Several studies have shown that periodontal treatment may improve certain cardiovascular markers. 

There has for several decades been a real revival of focal infection theory, which advocates a distant relationship, either direct or indirect, between oral pathologies and the rest of the body, and vice versa⁽¹⁾. 

The clearest and best researched archetype of this association is the bidirectional relationship between diabetes mellitus and periodontal diseases (PD), along with aspiration pneumonia. Similarly, both cardiovascular disease (CVD) and the adverse effects of pregnancy have also been studied extensively. In particular, cardiovascular disease has become especially important because of its fatal consequences for individuals and the social health costs arising thereof. 

The aetiopathogenic mechanisms between PD and CVD are common to other diseases and systemic disorders influenced by chronic periodontal disease and arise from interaction between the microorganisms in the subgingival biofilm and the host's inflammatory response⁽²⁾. 

Cardiovascular disease has become especially important because of its fatal consequences for individuals and the social health costs arising thereof 

We explain below the biological plausibility of this association, the epidemiology and the evidence that periodontal treatment can improve certain cardiovascular markers and, ultimately, the close relationship between periodontal disease and cardiovascular disease. 

Biological plausibility 

There are two mechanisms that describe this plausibility. The first is of an infectious nature and consists of the passage of bacteria into the bloodstream, or bacteraemia. The second is inflammatory and is caused by inflammatory mediators produced locally or systemically. 

Infection theory refers to the bacteria's capacity to interact and invade body cells directly, or indirectly stimulate the release of paracrine factors that modulate the functions of these cells. 

Cell invasion by periodontal pathogenic bacteria is a key virulence factor for the survival and spread of microorganisms in certain environments and for evading the host's defences. One of the most studied bacteria, both in vitro and in vivo, is Porphyromonas gingivalis. 

A recent study identified the ability of this periodontal pathogen to alter the expression of protein encoding genes, increasing inflammation and aetherosclerosis in the coronary arteries (the vessels that supply blood to the heart)⁽³⁾. 

Studies have also been made on other bacteria such as A. actinomycetemcomitans, P. intermedia, T. forsythia and F. nucleatum as well as others, which depending on the strains and their various mechanisms, may invade the host endothelial cells. 

The inflammation theories refer to the fact that both periodontitis and cardiovascular disease share inflammatory models that are interrelated and will vary from one individual to another depending on their genetic susceptibility. In studies so far, it has been observed that mediators and inflammatory markers increase in patients with periodontitis, and this could happen in two ways. 

One such way would be that used by mediators that travel from the periodontal lesion through the body, causing damage at a distance, and inducing formation of acute-phase reactant compounds in the liver, such as C-reactive protein. The other way is that the bacteria themselves or their products enter the bloodstream and stimulate the inflammatory response at a distance, and may even settle on the aetheroma plaques themselves⁽⁴⁾. 

The inflammatory response may also be affected by various types of antibodies associated with periodontal disease and that may interact with the host's antigens, inducing or accelerating aetherosclerotic processes. Other studies have shown that in these patients there is an increase in potentially inflammatory lipids such as LDL, triglycerides and VLDL, which would attach to aetherosclerotic plaques and accelerate their formation and maturation. 

Finally, it should be noted that these mechanisms may occur simultaneously and together impact on systemic inflammation in a patient. 

Epidemiology 

For the epidemiological study of the relationship between periodontal disease and cardiovascular disease, the most studied cardiovascular disease types are primary coronary, cerebrovascular, and peripheral arterial diseases. 

Furthermore, periodontal disease is clinically defined by probing depths and attachment levels, and by means of radiography. Most case-control and cohort studies conducted so far have found a clear association between the extent and severity of periodontal disease and the development of aetherosclerotic cardiovascular disease, independently of other risk factors such as smoking. The most affected groups, according to some studies, appear to be men and young adults⁽⁵⁾. 

One recent study at the University of Granada demonstrated for the first time a positive relationship between the severity and extent of periodontal disease and myocardial infarct size using two biomarkers of cardiac tissue necrosis, troponin I and myoglobin⁽⁶⁾. 

Evidence that periodontal treatment improves CVD biomarkers 

Cardiovascular disease remains the leading cause of death worldwide and any strategy or intervention set to manage such an epidemic is welcomed by the scientific community, governments and the general population. 

In this context, infectious chronic diseases like periodontitis may play an important role in the pathogenesis of aetherosclerotic cardiovascular disease, as it has been observed that the presence of periodontal disease might double the risk of death even when other risk factors are controlled. The European Society of Cardiology guidelines include periodontal disease as an independent risk factor for cardiovascular disease⁽⁷⁾. 

Studies to date have assessed the effects of periodontal therapy for both established risk factors for CVD, such as lipids and blood pressure, as well as for indirect CVD assessment criteria, such as endothelial function, the carotid intima-media thickness or sub-clinical aetherosclerosis, and systemic inflammation marker levels. 

Of these, the most significant results have been the improvement of the endothelial function, reduced IL-6 and a decrease in C-reactive protein after non-surgical periodontal treatment⁽⁸⁾. A recent meta-analysis also found an association between increased carotid intima-media thickness, impaired flow-mediated dilation, and periodontal disease⁽⁹⁾. 

For the remaining variables, evidence is still very limited and large-population, multi-centre, long-term intervention studies are required in order to validate the relationship between periodontal therapy and short- and long-term decreased risk of cardiovascular disease.