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Odontoblast dysfunction in osteogenesis imperfecta: an LM, SEM, and ultrastructural study.
Connect Tissue Res. 2002; 43(2-3):401-5.CT

Abstract

The inherited dentin defect dentinogenesis imperfecta (DI), while clinically obvious in osteogenesis imperfecta (OI) Types IB and IC, II, III, and IVB, is now thought to be present in all children with OI, in a continuum from minimal to severe dentin pathology. This collaborative study further clarifies the structural and ultrastructural dentin changes in the teeth of OI children with clinically obvious DI, and attempts to explain these in terms of odontoblast dysfunction. Collaborative studies were carried out in Melbourne, Australia, and Strasbourg, France, using light and polarized-light microscopy, scanning and transmission electron microscopy (SEM, TEM), selected-area diffraction (SAD), and x-ray spectroscopy (EDX). These showed structurally normal enamel (but containing long and broad lamellae) and a normally scalloped dentino-enamel junction (DEJ), but severe pathologic changes in the dentin. An initial narrow band of normal-appearing dentin tubules (including the mantle layer) ceased abruptly and was replaced by a wavelike laminar zone parallel to the DEJ with occluded tubules. Multiple parallel channels of 5-10 microns diameter were present at right angles to the DEJ indenting this zone, some terminating in retro-curved "processes." The abnormal dentin containing these channels almost completely occluded the pulp chamber. The structural and ultrastructural changes seen can be explained on the basis of the collagen defect in OI resulting in odontoblast dysfunction, which produces a distinct phenotype and one that is different from that in bone.

Authors+Show Affiliations

University of Melbourne, Royal Children's Hospital, Melbourne, Australia. rkingsh@ozemail.com.auNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12489189

Citation

Hall, R K., et al. "Odontoblast Dysfunction in Osteogenesis Imperfecta: an LM, SEM, and Ultrastructural Study." Connective Tissue Research, vol. 43, no. 2-3, 2002, pp. 401-5.
Hall RK, Manière MC, Palamara J, et al. Odontoblast dysfunction in osteogenesis imperfecta: an LM, SEM, and ultrastructural study. Connect Tissue Res. 2002;43(2-3):401-5.
Hall, R. K., Manière, M. C., Palamara, J., & Hemmerlé, J. (2002). Odontoblast dysfunction in osteogenesis imperfecta: an LM, SEM, and ultrastructural study. Connective Tissue Research, 43(2-3), 401-5.
Hall RK, et al. Odontoblast Dysfunction in Osteogenesis Imperfecta: an LM, SEM, and Ultrastructural Study. Connect Tissue Res. 2002;43(2-3):401-5. PubMed PMID: 12489189.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Odontoblast dysfunction in osteogenesis imperfecta: an LM, SEM, and ultrastructural study. AU - Hall,R K, AU - Manière,M C, AU - Palamara,J, AU - Hemmerlé,J, PY - 2002/12/20/pubmed PY - 2003/4/2/medline PY - 2002/12/20/entrez SP - 401 EP - 5 JF - Connective tissue research JO - Connect Tissue Res VL - 43 IS - 2-3 N2 - The inherited dentin defect dentinogenesis imperfecta (DI), while clinically obvious in osteogenesis imperfecta (OI) Types IB and IC, II, III, and IVB, is now thought to be present in all children with OI, in a continuum from minimal to severe dentin pathology. This collaborative study further clarifies the structural and ultrastructural dentin changes in the teeth of OI children with clinically obvious DI, and attempts to explain these in terms of odontoblast dysfunction. Collaborative studies were carried out in Melbourne, Australia, and Strasbourg, France, using light and polarized-light microscopy, scanning and transmission electron microscopy (SEM, TEM), selected-area diffraction (SAD), and x-ray spectroscopy (EDX). These showed structurally normal enamel (but containing long and broad lamellae) and a normally scalloped dentino-enamel junction (DEJ), but severe pathologic changes in the dentin. An initial narrow band of normal-appearing dentin tubules (including the mantle layer) ceased abruptly and was replaced by a wavelike laminar zone parallel to the DEJ with occluded tubules. Multiple parallel channels of 5-10 microns diameter were present at right angles to the DEJ indenting this zone, some terminating in retro-curved "processes." The abnormal dentin containing these channels almost completely occluded the pulp chamber. The structural and ultrastructural changes seen can be explained on the basis of the collagen defect in OI resulting in odontoblast dysfunction, which produces a distinct phenotype and one that is different from that in bone. SN - 0300-8207 UR - https://www.unboundmedicine.com/medline/citation/12489189/Odontoblast_dysfunction_in_osteogenesis_imperfecta:_an_LM_SEM_and_ultrastructural_study_ L2 - https://www.tandfonline.com/doi/full/10.1080/03008200290001005 DB - PRIME DP - Unbound Medicine ER -