The Periodontitis and Vascular Events (PAVE) pilot study: recruitment, retention, and community care controls.
ABSTRACT Population-based clinical and laboratory studies have reported findings providing support for a possible relationship between periodontal disease and cardiovascular disease. The Periodontitis and Vascular Events (PAVE) pilot study was conducted to investigate the feasibility of a randomized secondary prevention trial to test whether treatment of periodontal disease reduces the risk for cardiovascular disease.
Five clinical centers recruited participants who had documented coronary heart disease and met study criteria for periodontal disease. Eligible participants were randomized to receive periodontal therapy provided by the study or community dental care. Follow-up telephone calls and clinic visits were planned to alternate at 3-month intervals after randomization, with all participants followed until at least the 6-month clinic visit. Participants were followed for adverse events and periodontal and cardiovascular outcomes.
A total of 303 participants were randomized. Recruitment that involved active participation of a cardiologist with responsibility for the patients worked best among the strategies used. Of those who had not withdrawn, 93% completed the 6-month contact. During follow-up, 11% of the 152 subjects in the community dental care group reported receiving periodontal therapy outside of the study.
If appropriate recruitment strategies are used, this pilot study demonstrated that it is feasible to conduct a secondary prevention trial of periodontal therapy in patients who have had coronary heart disease. If a community dental care group is used, sample size estimation needs to take into account that a non-trivial proportion of participants in this group may receive periodontal therapy outside of the study.
- [Show abstract] [Hide abstract]
ABSTRACT: Abstract Aim: The aim of this review was to critically appraise the evidence on the impact of periodontal treatment of cardiovascular diseases (CVDs) biomarkers and outcomes. Methods: A systematic search was performed in Cinhal, Cochrane, Embase and Medline for relevant articles up to July 2012. Duplicate screening and reference hand searching were performed. Data were then summarized and evidence graded in tables. Results: The search resulted in: (a) no evidence on the effects of periodontal therapy on subclinical atherosclerosis, serum levels of CD40 ligand, serum amyloid A and monocyte chemoattractant protein-1, (b) limited evidence on the effects of periodontal therapy on arterial blood pressure, leucocyte counts, fibrinogen, tissue necrosis factor-a, sE-selectin, von Willebrand factors, d-dimers, matrix metalloproteinases, oxidative stress and CVD events, and (c) moderate evidence suggesting a negligible effect of periodontal therapy in reducing interleukin-6 and lipids levels, whilst a positive effect in reducing serum C-reactive protein levels and improving endothelial function. Conclusions: Periodontal therapy triggers a short-term inflammatory response followed by (a) a progressive and consistent reduction of systemic inflammation and (b) an improvement in endothelial function. There is however limited evidence that these acute and chronic changes will either increase or reduce CVD burden of individuals suffering from periodontitis in the long term.Journal of Periodontology 04/2013; 84(4 Suppl):S85-S105. · 2.40 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Periodontitis is a bacterially-induced, localized chronic inflammatory disease destroying both the connective tissue and the supporting bone of the teeth. In the general population, severe forms of the disease demonstrate a prevalence of almost 5%, whereas initial epidemiological evidence suggests an association between periodontitis and coronary artery disease (CAD). Both the infectious nature of periodontitis and the yet etiologically unconfirmed infectious hypothesis of CAD, question their potential association. Ephemeral bacteremia, systemic inflammation and immune-pathological reactions constitute a triad of mechanisms supporting a cross-talk between periodontal and vascular damage. To which extent each of these periodontitis-mediated components contribute to vascular damage still remains uncertain. More than twenty years from the initial epidemiological association, the positive weight of evidence remains still alive but rather debated, because of both the presence of many uncontrolled confounding factors and the different assessment of periodontal disease. From the clinical point of view, advising periodontal prevention or treatment targeting on the prevention of CAD it is unjustified. By contrast, oral hygiene including periodontal health might contribute to the overall well-being and healthy lifestyle and hence as might at least partially contribute to cardiovascular prevention.American journal of cardiovascular disease. 01/2011; 1(1):76-83.
- [Show abstract] [Hide abstract]
ABSTRACT: Aim: To study if preceding assessment of periodontal status in patients with established coronary artery disease (CAD) can predict future CAD endpoints (myocardial infarction, new revascularization procedure or CAD-related death) during 8-year follow-up, and if the changes in periodontal status over time differ in patients with CAD compared to healthy controls. Methods: In 2003, periodontal status was examined in 161 CAD patients who underwent percutaneous coronary intervention or coronary artery by-pass graft due to significant stenosis in the coronary arteries, and in 162 controls without CAD history. Eight years later, 126 CAD patients (mean age 68± 8.9, 102 men) and 121 controls (mean age 69± 9.0, 101 men) were periodontally re-examined. A standard classification of periodontal disease in three groups (mild, moderate and severe) was used. CAD endpoints during follow-up were obtained by review of medical records. Cause of death due to CAD was confirmed from the Swedish Cause of Death Register. Results: No significant differences were found among CAD patients with or without CAD related endpoints at 8 year follow-up and severity of periodontitis at baseline (P =0.7). CAD did not influence the incidence or severity of periodontitis over time. Significant differences were found at the final examination in periodontitis prevalence and severity (P =0.001), number of teeth (P =0.006), probing pocket depth 4-6 mm (P =0.016), bleeding on probing (P =0.001) and radiographic bone level (P =0.042) between CAD-patients and controls, all in favour of controls Conclusion: The study results did not show a significant association between CAD endpoints during 8 years and periodontal status at baseline. The progression of periodontitis was low in booth groups although the higher proportion of individuals with severe periodontitis among CAD patients compared to controls remained unchanged over the 8 year follow up. Further long-term prospective studies are needed to show whether periodontitis can be considered a risk or prognostic factor for CAD, in terms of endpoints including myocardial infarction, new revascularization procedure or CAD-related death.Journal of Periodontology 05/2013; · 2.40 Impact Factor