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(JOP 2009;80:1021-1032.) The American Journal of Cardiology (AJC) and the Journal of Periodontology (JOP) released a consensus paper on the relationship between heart disease and gum disease with the above title. Inflammation is one of the main causes of atherosclerotic cardiovascular disease (CVD) and periodontitis. Periodontal disease may increase the inflammation level throughout the body.Several studies have shown that patients with periodontal disease have an increased risk for cardiovascular disease . The immune system, once believed to be only a vital defense against infection and a promoter of healing—except in the instances of a few uncommon connective tissue disorders—is now recognized as a significant active participant in many chronic diseases, including hypertension, diabetes mellitus, arthritis, inflammatory bowel disease, psoriasis, and the two diseases addressed in this Editors’ Consensus: atherosclerotic cardiovascular disease (CVD) and periodontitis. Periodontitis, a bacterially induced, localized, chronic inflammatory disease, destroys connective tissue and bone that support the teeth. Periodontitis is common, with mild to moderate forms affecting 30% to 50% of adults and the severe generalized form affecting 5% to 15% of all adults in the United States. When bacterial biofilms on the teeth are not disrupted on a regular basis, ecologic changes lead to the emergence of a small set of gram-negative anaerobic bacterial species, including Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia (previously T. forsythensis), which consistently associate with periodontitis. Environmental and genetic factors as well as acquired risk factors such as diabetes mellitus and exposure to tobacco accelerate inflammatory processes in periodontitis. Approximately 50% of the variation in clinical severity of chronic periodontitis is explainable by genetic influences. Inflammation has emerged as an integrative CVD factor. Inflammation can operate in ‘‘all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. Higher quantiles of C-reactive protein (CRP) predict future acute myocardial infarction and unstable angina pectoris and the onset of systemic arterial hypertension, diabetes mellitus, and stroke, independent of blood lipid levels. The erythrocyte sedimentation rate, chemokines, and cytokines including IL-6, IL-8, IL-10, IL-18, TNF-a, and monocyte chemoattractant protein–1 also are frequently abnormal in patients with acute coronary syndromes and in many other conditions. The incidence of atherosclerotic CVD events increases in patients with chronic inflammatory diseases, in addition to periodontitis, including rheumatoid arthritis, psoriasis, systemic lupus erythematosus, and some types of infections.

The precise role of inflammation as a direct, causative factor in chronic atherogenesis and in the acute complications of atherosclerosis remains an area of intense current investigation.

Specific questions that the consensus panel believes should be addressed in future research include the following:

1. Is periodontitis an independent risk factor for atherosclerotic CVD?

(2) If periodontitis is an independent risk factor for atherosclerotic CVD, what is the mechanism of the relationship, and at what stage(s) of atherogenesis is it important?

(3) Regardless of whether periodontitis is an independent risk factor for atheroscleroticCVD, should risk factors for atherosclerotic CVD be treated more aggressively in patients with periodontitis than current guidelines recommend for the general population?

(4) Do periodontal therapeutic interventions, such as infection and inflammation control, directly reduce the rate of atherosclerotic plaque development and its complications, especially acute myocardial infarction and stroke?

(5) Because periodontitis in the general population is greatly underdiagnosed and undertreated, what measures can improve its detection and management in persons at increased risk for primary and secondary atherosclerotic CVD events?

(6) Are there specific oral microbial pathogens that add to CVD risk and therefore should be targeted for antibiotic treatment?

(7) In addition to the possible role of periodontal inflammation caused by infection, does secondary endotoxemia play a causative role in thIs periodontitis an independent risk factor for atherosclerotic CVD?

(8) Are acute events such as acute myocardial infarction and stroke more likely to occur during periods of worsening periodontitis?

(9) Do calcium channel blockers have any adverse effect on periodontitis other than causing gingival hyperplasia in some persons, and if so, what is the magnitude of this effect?

(10) In addition to calcium channel blockers, are there other cardiovascular medications that may adversely affect periodontitis?