“…In addition to bacterial components (e.g., lipopolysaccharide or LPS), periodontal disease allows locally‐produced proinflammatory mediators (e.g., interleukin‐(IL‐1) 1β, tumor necrosis factor‐α (TNF‐α), IL‐6, and prostaglandin E2 (PGE2)) to pour into the bloodstream, initiating responses in more distant tissues (Gemmell, Marshall, & Seymour, ; Loos, ; Loos, Craandijk, Hoek, Wertheim‐van Dillen, & van der Velden, ; Moutsopoulos & Madianos, ). The dissemination of bacteria and their biproducts into the bloodstream have the added effect of inducing system‐level infection responses that may instigate or affect the progression of cardiovascular diseases (for reviews of the evidence, see Dietrich, Sharma, Walter, Weston, & Beck, ; Dietrich et al, ), chronic obstructive pulmonary disease (Liu et al, ; Wang et al, ; Zeng et al, ), pneumonia (Awano et al, ; El Attar, Zaghloul, & El Menoufy, ; Scannapieco & Mylotte, ; Sharma & Shamsuddin, ; Terpenning et al, ), and diabetes (Bissett, Stone, Rapley, & Preshaw, ; Borgnakke, Ylöstalo, Taylor, & Genco, ; Lalla et al, ; Nelson et al, ; Taylor, Burt, Becker, Genco, & Shlossman, ). For example, platelet aggregation can be induced by oral bacteria such as P. gingivalis and S. sanguis or by the proinflammatory immune cytokines generated in response to them, affecting the formation of thrombi in the arteries and veins (Herzberg & Meyer, ).…”