Premium
Les lésions postnatales du système nerveux central dues au glutamate diminuent la susceptibilité aux maladies parodontales
Author(s) -
Breivik Torbjørn,
Thrane Per S.,
Gjermo Per,
Fonnum Frode
Publication year - 2001
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1034/j.1600-051x.2001.028010904.x
Subject(s) - monosodium glutamate , medicine , glutamate receptor , ligature , molar , central nervous system , immune system , disease , periodontal disease , saline , endocrinology , pathology , immunology , dentistry , receptor
Background: Inability to mount a suitable brain‐neuroendocrine response to bacterial or other antigenic challenges has been found to play an important rôle in infectious and inflammatory disease susceptibility and progression, including periodontal disease. Objective: The present study was designed to determine the effects of glutamate administration to new‐born Wistar rats on the development and progression of naturally occurring and ligature‐induced periodontal disease in the rats as adults. Postnatal glutamate administration is known to permanently damage neurones in the hypothalamic arcuate nucleus. Method: New‐born rats were treated 1× daily subcutaniously with 2 mg/g of monosodium‐L‐glutamate (MSG) for 5 days from day 3 to 6. Control animals were injected with similar amounts of saline. Experimental ligature‐induced periodontal disease was induced in the rats at the age of 12 weeks at maxillary right 2nd molar teeth. The contralateral maxillary left 2nd molars served as control teeth, and for assessment of naturally occurring periodontal disease. Disease progression was evaluated histometrically. Results: The results revealed that the glutamate‐lesioned rats developed significantly more periodontal tissue destruction compared to sham‐lesioned control rats in both the ligated and non‐ligated teeth. Conclusions: This study supports our resent findings indicating that inappropriate brain‐neuroendocrine‐immune regulation may play a rôle in periodontal disease susceptibility and progression.