Loss of cognitive function in the aging population, particular those with Alzheimer disease, presents unique challenges to health practitioners. For the dental practitioner these include management of periodontal diseases, caries, and other dental conditions in this special population. It is well established in the cognitively impaired patient that a lack of adherence to dental hygiene routines and professional care leads to increases in the prevalence and severity of these dental conditions, leading to increased loss of teeth. More recent evidence has indicated a possible role of the microbiota of dental plaque associated with periodontal diseases in the development and progression of Alzheimer disease, thereby supporting a two-way interaction of these two diseases. New therapies are needed to address the potential upstream events that may precede overt signs of Alzheimer disease. One of these approaches would be to target these various bacterial, viral, and other microbial pathogens associated with periodontal disease that can translocate into the bloodstream and then to distal sites, such as the brain. Such microbial translocation would lead to local inflammation and buildup of the hallmark signs of Alzheimer disease, including amyloid beta deposits, tau fragmentation and tangles, breakdown of host protective molecules, such as the apolipoproteins, and neuron toxicity. In this review, evidence for the biological basis of the role of the periodontal disease microflora on the initiation and progression of Alzheimer disease will be presented with a focus on the potential role of the keystone pathogen Porphyromonas gingivalis with its family of gingipain enzymes. The various mechanisms for which P. gingivalis gingipains may contribute to the initiation and progression of Alzheimer disease are presented. Small-molecule inhibitors of these gingipains and their effects on reducing biological markers of Alzheimer disease may have beneficial effects for the initiation and progression of loss of cognitive function in Alzheimer disease. In addition to these targeted therapies for specific periodontal pathogens, considerations for the dental practitioner in applying more general approaches to reducing the periodontal plaque microflora in the management of the cognitively impaired patient are discussed for this special population.

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阿尔茨海默病和牙周病患者：新见解、联系和治疗

老龄化人口的认知功能丧失，尤其是那些患有阿尔茨海默病的人，给健康从业者带来了独特的挑战。对于牙科医生来说，这些包括治疗这个特殊人群的牙周病、龋齿和其他牙科疾病。在认知障碍患者中，不遵守牙齿卫生常规和专业护理会导致这些牙齿状况的患病率和严重程度增加，从而导致牙齿脱落增加，这一点已得到充分证实。最近的证据表明，与牙周病相关的牙菌斑微生物群可能在阿尔茨海默病的发展和进展中发挥作用，从而支持这两种疾病的双向相互作用。需要新的疗法来解决可能出现阿尔茨海默病明显迹象之前的潜在上游事件。其中一种方法是针对与牙周病相关的各种细菌、病毒和其他微生物病原体，这些病原体可以转移到血液中，然后转移到远端部位，例如大脑。这种微生物易位会导致局部炎症和阿尔茨海默病标志性迹象的积累，包括淀粉样蛋白 β 沉积、tau 碎片和缠结、宿主保护性分子（如载脂蛋白）的分解和神经元毒性。在这篇综述中，牙周病微生物群在阿尔茨海默病的发生和发展中的作用的生物学基础的证据将被提出，重点是关键病原体的潜在作用牙龈卟啉单胞菌及其牙龈蛋白酶家族。介绍了P. gingivalis gingipains 可能导致阿尔茨海默病的发生和进展的各种机制。这些牙龈蛋白酶的小分子抑制剂及其对减少阿尔茨海默病生物标志物的作用可能对阿尔茨海默病认知功能丧失的开始和进展具有有益作用。除了针对特定牙周病原体的这些靶向治疗外，还针对这一特殊人群讨论了牙科医生在治疗认知障碍患者时采用更通用的方法来减少牙周菌斑菌群的注意事项。