Treatment of periodontal disease results in improvements in endothelial dysfunction and reduction of the carotid intima‐media thickness

Abstract

Several cohort studies reported a relation of cardiovascular events and periodontal disease. In particular, Porphyromonas gingivalis is associated with the development of atherosclerotic plaques. We verified in a longitudinal study whether inflammation biomarkers, endothelial adhesion molecules, leukocyte activation markers, and intima-media thickness could be beneficially modified by periodontal treatment alone. Thirty-five otherwise healthy individuals affected by mild to moderate parodontopathy were enrolled in the study. Echo-Doppler cardiography of the carotid artery, fluorescence-activated cell sorting analyses on lymphocytes and monocytes, and plasma inflammatory indices were evaluated at baseline and at multiple time points after the periodontal treatment. Results showed that inflammation biomarkers were abnormally increased at baseline. Periodontal treatment resulted in a significant reduction of the total oral bacterial load that was associated with a significant amelioration of inflammation biomarkers and of adhesion and activation proteins. Notably, intima-media thickness was significantly diminished after treatment. Inflammatory alterations associated with the genesis of atherosclerotic plaques are detected in otherwise healthy individuals affected by parodontopathy and are positively influenced by periodontal treatment. Reduction of oral bacterial load results in a modification of an anatomical parameter directly responsible for atherosclerosis. These results shed light on the pathogenesis of atherosclerosis and could have practical implications for public health.

Evidence that periodontal treatment improves biomarkers and CVD outcomes

“…Christgau et al (1998) failed to show any differences in WBC in patients with diabetes and healthy controls 4 months after periodontal treatment; these findings were confirmed in other trials (Montebugnoli et al 2005, Seinost et al 2005, Marcaccini et al 2009a, Graziani et al 2010, Siribamrungwong & Puangpanngam 2012 (Rastogi et al 2012). That efficacy was further confirmed in three additional clinical trials (Fokkema et al 2003, Hussain Bokhari et al 2009, Piconi et al 2009). Based on the evidence examined, only five trials reported a statistically significant reduction of WBC following periodontal therapy, whilst nine other trials reported the opposite finding.…”

“…The only published intervention study observing the impact of periodontal therapy on c-IMT was conducted in Italy by Piconi et al (2009). Also, 35 otherwise healthy individuals affected by mild to moderate periodontitis took part in the trial without control group and received a scan of their carotids before and after periodontal therapy.…”

Periodontal Disease and Atherosclerotic Vascular Disease: Does the Evidence Support an Independent Association?

“…279 A recent pilot study indicated that nonsurgical treatment of mild to moderate periodontitis in otherwise healthy individuals may significantly reduce cIMT at 12 months after completion of treatment. 280 To date, only a single multicenter pilot study has examined the effects of periodontal therapy on the secondary prevention of cardiac events. The Periodontitis and Vascular Events (PAVE) investigation 281,282 randomized patients with periodontitis and a history of CHD (angiographically proven coronary artery disease or recent MI or surgical or percutaneous coronary revascularization) to either community care (generally consisting of supragingival debridement only; control group) or a study protocol that consisted of oral hygiene instruction and nonsurgical periodontal therapy.…”

Increasing Evidence for an Association Between Periodontitis and Cardiovascular Disease

“…13 Small studies have reported reduction in carotid intimal-medial thickness 6 months after treatment of severe periodontal disease. 14 The systemic inflammatory or immune response to periodontal infection may increase cardiovascular risk. Also, pathogens from the mouth can enter atherosclerotic plaques via the blood stream, and this could promote an inflammatory or immune response within the atherosclerotic plaque.…”