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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/2498

Title: Odontoblast microstructure and possible compensation in the NOS-3 knockout mouse
Authors: Krage, T
Raab, WHM
Issue Date: 2002
Citation: JOURNAL OF DENTAL RESEARCH, 81. p. A61-A61
Abstract: The nitric oxide synthase-3 knockout mouse has been used as a study model to look at the effect of reduction in microcirculation on dentin development. It has been reported in the past that the dentin tubuli found at the predentin-dentin interface are approximately 2-fold larger in diameter as those observed in the wild type mouse. The aim of this study was to investigate the microstructure of the odontoblast cell bodies and their cell processes in order to gain a better understanding of the physiological and structural effects of the genetic elimination of the 3rd isoform of nitric oxide synthase. Methods: 5 NOS-3 Knockout mice and 5 WT mice were euthanized at 150 days, fixated in a (2%) gluteraldehyde solution and prepared for transmission electron microscopy(TEM). Results: A higher density of mitochondria was noted in the odontoblast cell bodies, as well as the odontoblast processes, in the NOS-3 knockout mouse when compared to that of the WT mouse. While it is known that NO has an inhibitory effect on cell respiration, it has also been reported that mitochondria have the ability to produce their own form of nitric oxide (mitNOS). Thus, the genetic elimination of endothelial nitric oxide synthase may be producing a form of "feedback" mechanism in the odontoblast cellular structure, in which the mitochondria are not inhibited by normal systemic endothelial nitric oxide. Thus, this lack of systemic inhibition may be causing the odontoblast to produce a physiological compensation by increasing the number of their mitochondria which can then produce their own NOS. Conclusions: We may conclude from our results that the higher mitochondrial density seen in the odontoblast of the NOS-3 knockout mouse may be a form of physiological compensation in these animals.
Notes: Univ Dusseldorf, D-4000 Dusseldorf, Germany. Limburgs Univ Centrum, Diepenbeek, Belgium.
URI: http://hdl.handle.net/1942/2498
ISI #: 000176024700272
ISSN: 0022-0345
Category: M
Type: Journal Contribution
Appears in Collections: Research publications

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