Department of Periodontology, Faculty of Odontology, Rio de Janeiro State University, Rio de Janeiro, CEP: 20551-030, Brazil.
Exp Biol Med (Maywood). 2013 Jun;238(6):713-22. doi: 10.1177/1535370213480690.
Several studies have suggested an increase of cardiovascular disease (CVD) risk on periodontitis patients. An enhancement has been demonstrated on both platelet activation and oxidative stress on periodontitis patients, which may contribute for this association. Therefore, the aim of this study was to evaluate the effects of non-surgical periodontal treatment on the l-arginine-nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway and oxidative status in platelets. A total of eight periodontitis patients and eight controls were included in this study. Clinical, laboratory and experimental evaluations were performed on baseline and 90 days after periodontal treatment (except for western blot analysis). The clinical periodontal evaluation included measurements of probing pocket depth (PPD), clinical attachment loss (CAL), % of sites with plaque and % of sites with bleeding on probing. We evaluated: l-[(3)H]arginine influx; nitric oxide synthase (NOS) and arginase enzymes activity and expression; expression of guanylate cyclase and phosphodiesterase-5 enzymes; cGMP levels; platelet aggregation; oxidative status through superoxide dismutase (SOD) and catalase activities, and measurement of reactive oxygen species (ROS) levels and C-reactive protein (CRP) levels. The initial results showed an activation of both l-arginine influx and via system y (+ )L associated with reduced intraplatelet cGMP levels in periodontitis patients and increased systemic levels of CRP. After periodontal treatment, there was a significant reduction of the % of sites with PPD 4-5mm, % of sites with CAL 4-5 mm, and an enhancement in cGMP levels and SOD activity. Moreover, CRP levels were reduced after treatment. Therefore, alterations in the intraplatelet l-arginine-NO-cGMP pathway and oxidant-antioxidant balance associated with a systemic inflammatory response may lead to platelet dysfunction, which may contribute to a higher risk of CVD in periodontitis.
几项研究表明，牙周炎患者的心血管疾病（CVD）风险增加。牙周炎患者的血小板活化和氧化应激增强，这可能是导致这种关联的原因。因此，本研究旨在评估非手术牙周治疗对血小板中 l-精氨酸-一氧化氮（NO）-环鸟苷单磷酸（cGMP）途径和氧化状态的影响。本研究共纳入 8 例牙周炎患者和 8 例对照者。在牙周治疗前（除了 Western blot 分析外）和 90 天后进行临床、实验室和实验评估。临床牙周评估包括测量探诊深度（PPD）、临床附着丧失（CAL）、菌斑百分比和探诊出血百分比。我们评估了：l-[(3)H]精氨酸内流；一氧化氮合酶（NOS）和精氨酸酶的活性和表达；鸟苷酸环化酶和磷酸二酯酶-5 酶的表达；cGMP 水平；血小板聚集；通过超氧化物歧化酶（SOD）和过氧化氢酶活性评估氧化状态，以及测量活性氧（ROS）水平和 C 反应蛋白（CRP）水平。初步结果显示，牙周炎患者的 l-精氨酸内流和系统 y (+ )L 均被激活，导致血小板内 cGMP 水平降低，系统性 CRP 水平升高。牙周治疗后，PPD 为 4-5mm 的位点百分比、CAL 为 4-5mm 的位点百分比显著降低，cGMP 水平和 SOD 活性增强。此外，治疗后 CRP 水平降低。因此，血小板内 l-精氨酸-NO-cGMP 途径和氧化还原平衡的改变与系统性炎症反应相关，可能导致血小板功能障碍，从而增加牙周炎患者 CVD 的风险。
