A body of scientific evidence supports the view that periodontal disease and Alzheimer’s disease (AD) are comorbid. While periodontal disease affects tooth-supporting tissues and the host’s immune responses, leading to eventual tooth loss, AD is characterized by 2 histologic diagnostic markers at autopsy: the extraneuronal amyloid plaques and the intraneuronal neurofibrillary tangles (Hyman et al. 2012). Other lesions without a role in the neuropathologic diagnosis of AD include neuronal and synaptic loss, neuroinflammation, and cerebral amyloid angiopathy (Dugger and Dickson 2017), which are of importance in understanding the disease process. Understanding the relationship between AD and periodontitis is hindered by the long-standing dogma that those with dementia or AD-associated dementia are at greater incidence of longitudinally manifesting periodontal disease than those without it. This view clearly assumes that AD-associated dementia is a risk factor for periodontal disease. The assumption would be that the behavioral changes associated with the onset of dementia, namely poorer levels of oral hygiene, are the predominant cause rendering an individual with AD more susceptible to periodontal disease. This currently held dogmatic view is behind the proposal of a bidirectional relationship between AD and periodontitis! Given that a growing body of literature (Stein et al. 2007; Sparks Stein et al. 2012; Farhad et al. 2014; Demmer et al. 2020; Nadim et al. 2020) suggests that periodontal disease can precede AD-associated dementia manifestation, the suggestion is that a converse relationship also exists. This was something that Ma et al. (2021) also identified in their cases over the course of their study, but they correctly rejected these cases due to the possibility of confounding factor interferences. To this end, Ma et al. assessed the effect of AD without diverse pathologies that may act as confounding factors on conditions that develop because of the human aging process.

中文翻译：

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牙周炎和痴呆：双向关系？

大量科学证据支持牙周病和阿尔茨海默病 (AD) 共病的观点。虽然牙周病影响牙齿支持组织和宿主的免疫反应，最终导致牙齿脱落，但 AD 的特征在于尸检时的 2 个组织学诊断标志物：神经元外淀粉样蛋白斑块和神经元内神经原纤维缠结 (Hyman et al. 2012)。在 AD 的神经病理学诊断中没有作用的其他病变包括神经元和突触丢失、神经炎症和脑淀粉样血管病（Dugger 和 Dickson 2017），这些对于了解疾病过程很重要。长期存在的教条阻碍了对 AD 与牙周炎之间关系的理解，即患有痴呆症或 AD 相关性痴呆症的人比没有患痴呆症的人纵向表现出牙周病的发病率更高。这种观点清楚地假设 AD 相关性痴呆是牙周病的危险因素。假设是与痴呆症发作相关的行为变化，即较差的口腔卫生水平，是导致 AD 个体更容易患牙周病的主要原因。这种目前持有的教条主义观点是AD和牙周炎之间双向关系的提议背后的原因！鉴于越来越多的文献（Stein 等人，2007；Sparks Stein 等人，2012；Farhad 等人，2014；Demmer 等人，2020；Nadim 等人。2020) 表明牙周病可能先于 AD 相关的痴呆表现，这表明也存在相反的关系。这是马等人的事情。（2021）也在他们的研究过程中发现了他们的案例，但由于混杂因素干扰的可能性，他们正确地拒绝了这些案例。为此，马等人。评估了 AD 的影响，而没有可能作为混杂因素影响因人类衰老过程而发展的各种病理。为此，马等人。评估了 AD 的影响，而没有可能作为混杂因素影响因人类衰老过程而发展的各种病理。为此，马等人。评估了 AD 的影响，而没有可能作为混杂因素影响因人类衰老过程而发展的各种病理。