Postnatal glutamate-induced central nervous system lesions alter periodontal disease susceptibility in adult Wistar rats

Background: Inability to mount a suitable brain-neuroendocrine response to bacterial or other antigenic challenges has been found to play an important role in infectious and inflammatory disease susceptibility and progression , including periodontal disease. Objective: The present study was designed to determine the effects of gluta mate administration to new-born Wistar rats on the development and progress ion 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 X daily subcutaniously with 2 mg/g of monosodium-L-glutamate (MSG) for 5 days from day 3 to 6. Control animals we re injected with similar amounts of saline. Experimental ligature-induced p eriodontal disease was induced in the rats at the age of 12 weeks at maxill ary right 2nd molar teeth. The contralateral maxillary left 2nd molars serv ed 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 si gnificantly more periodontal tissue destruction compared to sham-lesioned c ontrol rats in both the ligated and non-ligated teeth. Conclusions: This study supports our resent findings indicating that inappr opriate bra in-neuroendocrine-immune regulation may play a role in periodon tal disease susceptibility and progression.