Department of Pharmacology, ICB, USP, São Paulo, SP, Brazil.
Arch Oral Biol. 2011 Jan;56(1):41-7. doi: 10.1016/j.archoralbio.2010.08.011. Epub 2010 Sep 22.
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.
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.
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.
in addition to mediating alveolar bone loss, NO contributes to systemic effects of periodontitis in the heart and kidney.
本研究旨在评估结扎诱导的牙周炎对正常血压和一氧化氮（NO）缺乏（L-NAME 处理）高血压大鼠的肾脏和心脏的影响。
在诱导牙周炎前两周开始进行口腔 L-NAME（或水）处理。结扎放置后 3、7 或 14 天处死大鼠，并通过放射照相评估牙槽骨丧失。在心脏和肾脏中测定硫代巴比妥酸反应性物质（TBARS；脂质过氧化指标）、蛋白硝基酪氨酸（NT；蛋白硝化的标志物）和髓过氧化物酶活性（MPO；中性粒细胞标志物）。
在 NO 缺乏的高血压大鼠中，牙周炎诱导的牙槽骨丧失明显减少。此外，L-NAME 处理完全阻止了牙周炎诱导的心脏 NT 升高。另一方面，L-NAME 处理增强了牙周炎大鼠心脏和肾脏中 MPO 的产生。牙周炎未引起心脏或肾脏 TBARS 含量的变化。
除了介导牙槽骨丧失外，NO 还会导致牙周炎对心脏和肾脏的全身影响。
