More evidence for dentists being part of the diabetes team: cardiologists and other physicians who manage patients with CVD should collaborate with dentists to moderate cardiovascular risk in patients who also suffer from periodontitis…
The association between periodontitis and other chronic diseases, such as cardiovascular disease (CVD) and Type 2 diabetes, could be related to systemic inflammation initiated by a local inflammatory challenge. Oliveira et al. have added lack of oral hygiene, and its link with systemic inflammation, to the spectrum of risk factors for CVD.
The inflammatory response has an important role in several chronic diseases, including atherosclerotic cardiovascular disease (CVD) and periodontitis. The association between chronic diseases such as CVD, Type 2 diabetes, and periodontitis is also becoming increasingly clear, and could at least in part be related to induction of systemic inflammation by a local inflammatory challenge. Oliveira et al. have now added an important health behavior — failure to maintain oral hygiene — to the spectrum of risk factors for CVD. Furthermore, they have reported a link between poor oral hygiene and elevated levels of the inflammatory molecules C-reactive protein (CRP) and fibrinogen, which are risk markers for CVD.
In this commentary, we aim to provide health professionals, including cardiologists and dentists, with an approach to reducing risk of primary and secondary atherosclerotic CVD events in patients with periodontitis and poor oral hygiene.
The observation by Oliveira et al. that poor oral hygiene, which is often found in patients who develop periodontitis, is associated with increased risk of CVD is relevant to current clinical practice. Systemic inflammation and alterations in lipid metabolism are common traits of periodontal disease that could explain the link between CVD and periodontitis. Although randomized, controlled intervention trials are necessary to prove a causal link between periodontitis and CVD, periodontal disease is highly prevalent in the general population and should not be ignored as a possible important risk factor. We will highlight the evidence for the existence of an association between periodontitis and CVD and the extent to which we understand the plausible biological mechanisms underlying this link.
The concept that periodontitis is associated with atherosclerotic vascular diseases was supported by an analysis of data from NHANES I, which demonstrated that periodontal disease is a risk factor for nonhemorrhagic stroke. In a meta-analysis, Bahekar and colleagues found an increased incidence of CVD among patients with periodontitis. In another meta-analysis of cross-sectional and longitudinal studies of the association between CVD and periodontitis, Humphrey and colleagues concluded that periodontal disease is a risk factor for CVD, with relative risk estimates ranging from 1.24 to 1.35 after adjustment for possible confounding factors. A relationship between peripheral arterial disease and history of periodontitis has also been reported. This body of literature indicates that periodontitis might be an independent risk factor for CVD. Moreover, these studies point to the need for further research to better define the relationship between these two diseases and determine the extent to which chronic inflammatory diseases such as periodontitis contribute to the pathogenesis of CVD.
A consensus report published in 2009 by the editors of the American Journal of Cardiology and the Journal of Periodontology stated that the available evidence supports at least two biologically plausible mechanisms for a causative link between periodontitis and CVD. The increase in levels of systemic inflammation among patients with periodontitis has been clearly demonstrated, and treatment of periodontitis has been shown to reduce systemic inflammation in patients with a history of cardiovascular events, suggesting that inflammatory cytokines induced by periodontitis could mediate the link with CVD. The second mechanism derives from the observation that the 108-1012 Gram-negative bacteria found in the periodontal pockets surrounding the diseased tooth often migrate to the blood stream (bacteremia). Periodontal bacteria have been identified in atheromas and could provide the inflammatory stimulus leading to atheroma formation. In addition, studies of animal models, for example a study in rabbits by Jain and colleagues, have demonstrated that atheroma formation is increased in animals with periodontitis, which suggests a potential causal role for periodontal infection in CVD.
Link between periodontitis and cardiovascular disease. Dental inflammation induced by bacterial biofilm (periodontitis) causes a local and systemic cytokine response. Proinflammatory cytokines induce an acute phase response in the liver characterized by elevated levels of C-reactive protein and fibrinogen, which in turn promote atherogenesis. Gingival ulceration in periodontitis allows the migration of bacteria into the blood (bacteremia), which could provide a second inflammatory stimulus leading to atheroma formation. Risk factors common to both cardiovascular disease and periodontitis are also thought to be related to increased systemic inflammation. Abbreviations: CRP, C-reactive protein; IL-1, interleukin 1; IL-6, interleukin 6; TNF, tumor necrosis factor.
The risk factors shared between periodontitis and CVD present the possibility that the association between the two conditions is, at least in part, the expression of two unrelated inflammatory diseases in a susceptible individual. Type 2 diabetes, cigarette smoking, obesity, lipid alterations, hypertension, physical inactivity, family history of CVD and periodontal disease, advancing age, and male sex are all risk factors for CVD and are commonly found in patients with periodontitis.
On the strength of the current evidence for an association between CVD and periodontitis, a series of clinical recommendations were made in the aforementioned consensus report. Patients with periodontitis who have two or more known risk factors for atherosclerosis should be referred by the dental team for evaluation of atherosclerotic risk, which should include physical examination and annual measurement of blood pressure and blood lipid profile. Patients with periodontitis and abnormal serum lipid values, elevated levels of plasma CRP (as measured by the high-sensitivity CRP test), or both are recommended to follow a multifaceted lifestyle modification program to reduce CVD risk. Cessation of cigarette smoking is recommended for all patients with periodontitis. Furthermore, all patients with periodontitis who have elevated blood pressure (>140/90 mmHg) should be treated according to standard hypertension management protocols and should undertake lifestyle changes, including reduction of weight and dietary sodium intake, as appropriate. Periodontal evaluation should be considered in patients with CVD who have signs or symptoms of gingival disease or unexplained tooth loss. Moreover, when periodontitis is newly diagnosed in patients with CVD, dentists and physicians should closely collaborate to optimize CVD risk reduction and periodontal care.
On the basis of current knowledge, cardiologists and other physicians who manage patients with CVD should collaborate with dentists to moderate cardiovascular risk in patients who also suffer from periodontitis.
Nat Rev Cardiol 09/07/2010