Chronic inflammatory disease of the supporting tissues of the teeth, periodontitis, is primarily caused by periodontal pathogenic bacteria found in the dysbiotic subgingival biofilm. One of these specific bacteria is Porphyromonas gingivalis, a gram-negative anaerobic bacterium, which is also a key periodontal pathogen. P.gingivalis and its virulence factors, such as fimbriae, gingipain and lipopolysaccharide (LPS) are closely related to the onset of the disease. The clinical presentation of periodontitis is characterized by the presence of gingival erythema, edema, periodontal pockets and the destruction of supporting tissues, manifested by their visible loss. Periodontal pathogenic microorganisms and their products can enter the circulation, which leads to transient bacteremia and systemic dissemination of bacterial products. Moreover, periodontitis can induce systemic effects by promoting the expression of inflammatory mediators such as proinflammatory cytokines. It is through this mechanism that today periodontitis is associated with systemic diseases. Alzheimer's disease (AD), known as a progressive neurodegenerative disease, is recognized as a leading cause of cognitive and behavioral impairment. New findings suggest that peripheral infections can activate microglial cells within the central nervous system that promote the development of neurodegeneration in AD. The mechanism by which peripheral proinflammatory molecules can increase the amount of inflammatory molecules in the brain involves at least two pathways, systemic circulation and/or neural pathways. It was suggested that the amount of inflammatory molecules in the brain could be increased by periodontitis, which itself is characterized by an increased level of inflammation, and this would consequently affect the development of AD. The aim of this review is to provide a literature review of the mechanisms of the connection between periodontitis and the periodontopathogen P. gingivalis, and Alzheimer's disease.