Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/2496
Title: Apoptosis in nociceptive desensitized animals after application of capsaicin
Authors: Krage, T
VANDENABEELE, Frank 
LAMBRICHTS, Ivo 
Raab, WHM
Issue Date: 2002
Publisher: INT AMER ASSOC DENTAL RESEARCHI
Source: JOURNAL OF DENTAL RESEARCH, 81. p. A62-A62
Abstract: Objectives: Capsaicin, the pungent ingredient in chili peppers, has the ability systemically to selectively desensitize nociceptive fibers. Furthermore, it is known that the dentinal development in these nociceptive desensitized animals is drastically altered. The aim of this study was to better understand the physiological effects of the neonatal systemic application of capsaicin by investigating the apoptosis, or programmed cell death, in their pulpal tissue. Methods: 20 rats were given a dose of 40mg/kg body weight capsaicin on the first post-natal day. A 50% death rate was observed immediately after capsaicin application. An equal sum of untreated rats served as the control group. All animals were intravitally perfused with a 4% paraformaldehyde and 0.2% picric acid solution at 150 days of age and jaws were dissected. The molars of 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 apoptosis was observed in both groups, the capsaicin-treated group showed higher numbers of TUNEL-positive cells in the odonblast layer. This finding is a possible explanation for defects seen in dentinal development of capsaicin-treated animals. Conclusion: We may conclude that the systemic neonatal application with capsaicin is in relation with an increase in apoptosis of odontoblasts, thus possibly causing an alteration in the dentin production in these nociceptive desensitized animals.
Notes: Univ Dusseldorf, D-4000 Dusseldorf, Germany. Limburgs Univ Centrum, Diepenbeek, Belgium.
Document URI: http://hdl.handle.net/1942/2496
ISSN: 0022-0345
e-ISSN: 1544-0591
ISI #: 000176024700286
Category: M
Type: Journal Contribution
Appears in Collections:Research publications

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