Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/8290
Title: Apoptosis in pulpal tissue of the NOS-3 knockout mouse.
Authors: Krage, T.
LAMBRICHTS, Ivo 
VANDENABEELE, Frank 
Goedecke, A.
Raab, WHM
Issue Date: 2003
Publisher: INT AMER ASSOC DENTAL RESEARCHI A D R/A A D R
Source: JOURNAL OF DENTAL RESEARCH, 82. p. B325-B325
Abstract: It has been observed that in a previous study that there is an increased apoptotic rate in the odontoblast cell layer of the nocioceptive-desensitized capsaicin-treated rat. Objectives: To answer this question we have turned to a new study model, the nitric oxide synthase-3 (NOS-3) knockout mouse, where we have a perfect study model to look at effects of reduction in microcirculation in the nociceptive-intact pulp. The aim of this study was to look at the rate of TUNEL positive cell reactions in the pulpal tissue of the NOS-3 knockout mouse. Methods: To carry this out 5 NOS-3 knockout mice and 5 wild type (WT) mice were intravitally perfused on day 150 with a 4% paraformaldehyde/ 0.2% picric acid solution and jaws were dissected. The animals from both study groups were cryosectioned at 20µm and the In Situ Cell Death Detection POD (Roche) TUNEL reaction was applied to detect DNA strand breakage. Results: While a general observation of TUNEL positive cell reaction was observed in NOS-3 knockout mice and WT mice, a more pronounced reaction was detected in the NOS-3 knockout group. This observation was not, however, more pronounced in the odontoblas layer. Conclusions: We may conclude from our results that the reduction in microcirculation of the NOS-3 knockout has an influence on apostosis in dental pulp tissue. This influence on apoptosis does not, however, extend to the odontoblast layer, as was previously observed in the nociceptive desensitized capsaicin-treated rat.
Notes: Univ Dusseldorf, D-4000 Dusseldorf, Germany. Limburgs Univ Ctr, Diepenbeek, Belgium.
Document URI: http://hdl.handle.net/1942/8290
ISSN: 0022-0345
e-ISSN: 1544-0591
ISI #: 000202893603185
Category: M
Type: Journal Contribution
Appears in Collections:Research publications

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