**1. Introduction**

Periodontitis is a noncommunicable infectious disease associated with an important inflammatory component affecting around 50% of the population worldwide and with a prevalence of its severe forms of 11.2% [1]. The Global Burden of Diseases, Injuries, and Risk Factors Study (2017) reported periodontitis as the sixth most prevalent chronic human disease [2].

Periodontitis is characterized by loss of connective tissue attachment that is normally located at the tooth neck (cementoenamel junction) as well as by alveolar bone destruction. Periodontitis is accompanied by the transformation of the shallow gingival sulcus into a deep periodontal pocket and a marked apical diffusion of the dysbiotic subgingival biofilm [3]. In generalized severe periodontitis, the surface area of the epithelial lining of the periodontal pockets is enormous and could favor the direct contact of subgingival bacteria with gingival connective tissue through focal ulcerated areas. Moreover, epithelial ulcerations constitute biological entries for the systemic dissemination of subgingival Gram-negative bacteria and local products eliciting different general biological responses [3, 4].

There is important evidence suggesting periodontitis as a biologically plausible risk factor for the development of other chronic, systemic, inflammatory conditions such as diabetes mellitus, cardiovascular disease (CVD), and adverse pregnancy outcomes [5]. Relationships between periodontitis and chronic obstructive pulmonary disease, rheumatoid arthritis, metabolic syndrome, obesity, cancers, and chronic renal disease have also been reported [6]. An inverse influence of systemic conditions on periodontal status has also been described [7]. Current epidemiological evidence sustains that periodontitis induces an increased risk for future atherosclerotic CVD [8].

The term CVD refers to atherosclerotic conditions such as coronary heart disease, cerebrovascular disease and peripheral vascular disease representing a leading cause of death, impairments, and quality of life alterations [8]. CVDs are the most prevalent noncommunicable diseases globally due to the increasingly aging population as well as to profound alterations of diets and lifestyles. Eurostat, the statistical office of the European Union, reported that in 2016 in UE 1.68 million deaths were resulting from diseases of the circulatory system, which was equivalent to 37.1% of all deaths—considerably higher than the second most prevalent cause of death, cancer (malignant neoplasms 25.8%). They accounted for 50–60% of all deaths in the Baltic Member States and Romania and 65.8% of all deaths in Bulgaria. By contrast, less than one-quarter of all deaths in Denmark (22.6%), France (24.3% 2016 data) and the Netherlands (25.0%) were caused by diseases of the circulatory system [9].

Periodontitis has a negative impact on cardiovascular outcomes. Also, periodontal treatment has been associated with potential risks and complications in patients on anti-thrombotic therapy which must be considered in clinical practice [8].

Due to significant advancement and the accumulation of new evidence on periodontitis-CVD relationships as well as to the major medical, economic and social burden represented by both periodontitis and CVD, this chapter aims to review existing epidemiological and pathogenetic links related to this topic as wells to highlight the impact of the periodontitis-CVD associative relationships on clinical practice and to provide some clinical recommendations for both periodontists and cardiologists on this topic.
