Kinane D F, Zhang P, Benakanakere M, Singleton J, Biesbrock A, Nonnenmacher C, He T
Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Department of Periodontics, Endodontics and Dental Hygiene, Center for Oral Health and Systemic Disease, University of Louisville School of Dentistry, Louisville, KY, USA.
J Periodontal Res. 2015 Dec;50(6):864-9. doi: 10.1111/jre.12280. Epub 2015 May 9.
Bacteremia and systemic inflammatory markers are associated with periodontal and systemic diseases and may be linking mechanisms between these conditions. We hypothesized that in the development of gingival inflammation, systemic markers of inflammation and bacteremia would increase.
To study the effect of bacteremia on systemic inflammatory markers, we recruited 80 subjects to participate in an experimental gingivitis study. Subjects were stratified based on gender, smoking and the number of bleeding sites and then randomized to one of two groups: control group (n = 40) or experimental gingivitis group (n = 40). Subjects in the control group conducted an oral hygiene regimen: brushing twice daily with a regular sodium fluoride cavity protection dentifrice and a standard manual toothbrush, flossing twice daily, and mouth rinsing with an anti-cavity fluoride rinse once daily. The experimental group stopped brushing and flossing, and used only the fluoride anti-cavity mouth rinse for 21 d.
Seventy-nine of 80 subjects were evaluable. One subject in the control group was excluded from the results due to antibiotic use during the study. Our data showed the experimental gingivitis group exhibited a significant (p < 0.05) increase in dental plaque level and gingival inflammatory indices relative to baseline and the control group but a decrease in bacteremia and soluble intercellular adhesion molecule-1 levels vs. baseline. Bacteremia was negatively correlated with gingival inflammatory indices and soluble intercellular adhesion molecule-1 levels in the experimental gingivitis group, thus negating our hypothesis.
We conclude that there are marked differences in systemic cytokine levels over the course of short-term experimentally induced gingivitis and further conclude that a long-term periodontitis study must be considered to address mechanisms whereby oral diseases may affect systemic diseases.
菌血症和全身炎症标志物与牙周疾病及全身疾病相关，可能是这些病症之间的联系机制。我们假设在牙龈炎症发展过程中，全身炎症标志物和菌血症会增加。
为研究菌血症对全身炎症标志物的影响，我们招募了80名受试者参与一项实验性牙龈炎研究。受试者根据性别、吸烟情况和出血部位数量进行分层，然后随机分为两组之一：对照组（n = 40）或实验性牙龈炎组（n = 40）。对照组受试者进行口腔卫生护理：每天用含氟防龋牙膏和标准手动牙刷刷牙两次，每天使用牙线两次，每天用含氟防龋漱口水漱口一次。实验组停止刷牙和使用牙线，仅使用含氟防龋漱口水21天。
80名受试者中有79名可进行评估。对照组中有一名受试者因在研究期间使用抗生素而被排除在结果之外。我们的数据显示，与基线和对照组相比，实验性牙龈炎组的牙菌斑水平和牙龈炎症指数显著升高（p < 0.05），但菌血症和可溶性细胞间粘附分子-1水平相对于基线有所下降。在实验性牙龈炎组中，菌血症与牙龈炎症指数和可溶性细胞间粘附分子-1水平呈负相关，从而否定了我们的假设。
我们得出结论，在短期实验性诱导的牙龈炎过程中，全身细胞因子水平存在显著差异，并进一步得出结论，必须考虑进行长期牙周炎研究，以探讨口腔疾病可能影响全身疾病的机制。
