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Disorders of human dentin.
Cells Tissues Organs. 2007; 186(1):70-7.CT

Abstract

Dentin, the most abundant tissue in teeth, is produced by odontoblasts, which differentiate from mesenchymal cells of the dental papilla. Dentinogenesis is a highly controlled process that results in the conversion of unmineralized predentin to mineralized dentin. By weight, 70% of the dentin matrix is mineralized, while the organic phase accounts for 20% and water constitutes the remaining 10%. Type I collagen is the primary component (>85%) of the organic portion of dentin. The non-collagenous part of the organic matrix is composed of various proteins, with dentin phosphoprotein predominating, accounting for about 50% of the non-collagenous part. Dentin defects are broadly classified into two major types: dentinogenesis imperfectas (DIs, types I-III) and dentin dysplasias (DDs, types I and II). To date, mutations in DSPP have been found to underlie the dentin disorders DI types II and III and DD type II. With the elucidation of the underlying genetic mechanisms has come the realization that the clinical characteristics associated with DSPP mutations appear to represent a continuum of phenotypes. Thus, these disorders should likely be called DSPP-associated dentin defects, with DD type II representing the mild end of the phenotypic spectrum and DI type III representing the severe end.

Authors+Show Affiliations

National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. shart@mail.nih.govNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Intramural

Language

eng

PubMed ID

17627120

Citation

Hart, P Suzanne, and Thomas C. Hart. "Disorders of Human Dentin." Cells, Tissues, Organs, vol. 186, no. 1, 2007, pp. 70-7.
Hart PS, Hart TC. Disorders of human dentin. Cells Tissues Organs. 2007;186(1):70-7.
Hart, P. S., & Hart, T. C. (2007). Disorders of human dentin. Cells, Tissues, Organs, 186(1), 70-7.
Hart PS, Hart TC. Disorders of Human Dentin. Cells Tissues Organs. 2007;186(1):70-7. PubMed PMID: 17627120.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Disorders of human dentin. AU - Hart,P Suzanne, AU - Hart,Thomas C, PY - 2007/7/14/pubmed PY - 2007/8/30/medline PY - 2007/7/14/entrez SP - 70 EP - 7 JF - Cells, tissues, organs JO - Cells Tissues Organs VL - 186 IS - 1 N2 - Dentin, the most abundant tissue in teeth, is produced by odontoblasts, which differentiate from mesenchymal cells of the dental papilla. Dentinogenesis is a highly controlled process that results in the conversion of unmineralized predentin to mineralized dentin. By weight, 70% of the dentin matrix is mineralized, while the organic phase accounts for 20% and water constitutes the remaining 10%. Type I collagen is the primary component (>85%) of the organic portion of dentin. The non-collagenous part of the organic matrix is composed of various proteins, with dentin phosphoprotein predominating, accounting for about 50% of the non-collagenous part. Dentin defects are broadly classified into two major types: dentinogenesis imperfectas (DIs, types I-III) and dentin dysplasias (DDs, types I and II). To date, mutations in DSPP have been found to underlie the dentin disorders DI types II and III and DD type II. With the elucidation of the underlying genetic mechanisms has come the realization that the clinical characteristics associated with DSPP mutations appear to represent a continuum of phenotypes. Thus, these disorders should likely be called DSPP-associated dentin defects, with DD type II representing the mild end of the phenotypic spectrum and DI type III representing the severe end. SN - 1422-6421 UR - https://www.unboundmedicine.com/medline/citation/17627120/Disorders_of_human_dentin_ L2 - https://www.karger.com?DOI=10.1159/000102682 DB - PRIME DP - Unbound Medicine ER -