Archives of oral biology · 2010
Local and cardiorenal effects of periodontitis in nitric oxide-deficient hypertensive rats.
Сравнительное исследованиеСтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Herrera Bruno S, Martins-Porto Rodrigo, Campi Paula, Holzhausen Marinella, Teixeira Simone A, Mendes Gustavo D, Costa Soraia K P, Gyurko Robert, Van Dyke Thomas E, Spolidório Luis C, Muscará Marcelo N
Аннотация
OBJECTIVE: in this study we have assessed the renal and cardiac consequences of ligature-induced periodontitis in both normotensive and nitric oxide (NO)-deficient (L-NAME-treated) hypertensive rats.
MATERIALS AND METHODS: oral L-NAME (or water) treatment was started two weeks prior to induction of periodontitis. Rats were sacrificed 3, 7 or 14 days after ligature placement, and alveolar bone loss was evaluated radiographically. Thiobarbituric reactive species (TBARS; a lipid peroxidation index), protein nitrotyrosine (NT; a marker of protein nitration) and myeloperoxidase activity (MPO; a neutrophil marker) were determined in the heart and kidney.
RESULTS: in NO-deficient hypertensive rats, periodontitis-induced alveolar bone loss was significantly diminished. In addition, periodontitis-induced cardiac NT elevation was completely prevented by L-NAME treatment. On the other hand L-NAME treatment enhanced MPO production in both heart and kidneys of rats with periodontitis. No changes due to periodontitis were observed in cardiac or renal TBARS content.
CONCLUSIONS: in addition to mediating alveolar bone loss, NO contributes to systemic effects of periodontitis in the heart and kidney.
MATERIALS AND METHODS: oral L-NAME (or water) treatment was started two weeks prior to induction of periodontitis. Rats were sacrificed 3, 7 or 14 days after ligature placement, and alveolar bone loss was evaluated radiographically. Thiobarbituric reactive species (TBARS; a lipid peroxidation index), protein nitrotyrosine (NT; a marker of protein nitration) and myeloperoxidase activity (MPO; a neutrophil marker) were determined in the heart and kidney.
RESULTS: in NO-deficient hypertensive rats, periodontitis-induced alveolar bone loss was significantly diminished. In addition, periodontitis-induced cardiac NT elevation was completely prevented by L-NAME treatment. On the other hand L-NAME treatment enhanced MPO production in both heart and kidneys of rats with periodontitis. No changes due to periodontitis were observed in cardiac or renal TBARS content.
CONCLUSIONS: in addition to mediating alveolar bone loss, NO contributes to systemic effects of periodontitis in the heart and kidney.