This paper reviews a current view regarding the association between periodontitis and atherosclerotic cardiovascular diseases (ACVD). Many evidences have suggested that there exist biological mechanisms by which periodontitis can lead to ACVD. Periodontal infection can lead to direct bacterial invasion into endothelial tissues through the blood stream, then the bacteria can activate the host inflammatory response followed by atheroma formation, maturation and exacerbation. Also, chronic periodontal infections may indirectly induce endothelial activation or dysfunction through a state of systemic inflammation as evidenced by elevated plasma acute proteins, IL-6 and fibrinogen as well. There is moderate evidence that periodontal treatment can reduce systemic inflammation and improvement of both clinical surrogate markers. But there is no periodontal intervention study available on primary ACVD prevention. There is consistent and strong epidemiologic evidence, including in vitro, animal and clinical studies, that periodontitis imparts increased risk for future ACVD. However, evidences from intervention trials to date are not sufficient to confirm the multi directional causality of periodontitis in ACVD etiology. Well-designed intervention trials on the impact of periodontal treatment on the prevention of ACVD outcomes are needed.