone, and periapical radiolucencies are the characteristics of DD type I. Conclusion:There are many problems in the management of a patient with DD. Depending on root development and pulp canal situation, endodontic treatment and tooth extraction are applied in teeth with pulp necrosis and periapical abscess. The prognosis of DD largely depends upon the age at which the diagnosis is made, and the quality of the treatment provided.

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Rootless teeth: Dentin dysplasia type I

Cited by 12 publications

References 7 publications

Mutation inSSUH2Causes Autosomal-Dominant Dentin Dysplasia Type I

Mutation inSSUH2Causes Autosomal-Dominant Dentin Dysplasia Type I

Dentin dysplasia type I

Dentin Dysplasia Type I: Report of Two Cases

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