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The classification and prevalence of amelogenesis imperfecta is updated based upon new information in the literature. Problems with the currently used classification of inherited dentin defects are discussed.
Dentinogenesis imperfecta (DGI) is an autosomal dominant inherited dental disease which affects dentin production and mineralization. Genetic linkage studies have determined linkage between DGI type II and group-specific component (Gc, vitamin D binding protein), interferon (gamma)-induced cytokine protein 10 (INP10) and secreted phosphoprotein 1 (SSP1, osteopontin, bone sialoprotein 1, early T-lymphocyte activation 1). Therefore, the gene locus has been localized to the long arm of human chromosome 4 in the region 4q13-q21. Dentin matrix protein-1 (DMP-1, AG-1) is a new acidic, phosphorylated dentin extracellular matrix protein which has recently been identified by cDNA cloning. The purpose of this study was to establish the possible association of DMP-1 with DGI type II by determining the human chromosomal localization of this protein. A DMP-1 DNA probe was generated1using PCR amplification of the mouse full-length DMP-1 and labeled with [32P] d-CTP. A panel of rodent somatic cell hybrid clones, previously cytogenetically characterized, was used for the assignment. High stringently DNA hybridization studies and analysis of the chromosomal cell panel indicated that the DMP-1 gene locus is located on human chromosome 4. This data supports the hypothesis that DMP-1 is a candidate gene for the genetic disease DGI type II. This is based on chromosomal localization to human chromosome 4, the expression of DMP-1 mostly by odontoblasts, and its purported physical-chemical properties.
Based on four personal cases of osteogenesis imperfecta and dentinogenesis imperfecta, the authors review the semiological elements constituting the syndrome, and assign each case to the Sillence (1979) classification. The author established his classification on clinical criteria and the genetic nature of the various forms of osteogenesis imperfecta, however, the most recent discoveries concerning collagen biochemistry confirm that the condition is without doubt more heterogenous than suggested clinically, thereby better explaining the wide range of mutations encountered.
This paper presents a case of dentinogenesis imperfecta Type I occurring in a patient with familial tarda type osteogenesis imperfecta. The investigation and management of this patient is described.
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Dentinogenesis imperfecta is a hereditary disorder resulting in defective dentin in both the primary and secondary dentitions. The complications of dentinogenesis imperfecta are difficult to manage and provide a challenge to the dentist. This case report concerns treating an African American patient with dentinogenesis imperfecta who appeared for treatment with endodontic pathosis. It illustrates the need for appropriate and timely restorative treatment to prevent pulpal pathosis. Also demonstrated is the difficulty of endodontically treating dentinogenesis imperfecta teeth because of pulpal obliteration and abnormal dentin mineralization. Early and correct diagnosis of dentinogenesis imperfecta is imperative to enable appropriate preventive interventions and optimal dental treatment. Although pulpal pathosis is rarely reported with dentinogenesis imperfecta, endodontic treatment is occasionally necessary and has a guarded prognosis if initiated after pulp canal obliteration has occurred.
Dentinogenesis imperfecta is a localized form of mesodermal dysplasia of the dentin affecting both the primary and permanent dentitions. Most previous reports on dentinogenesis imperfecta describe treatment with overdentures, which have several disadvantages. The present report describes a case of dentinogenesis imperfecta in an 11-year-old girl. A combination of restorative, prosthetic, and surgical treatment was used to resolve the condition.
The rare hereditary disease, dentinogenesis imperfecta, is a disturbance of dentin formation in both the deciduous and permanent dentitions. It may be associated with osteogenesis imperfecta, though it is probably that the two diseases are carried by different genes. This association was recognized in a 19-year-old man. Dentinogenesis imperfecta had been diagnosed at the age of 6 and had been regarded as a mutation; 11 years later, an atypical form of osteogenesis imperfecta developed. The case is atypical because of the apparent absence of dentinogenesis imperfecta in the patient's family. The dental manifestations may have heralded the bone disease.
We present a case of Amelogenesis imperfecta associated with Dentinogenesis imperfecta, affecting the primary dentition which is rehabilitated under general anesthesia. Dentinogenesis imperfecta is a tooth abnormality which presents clinical, radiological and histological characteristics, they should be recognized by the dentist who will determine the treatment depending on age and grade of affection. In the primary dentition we recommend the use of stainless steel crowns do to it's resistance and easy adaptation which will remain in the mouth until it's normal exfoliation.
The inorganic phase in dentin with dentinogenesis imperfecta was investigated, using the correlated techniques of high resolution TEM, X-ray diffraction analyses, infrared absorption spectroscopy, thermogravimetry, and chemical and electron microprobe analyses. It was shown that crystallites in dentin with dentinogenesis imperfecta are of normal size (from 3 to 6 lattice planes thick), but less numerous than in normal dentin. Electron microprobe analyses indicated significant differences in the mineral content of dentin with dentinogenesis imperfecta compared to normal dentin. A higher Ca/P ratio, a loss in Ca and P, and a severe significant loss in Mg, corroborated by chemical analyses, were recorded. The main component of the inorganic phase in dentin with dentinogenesis imperfecta was found to be poorly crystallized carbonated apatite. It is suggested that the water content, greatly increased in dentin with dentinogenesis imperfecta, is at least partly related to lattice water tightly bound to the inorganic phase.