Morphology of dental enamel and dentine–enamel junction in osteogenesis imperfecta

Lindau, B.; Dietz, Wolfram; I, Hoyer; Lundgren, Ted; Storhaug, Kari; Norén, Jörgen G.

doi:10.1046/j.1365-263x.1999.00101.x

Cited by 27 publications

(28 citation statements)

References 22 publications

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“…Gallusi et al [15], Salvolini et al [8], De Coster et al [16], Barron et al [9], and Lindau et al [17] have www.fhc.viamedica.pl all reported irregular anomalies in the enamel-dentin junction. According to their observations, dentinal tubules are absent from large areas of the dentin; they also observed the presence of large channels in the dentin, just as we did in the present study.…”

Section: Discussionmentioning

confidence: 99%

Dentinogenesis imperfecta type II: Ultrastructure of teeth in sagittal sections

Wieczorek

Loster

2013

Folia Histochem Cytobiol.

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Abstract:The morphological abnormalities of the teeth of patients affected by dentinogenesis imperfecta type 2 (DI-II) may underlie the difficulties with the clinical restoration of such teeth. We therefore performed a scanning electron microscopy (SEM) study of four permanent first mandibular molars of four DI-II patients with periapical pathosis. The teeth were prepared for SEM evaluation by standard methods. In the crown, the enamel presented a highly irregular surface with a number of cracks and crevices. In some places, only granular remains of the enamel were found, while in other parts of the crown, the enamel was absent. SEM examination revealed the structural changes responsible for the lower enamel's hardness and resistance to attrition, and for tooth wear, while the structural changes in the dentin may explain the failure of some adhesive restorative materials. This SEM study thus revealed structural defects which underlie the problems of attrition and restoration loss found in patients with this genetic dental condition.

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Section: Discussionmentioning

confidence: 99%

Dentinogenesis imperfecta type II: Ultrastructure of teeth in sagittal sections

Wieczorek

Loster

2013

Folia Histochem Cytobiol.

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“…This difference may be explained by a faster formation of the primary teeth and a greater expression of collagen during the embryonic developmental stage [83,86]. The enamel, which shows normal structure and normal or infrequently decreased mineral content [87], is often dislodged, exposing the soft dysplastic dentin. Teeth show a greyish-blue to brown-yellow colour with a typical amber translucent appearance [88].…”

Section: Osteogenesis Imperfectamentioning

confidence: 99%

“…Teeth show a greyish-blue to brown-yellow colour with a typical amber translucent appearance [88]. These discolorations are the results of light diffraction through the defective dentin–enamel junction [87]. …”

Section: Osteogenesis Imperfectamentioning

confidence: 99%

Tooth dentin defects reflect genetic disorders affecting bone mineralization

Vital

Gaucher

Bardet

et al. 2012

Bone

123

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Several genetic disorders affecting bone mineralization may manifest during dentin mineralization. Dentin and bone are similar in several aspects, especially pertaining to the composition of the extracellular matrix (ECM) which is secreted by well-differentiated odontoblasts and osteoblasts, respectively. However, unlike bone, dentin is not remodelled and is not involved in the regulation of calcium and phosphate metabolism. In contrast to bone, teeth are accessible tissues with the shedding of deciduous teeth and the extractions of premolars and third molars for orthodontic treatment. The feasibility of obtaining dentin makes this a good model to study biomineralization in physiological and pathological conditions. In this review, we focus on two genetic diseases that disrupt both bone and dentin mineralization. Hypophosphatemic rickets is related to abnormal secretory proteins involved in the ECM organization of both bone and dentin, as well as in the calcium and phosphate metabolism. Osteogenesis imperfecta affects proteins involved in the local organization of the ECM. In addition, dentin examination permits evaluation of the effects of the systemic treatment prescribed to hypophosphatemic patients during growth. In conclusion, dentin constitutes a valuable tool for better understanding of the pathological processes affecting biomineralization.

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“…The teeth show a grayish-blue to brown hue varying among individuals and within the same individual over time. The enamel, which shows normal structure and normal or infrequently decreased mineral content (20), is often dislodged, exposing the soft dysplastic dentin. This may lead to a rapid and extensive attrition (7,14,15).…”

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confidence: 99%

Dental aberrations in children and adolescents with osteogenesis imperfecta

Malmgren

Norgren

2002

Acta Odontologica Scandinavica

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The aim of this investigation was to study dental aberrations in a large sample of unrelated patients with different types and forms of osteogenesis imperfecta (OI). Sixty-eight non-related index patients aged 0.3 to 20 years (mean, 10 years) were examined clinically. Panoramic radiographs from 49 patients were analyzed. Dentinogenesis imperfecta (DI) type I was found in 27 of 65 patients and was significantly more common in OI type III than in types I and IV and in patients with a severe form of the disease. The presence or absence of DI showed almost complete accordance between affected parents and children and between affected siblings. Moreover, agenesis was found in 11 of 49 patients, apically extended pulp chambers in 20 of 48 patients, and impaction of second permanent molars in 7 of 19 patients older than 15 years. The percentage of patients with no apparent dental aberrations was approximately the same in patients with OI type I and type III and in patients with mild and severe form of the disease. The high prevalence of dental aberrations in OI stresses the importance of clinical and radiographic odontologic examination as part of the clinical investigation. In patients with mild forms of the disease, in whom the medical diagnosis is uncertain, demonstration of disturbances in dental development can be crucial for establishing the OI diagnosis. C

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Morphology of dental enamel and dentine–enamel junction in osteogenesis imperfecta

Abstract: The mesodermal disease OI might also be manifested in ectodermal enamel, probably because of suboptimal mesenchymal-ectodermal interactions during amelogenesis.

Cited by 27 publications

References 22 publications

Dentinogenesis imperfecta type II: Ultrastructure of teeth in sagittal sections

Dentinogenesis imperfecta type II: Ultrastructure of teeth in sagittal sections

Tooth dentin defects reflect genetic disorders affecting bone mineralization

Dental aberrations in children and adolescents with osteogenesis imperfecta

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