Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY 40536, USA.
Clin Exp Immunol. 2010 Dec;162(3):550-9. doi: 10.1111/j.1365-2249.2010.04202.x.
This study tested the hypothesis that pregnant female baboons exhibit increased levels of various inflammatory mediators in serum resulting from ligature-induced periodontitis, and that these profiles would relate to periodontal disease severity/extent in the animals. The animals were sampled at baseline (B), mid-pregnancy (MP; two quadrants ligated) and at delivery (D; four quadrants ligated). All baboons developed increased plaque, gingival inflammation and bleeding, pocket depths and attachment loss following placement of the ligatures. By MP, both prostaglandin E(2) (PGE(2)) and bactericidal permeability inducing factor (BPI) were greater than baseline, while increased levels of interleukin (IL)-6 occurred in the experimental animals by the time of delivery. IL-8, MCP-1 and LBP all decreased from baseline through the ligation phase of the study. Stratification of the animals by baseline clinical presentation demonstrated that PGE(2), LBP, IL-8 and MCP-1 levels were altered throughout the ligation interval, irrespective of baseline clinical values. IL-6, IL-8 and LBP were significantly lower in the subset of animals that demonstrated the least clinical response to ligation, indicative of progressing periodontal disease. PGE(2), macrophage chemotactic protein (MCP)-1, regulated upon activation, normal T cell expressed and secreted (RANTES) and LBP were decreased in the most diseased subset of animals at delivery. Systemic antibody responses to Fusobacterium nucleatum, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Campylobacter rectus were associated most frequently with variations in inflammatory mediator levels. These results provide a profile of systemic inflammatory mediators during ligature-induced periodontitis in pregnant baboons. The relationship of the oral clinical parameters to systemic inflammatory responses is consistent with a contribution to adverse pregnancy outcomes in a subset of the animals.
结扎诱导的牙周炎会使孕期雌性狒狒血清中各种炎症介质水平升高,且这些变化与动物牙周病的严重程度/范围有关。在基线(B)、妊娠中期(MP;结扎两个象限)和分娩时(D;结扎四个象限)对动物进行采样。所有狒狒在结扎放置后,菌斑、牙龈炎症和出血、牙周袋深度和附着丧失均增加。到 MP 时,前列腺素 E2(PGE2)和杀菌通透性增强因子(BPI)均高于基线,而实验组动物在分娩时 IL-6 水平升高。IL-8、MCP-1 和 LBP 均从基线降至结扎研究阶段。根据基线临床表现对动物进行分层,结果表明 PGE2、LBP、IL-8 和 MCP-1 水平在整个结扎间隔内发生变化,而与基线临床值无关。IL-6、IL-8 和 LBP 在结扎反应最小的动物亚组中显著降低,表明牙周病进展。分娩时,PGE2、巨噬细胞趋化蛋白 1(MCP-1)、活化正常 T 细胞表达和分泌因子(RANTES)和 LBP 在疾病最严重的动物亚组中降低。针对福赛斯坦纳菌、牙龈卟啉单胞菌、伴放线放线杆菌和直肠弯曲杆菌的系统抗体反应与炎症介质水平的变化最相关。这些结果提供了孕期狒狒结扎诱导牙周炎期间系统炎症介质的特征。口腔临床参数与全身炎症反应的关系与动物亚组不良妊娠结局的发生有关。