Clinical and Bacterial Markers of Periodontitis and Their Association with Incident All-Cause and Alzheimer's Disease Dementia in a Large National Survey
Clinical and Bacterial Markers of Periodontitis and Their Association with Incident All-Cause and Alzheimer's Disease Dementia in a Large National Survey
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DOI：
10.3233/jad-200064
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发表时间：
2020-01-01
影响因子：
4
通讯作者：
Zonderman, Alan B.
中科院分区：
文献类型：
--
作者：
Beydoun, May A.;Beydoun, Hind A.;Zonderman, Alan B.
包括牙周病原体在内的微生物制剂最近已成为阿尔茨海默病（AD）病理学的重要参与者。我们研究了临床牙周和细菌参数与美国中年和老年人的全因痴呆和AD痴呆以及AD死亡率的关系。临床[附件丢失（AL）;使用第三次全国健康和营养调查的数据，研究了牙周标志物[牙周袋深度（PPD）]和细菌[病原体免疫球蛋白G（IgG）]与AD和全因痴呆发病率以及AD死亡率的关系（NHANES III，1988-1994）与截至2014年1月1日的国家死亡指数和医疗保险数据纵向关联，随访时间长达26年。进行了性别和年龄特异性多变量校正的考克斯比例风险模型。在>= 65岁的人群中，AD发病率和死亡率与PPD、两个因素和一个簇一致相关，该簇由抗牙龈卟啉单胞菌（P. gingivalis）、产黑色素普雷沃菌（P melaninogenica）和直弯曲杆菌（C.直肌）等。具体而言，AD发病率与C.直肌和牙龈卟啉单胞菌滴度（根据SD，aHR =1.22; 95% CI，1.04-1.43，p= 0.012），而AD死亡风险随着另一复合物（根据SD，aHR =1.46; 95% CI，1.09-1.96，p =0.017）的增加而增加，该复合物高度负载牙龈卟啉单胞菌、中间普雷沃菌、变黑普雷沃菌、具核梭杆菌、梭形芽孢杆菌。直肌链球菌、嗜二氧化碳菌、产黑色素嗜菌。这项研究为牙周病原体与AD之间的关联提供了证据，老年人的相关性更强。牙周病原体治疗对减少神经变性后遗症的有效性应在随机对照试验中进行测试。
Microbial agents including periodontal pathogens have recently appeared as important actors in Alzheimer's disease (AD) pathology. We examined associations of clinical periodontal and bacterial parameters with incident all-cause and AD dementia as well as AD mortality among US middle-aged and older adults. Clinical [Attachment Loss (AL); probing pocket depth (PPD)] and bacterial [pathogen immunoglobulin G (IgG)] periodontal markers were investigated in relation to AD and all-cause dementia incidence and to AD mortality, using data from the third National Health and Nutrition Examination Surveys (NHANES III, 1988-1994) linked longitudinally with National Death Index and Medicare data through January 1, 2014, with up to 26 years of follow-up. Sex- and age-specific multivariable-adjusted Cox proportional hazards models were conducted. Among those >= 65 years, AD incidence and mortality were consistently associated with PPD, two factors and one cluster comprised of IgG titers against Porphyromonas gingivalis (P. gingivalis), Prevotella melaninogenica (P melaninogenica) and Campylobacter rectus (C. rectus) among others. Specifically, AD incidence was linked to a composite of C. rectus and P gingivalis titers (per SD, aHR =1.22; 95% CI, 1.04-1.43, p= 0.012), while AD mortality risk was increased with another composite (per SD, aHR =1.46; 95% CI, 1.09-1.96, p =0.017) loading highly on IgG for P gingivalis, Prevotella intermedia, Prevotella nigrescens, Fusobacterium nucleatum, C. rectus, Streptococcus intennedius, Capnocylophaga Ochracea, and P melaninogenica. This study provides evidence for an association between periodontal pathogens and AD, which was stronger for older adults. Effectiveness of periodontal pathogen treatment on reducing sequelae of neurodegeneration should be tested in randomized controlled trials.