{'fraction_non_alphanumeric': 0.023855702094647012, 'fraction_numerical': 0.009503491078355315, 'mean_word_length': 5.486792452830189, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Periodontal disease – important to consider in cardiovascular disease prevention

The possibility of a connection between oral infection and systemic health was suggested already during the nineteenth century [1] and a discussion on the oral focal infection theory continued, a debate that is still going on. In the late 1980s, after suggestions by Mattila and Beck and co-workers, an increased interest on the association between oral health and cardiovascular disease emerged [2,3]. Since then, the interest for this link has persevered. Periodontitis is a chronic inflammatory condition following bacterial colonization of the gingiva that successively degrades the tissues attaching the teeth to the alveolar bone. Its mildest form, gingivitis or a bleeding gum, does not affect the underlying supporting structures of the teeth and is reversible with treatment. Periodontitis is common and it has been estimated that 46% of US adults have periodontitis [4] and its severe form, which often result in tooth loss, affect 5–15% worldwide [5]. Furthermore, in the presence of an oral infection or inflammation, the inner wall of the gingival pocket will become ulcerated and its role as a barrier to the systemic circulation is disrupted. Under these conditions, bacteria as well as bacterial products and inflammatory mediators can move from the gingival pocket to the well vascularized periodontal tissues and into the circulation. Atherosclerosis is a multifactorial disease promoted by chronic inflammatory conditions. An activation of systemic inflammation increases the risk for rupture of the atherosclerotic plaques and is considered of importance for the onset of acute coronary syndromes [6,7]. Cardiovascular disease, an expression of atherosclerosis, is the major cause of mortality in the western world contributing to almost half of all deaths in Europe [8]. Although a multitude of risk factors including smoking, hypertension, dyslipidemia, and diabetes are known to be behind a large proportion of myocardial infarctions (MIs) [9], there are still gaps in the knowledge regarding causes that contribute to the progress of atherosclerosis and cardiovascular events. It has been postulated that an association between periodontal and cardiovascular diseases may be one of these gaps [10]. Both conditions are promoted by similar risk factors, which may be a likely, but perhaps not the only, reason for the connection. An alternate explanation is that systemic inflammation promoted by periodontitis accelerates the atherosclerotic vascular injury and plaque rupture. Then, periodontitis becomes a cause of, rather than just a condition that co-exists with cardiovascular disease [7,11]. That DNA from oral bacteria has been identified in arterial plaques further support that there is a link between the oral microflora and cardiovascular disease [12]. Together with studies in which periodontal intervention favorably influenced inflammatory markers of cardiovascular risk for up to six months after the intervention [13,14], these findings were taken as evidence of a causal relationship. These studies must, however, be interpreted with caution due to the limited study populations, an aggravation of systemic inflammation during the first days after the periodontal intervention, the use of surrogate endpoints as a substitute for cardiovascular morbidity and mortality and incomplete information on shared risk factors of potential importance. This was further supported by an American Heart Association (AHA) statement saying...‘statements that imply a causative association between periodontal disease and specific atherosclerotic vascular disease events or claim that therapeutic interventions may be useful on the basis of that assumption are unwarranted’ [15]. A large, Swedish, multicenter, case-control study, PAROK RANK, recently investigated periodontitis and its relation to coronary artery disease [16]. The study recruited 805 patients <75 years old with a first MI and 805 controls matched for age, gender, and geographical area. The main finding was that the presence of moderate to severe periodontitis was independently associated with a first MI, increasing the risk by 28%. This association was particularly apparent in participants below the age of 65 years and among women (data on file). Thus, PAROKRANK supports the possibility of an independent relationship between periodontitis and cardiovascular disease [17]. The study has several strengths, among them a study population recruited from a nationwide geographical area and covering a variety of educational and socioeconomic conditions. The upper age limit of 75 years and that a first MI, representing both atherosclerosis and plaque vulnerability, was used as the expression of cardiovascular disease made the investigation less influenced by a multiplicity of concomitant disorders. Moreover, the presence and severity of periodontitis was based on alveolar bone loss studied by means of a radiographic method and interpreted at one core center. Still, it is an observational investigation and as such, it cannot be used as proof of a causal relationship.