The ultrastructure of the dental tissues in dentinogenesis imperfecta in man

Wright, J. Timothy; Gantt, David G.

doi:10.1016/0003-9969(85)90116-5

Cited by 35 publications

(33 citation statements)

References 11 publications

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“…Enamel fractures occurred along stries of Retzius where prisms are discutinued. 36 Enamel dentin junction is also altered, this explains the phenomenon of enamel chipping. High-resolution synchrotron radiation computed tomography and small angle X-ray scattering showed anomalies of shape and thickness of crystallites.…”

Section: Dentinogenesis and Dental Biomineralizationmentioning

confidence: 99%

Isolated dentinogenesis imperfecta and dentin dysplasia: revision of the classification

Molla¹,

Fournier²,

Berdal³

2014

Eur J Hum Genet

111

134

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Dentinogenesis imperfecta is an autosomal dominant disease characterized by severe hypomineralization of dentin and altered dentin structure. Dentin extra cellular matrix is composed of 90% of collagen type I and 10% of non-collagenous proteins among which dentin sialoprotein (DSP), dentin glycoprotein (DGP) and dentin phosphoprotein (DPP) are crucial in dentinogenesis. These proteins are encoded by a single gene: dentin sialophosphoprotein (DSPP) and undergo several posttranslational modifications such as glycosylation and phosphorylation to contribute and to control mineralization. Human mutations of this DSPP gene are responsible for three isolated dentinal diseases classified by Shield in 1973: type II and III dentinogenesis imperfecta and type II dentin dysplasia. Shield classification was based on clinical phenotypes observed in patient. Genetics results show now that these three diseases are a severity variation of the same pathology. So this review aims to revise and to propose a new classification of the isolated forms of DI to simplify diagnosis for practitioners.

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Section: Dentinogenesis and Dental Biomineralizationmentioning

confidence: 99%

Isolated dentinogenesis imperfecta and dentin dysplasia: revision of the classification

Molla¹,

Fournier²,

Berdal³

2014

Eur J Hum Genet

111

134

View full text Add to dashboard Cite

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“…[3] Teeth with the DI show a mesodermal defect, in which there is an abnormality in the primary structure of dentine. [4] Studies by Kerebel et al [5] and Wright et al [6] showed abnormalities in the dentinal tubules and calcifi cation of dentine in such teeth. No changes were seen in enamel, cementum, and periodontal ligament of eff ected teeth.…”

Section: Discussionmentioning

confidence: 98%

A case report of dentinogenesis imperfecta inherited in a family of four generations

Okade¹,

Nagaraj²,

Shruthi³

et al. 2016

IJMDCR

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In dental anomaly, dentinogenesis imperfecta (DI) is one of the hereditary developmental disorders aff ecting both formation and maturation of dentin. This autosomal dominant disorder is characterized by discolored and translucent teeth ranging from gray to brownish-blue or amber. It can aff ect both primary and permanent teeth. The enamel may split readily from the dentin on occlusal stress. Radiographically, there is evidence of cervical constrictions, short root, and pulp chambers. The aff ected teeth may have smaller or completely obliterated root canals. This article reports a case of a family, which is aff ected by type I DI over four generations.

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“…The gene product is a precursor protein that is cleaved into 2 dentinspecific proteins, dentin sialoprotein (DSP) and dentin phosphoprotein (DPP). The genetic basis for this clinical heterogeneity is unknown (4)(5)(6)(7)(8). Examination of the family pedigree revealed that in each instance an affected child had an affected parent.…”

Section: Discussionmentioning

confidence: 99%

Dentinogenesis imperfecta type II: an affected family saga

Kamboj

Chandra

2007

J Oral Sci

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Dentinogenesis imperfecta (DI) type II orhereditary opalescent dentin is inherited in simple autosomal dominant mode with high penetrance and low mutation rate. It generally affects both the deciduous and permanent dentitions. DI type II corresponds to a localized form of mesodermal dysplasia, observed in histodifferentiation. Early diagnosis and treatment are therefore, fundamental, aiming at obtaining a favourable prognosis since late intervention makes treatment more complex. We present two cases of DI type II with the disease affecting three generations of a family in India, and briefly highlight the molecular basis of this disease. (J. Oral Sci. 49, [241][242][243][244] 2007)

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The ultrastructure of the dental tissues in dentinogenesis imperfecta in man

Cited by 35 publications

References 11 publications

Isolated dentinogenesis imperfecta and dentin dysplasia: revision of the classification

Isolated dentinogenesis imperfecta and dentin dysplasia: revision of the classification

A case report of dentinogenesis imperfecta inherited in a family of four generations

Dentinogenesis imperfecta type II: an affected family saga

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