Department of Periodontology, School of Dental Medicine, University of Muenster, Germany.
Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and Vrije Universiteit Amsterdam, The Netherlands.
J Alzheimers Dis. 2018;66(1):105-114. doi: 10.3233/JAD-180620.
Recent studies suggest a link between periodontitis and Alzheimer's disease (AD).
Verification of the presence of periodontal pathogens and the intrathecal generation of pathogen-specific antibodies in 20 patients with AD and 20 with other forms of dementia (DEM-noAD).
Clinical periodontal indices were recorded. Cerebrospinal fluid (CSF) was analyzed for total tau protein (T-tau) and amyloid-β (Aβ1-42). In serum and CSF, antibody levels against Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Treponema species were quantified. The presence of selected bacteria and inflammatory biomarkers were determined in periodontium, serum, and CSF.
In line with diagnoses, CSF-levels of Aβ1-42 were significantly lower in AD than DEM-noAD patients. Periodontal destruction and inflammation were omnipresent with no difference between groups. P. gingivalis, T. forsythia, and Treponema species were detected in more than 50% of subgingival biofilm samples, but neither in serum nor in the CSF. Elevated levels of anti-pathogen antibodies in CSF of 16 patients (7 AD; 9 DEM-noAD) compared to serum highlight a possibility of the intrathecal immune response to pathogens. There was no significant difference in antibodies levels against selected bacteria in CSF and serum between groups. Multivariate regression analysis and general linear models revealed an association of the T-tau level in AD group with both serum levels of anti-P. gingivalis antibodies and MCP-1/CCL-2.
Periodontal pathogens may enter the brain and stimulate a local immune response. However, in patients with dementia at the age up to 70 years, periodontal pathogens do not act as a trigger for developing AD.
最近的研究表明牙周炎与阿尔茨海默病（AD）之间存在关联。
验证 20 例 AD 患者和 20 例其他类型痴呆（非 AD 痴呆）患者的牙周病原体和鞘内产生病原体特异性抗体的情况。
记录临床牙周指数。分析脑脊液（CSF）中的总 tau 蛋白（T-tau）和淀粉样蛋白-β（Aβ1-42）。在血清和 CSF 中定量检测对牙龈卟啉单胞菌、伴放线放线杆菌和密螺旋体的抗体水平。在牙周组织、血清和 CSF 中检测选定细菌和炎症生物标志物的存在。
与诊断相符，AD 患者 CSF 中的 Aβ1-42 水平明显低于非 AD 痴呆患者。牙周破坏和炎症普遍存在，两组之间无差异。龈下生物膜样本中超过 50%检测到牙龈卟啉单胞菌、福赛斯坦纳密螺旋体和密螺旋体，但在血清和 CSF 中均未检测到。与血清相比，16 名患者（7 名 AD；9 名非 AD 痴呆）的 CSF 中抗病原体抗体水平升高，这提示了针对病原体的鞘内免疫反应的可能性。CSF 和血清中针对选定细菌的抗体水平在两组之间无显著差异。多变量回归分析和一般线性模型显示，AD 组的 T-tau 水平与血清中抗牙龈卟啉单胞菌抗体和 MCP-1/CCL-2 水平相关。
牙周病原体可能进入大脑并刺激局部免疫反应。然而，在 70 岁以下的痴呆患者中，牙周病原体不会作为引发 AD 的诱因。
