Effects of Non-Surgical Periodontal Therapy on Endothelial Function A Randomized Controlled Clinical Trial

In the last decade considerable evidence has supported the hypothesis that chronic low-grade infections, periodontitis included, and the inflammatory responses associated with them may play a significant role in the onset of atherosclerosis. An inflammatory alteration of the normal endothelial activity is thought to be one of the mechanisms that may link infection with atherosclerosis. It consists of loss of the normal vasodilation, antiplatelet and antithrombotic properties of the vascular walls and it is frequently called endothelial dysfunction. Impaired endothelium-dependent dilatation, an early functional marker of endothelial dysfunction has been demonstrated in young populations with family history of cardiovascular diseases. In the past 15 years a new non invasive and reproducible technique called Flow mediated dilatation (FMD) has been used to assess endothelial function.

Periodontitis is a chronic infection of the tooth supporting apparatus caused primarily by anaerobic gram negative bacteria organised in a biofilm (commonly known as sub-gingival dental plaque); it leads to inflammatory destruction of the periodontal ligament and alveolar bone and eventually to tooth exfoliation. Periodontitis is highly prevalent in both industrialised and developing countries with 10-15% of the adult population being affected by severe forms of this disease. Recognized risk factors include genetic polymorphisms in inflammatory genes, environmental exposures such as cigarette smoking, and systemic diseases such as diabetes. Local periodontal production of prostaglandins and pro-inflammatory cytokines has been associated with activation of matrix metalloproteinases and eventually to destruction of the periodontal ligament and alveolar bone. It is the primary cause of tooth loss in adult populations and as such leads to long term disability and increased treatment needs.

Local periodontal infections have been associated with a systemic response characterized by increased serum levels of C-reactive protein (CRP), hyper-fibrinogenemia, moderate leukocytosis, as well as increased serum levels of IL-1 and IL-6 when compared with unaffected control populations.

Several epidemiological studies have associated increased levels of acute phase markers with higher risk for cardiovascular atherosclerotic events. Among these markers, C-reactive protein is considered to be one of the most sensitive and probably to be an independent risk factor of atherosclerosis. It is produced by the liver presumably for adaptive or defensive reasons in response to a variety of inflammatory stimuli, including chronic low grade infections.

In a recently completed pilot trial we have been able to establish that treatment of periodontal infections resulted in a significant decrease in serum CRP. In that study, treatment of periodontal infections led to a significant decrease in serum CRP (0.5 mg/L, 95% CI 0.4 to 0.7 mg/L) and IL6 in otherwise healthy individuals affected with severe, generalized periodontitis and indicated that periodontitis contributed to the systemic inflammatory responses.