Perio disease and CVD

Are periodontal disease and cardiovascular disease linked? If so, how strong is the link?

23 March, 2016 / clinical
 Tegan Dowler  

This review looks at links between cardiovascular disease (CVD) and periodontal disease (PD). The literature for the review was acquired by searching databases that were available through UHI multisearch, ResearchGate, Pubmed, Wiley Online Library and the NHS Knowledge Network. The search terms used were cardiovascular disease, heart disease and periodontal disease. From an original 24 papers which were initially found, in total 17 papers fitted the criteria and were analysed for this review. The criteria included: the paper must be a free full text, written in English, from anywhere in the world, must be within 25 years of age, from an unbiased source, subjects could be male and/or female and of any age range.

The links between CVD and PD are often overlooked. In recent years a variety of research and studies have taken place and allowed the links to be strengthened. Despite this there is no mention of the connections on well-known websites such as the British Heart Foundation and the NHS, which are often patients’ first port of call after diagnosis. In this literature review, the target is to provide a detailed analysis of papers to aid the clinician to be able to give a more holistic approach to the treatment provided. 1,2

The link between CVD and PD has been a topic which has been well researched over previous decades and many correlation links have been found, suggesting that the bacteria from the oral cavity enters the blood stream when PD is present and gingival inflammation is existent and thus the bacteria in the blood stream can cause cardiovascular problems by contributing to atheroma formation. 1,2

The links between CVD and PD are often overlooked. In recent years, research has allowed the links to be strengthened

The effect this has on dental clinicians is that they should have the knowledge to educate and forewarn the patient on the links and increased CVD risks when PD is present. This could help to potentially aid the patient and thus stop the possibility of a fatality. A holistic understanding is the key to first-class patient care. Therefore, the aim of this literature review is to look at how strong the link between CVD and PD is which will then aid clinicians to further their understanding in this area before being competent to pass the understanding on to patients.

Review of papers

The studies that were analysed within this review were no older than 25 years, so as to avoid dated evidence but to keep the selection open for longer studies to be included. They were ranked on the hierarchy of evidence in order to check they were a good source of evidence to be included (Appendices one and two are available in the online version at

Only four of the papers looked at were pre-2000 so much of the evidence gathered was within 14 years of this review. With regards to the references, Grau et al. (2004) 4 had a reference 58 years old at time of publication, which is quite old. However, the other references within this review are up to date, and older references are often required to aid in the basic knowledge present today. The papers (DeStefano et al. 1993 5, Joshipura et al. 1996 6, Mattila et al. 1989 7, Mattila et al. 1995 8), which were pre-2000, together had references that were not older than 26 years old at time of publication, meaning they are still relevant and used to date and can aid the reasoning for current research.

The methodology used is similar within the papers, with links between CVD and PD trying to be found by clinical dental examinations and cardiovascular events recorded, although understandably the studies did vary from each other in some areas.

Three of the papers (DeStefano et al. 1993 5, Hujoel et al. 2000 9, Wu et al. 2000 10) look at the same data that was gathered from the First National Health and Nutrition Examination Survey in the US. It was a cohort study that included a dental examination recording number of decayed permanent teeth, oral hygiene index, periodontal classification and periodontal index. Recalls of the subjects happened on four occasions. Each paper looks at the data with slightly different interpretation and includes different sample sizes of different subjects involved, depending on what limitations the authors put in place, meaning there was a difference of between 8,032 and 20,749 included subjects among the studies. Despite this, they were in agreement that there was a correlation. However, they found that the data from this study was inconclusive or statistically inconclusive to PD having a causal association with CVD. Due to the difference in participants numbers, the exact percentages of increased risk varies and because each study presents the data differently, this makes it challenging to compare how different these figures are from each other. Nevertheless, findings which were in agreement were that African-Americans and men are higher risk factors, although this could be due to the fact they are more susceptible to PD and thus the correlation of CVD follows.

A different, yet similar study 11 with a much smaller sample size of 241 coronary heart disease (CHD) patients and 50 control patients, undertook a dental examination making note of the probe depth, recession and bleeding on probing. This study found that CHD patients had significantly higher loss of clinical attachment, probing depth and missing teeth compared to non-CHD patients.

In agreement with the previous papers discussed, 5,9, 10 it also found that men were a common risk factor. In addition, diabetes and smoking patients were found to increase this risk further, which is possibly due to the interconnection between diabetes and PD and how smoking effects the wound healing and thus regeneration, both of these would make the PD more severe. This paper again concluded that there was a positive association between CHD and PD, as in all areas patients with CHD had higher figures (pocket depths, clinical attachment loss, bleeding on probing and missing teeth) than the non-CHD subjects. 12,13

Some studies relied on questionnaires 14, 15, 16 to gather much of their initial data, meaning sample sizes could be larger as costs of clinical examinations are reduced. After the initial information from the questionnaires was gathered, national databases and medical records could be checked to follow cardiovascular events for the remaining study. This allowed the studies to be over a much greater time period and therefore more cardiovascular events can be recorded and the links looked into by the authors.

The Mucci et al. 15 study lasted for 37 years, in which time 15,273 Swedish twins could be considered. It was discovered that the shared genetic factors were responsible for an association between PD and CVD. In addition, twins with severe tooth mobility were at 30 per cent greater risk of developing CVD than those with no tooth mobility. Having mobile teeth means that PD must be present, so this risk can further strengthen the links.

To oppose this, Howell et al. 14 after studying 22,071 US male physicians, concluded that there was no risk factor between CVD and PD. However, it was noted that men who reported PD at baseline had elevated but statistically non-significant increased risk of nonfatal myocardial infarction, stroke and cardiovascular death (10-20 per cent). Although the information is non-significant, it still links in from the study on the increased risk men have found by other studies 5, 9, 10, 11.

Oliveira, Watt and Hamer 16 looked at the links between CVD and oral hygiene. As it is known that it is the bacteria in the plaque, which is the cause of PD, this study can be included. With a sample size of 11,869, it was found that there was no clear difference between age, sex and smokers or non-smokers. In this study it was found that there was a significant association between tooth brushing and CVD, a 70 per cent increased risk if oral hygiene is poor. In addition, frequency of tooth brushing and markers of low-grade systemic inflammation found a direct correlation with C-reactive protein and fibrinogen – the more times teeth were brushed, the lower the number of inflammatory markers. However, it was again concluded that the link between CVD and oral hygiene is present but whether it is a casual link or risk marker is not certain.

When looking at clinical measurements, Machuca et al. 17 undertook a 10-year longitudinal study directly comparing CVD patients and healthy control groups. A dental examination was done at baseline, 12 months and 10 years to try to see if there was any significant difference in the two groups. At baseline, CVD patients did have higher numerical values, but this has been classed as non-significant. After just 12 months, pocket depths were already significantly different with 3.0±1.3 (mm) in the control group and 4.1±1.5 (mm) in the CVD group, but by the 10-year follow-up visit this had once again dropped down to non-significant figures, consistent for clinical attachment loss.

The paper summarised by saying that patients with CVD had bad initial periodontal status and presented a worse response to treatment than the control group. Having said this the CVD patients had a significantly greater plaque index score in all three examinations, so this would effect the treatment. In addition, the control group was selected due to periodontal problems, so this would mean the figures were not accurately based on truly healthy subjects and actually patients who already had deeper periodontal pockets and thus this cannot be classed as genuine health. In addition to this, there were only nine patients in the control group and 35 in the CVD group which is a very small sample size and may not have a wide enough range of ages, sex, socio-economic group etc.

Grau et al. conducted a similar study, although it was a case-controlled study and patients were only examined once. The way it was completed was by examining 303 patients seven days after the cardiac event, including 300 population control patients and 168 hospital control patients. The results showed that the clinical attachment loss mean is higher in the cardiac patient group than both the control groups and this pattern remains for gingivitis, plaque levels and radiological bone loss.

The number of teeth is significantly lower in cardiac patients than the two control groups also. This shows that periodontitis is more severe in this cardiac patient group. The results were all collected in the same way using well-recognised indexes, e.g. Silness and Loe plaque index, allowing the possibility of bias to be reduced. From the results, it shows that an increased severity of periodontitis was associated with an increased risk factor of 4.3 for cerebral ischemia and thus there was a significant association. Looking at Machuca et al. 17 study in comparison it would be good to see Grau et al. 4 study done on a longer term or with follow up visits to see if and how the results change.

The two papers from Mattila et al. 7, 8 looked at the same study although the 1995 paper included an extra series. And, while the 1989 paper does not state dates of the examinations, it is clear they are the same as the 1995 due to sample size of patients, results and that the papers both have fundamentally the same authors. The dentist measured the severity of tooth infection and periodontium after discharge form Helsinki University Central Hospital due to acute myocardial infarction. Patients were then given a score on dental disease of 0-10.


The 1995 papers results agree with and then go further than the 1989 paper and found that with the additional observations the severity of dental disease correlates with the magnitude of coronary atheromatosis. However, it still only suggests that the association is correlation and not causality. A point that has to be remembered with these studies is that the dentist knew if the subject was a control or patient and so this may cause slightly influenced results.

Joshipura et al. 6 completed a six-year cohort study on 44,119 male health professionals to look at the incidence of coronary heart disease in relation to the number of teeth present and PD. An area, which this study looked at that other studies have overlooked, is the participants diet. Tooth loss can lead to changes in diet and thus increase the coronary heart disease risk. It was discovered that tooth loss was associated with an increased consumption of saturated fats and cholesterol and decreased consumption of fruits, vegetables, carotene and fibre. These food groups are connected with CVD and so this is a possible trigger that has been overlooked in other studies.

At baseline it was discovered that the number of teeth was negatively related to age, smoking and coronary risk factor. There was a significantly higher incidence of coronary heart disease when there were 10 or fewer teeth when compared to full dentition in both groups (positive periodontal history 5.4 per cent to 2 per cent and negative periodontal history 3.74 per cent to 1.42 per cent) with this study having a high follow up rate it thus reduces bias. The overall findings were that no overall association was found between PD and coronary heart disease, although tooth loss may increase the risk, which could mean there was a history of PD.

DeStefano et al. 5 makes a valid point by suggesting that dental infections and coronary artery disease share similar etiological factors, consequently leaving the possibility that it could be poor oral health which is distinctive of an individual’s lifestyle that increases the risk of coronary artery disease, which is a type of CVD. Things such as smoking, diabetes and low socio-economic status are these types of factors. Mattila et al. 7 found that the total dental index correlated significantly with social class, subjects in the lower classes had worse dental health, which agrees with the DeStefano et al. 5 argument.

Within Lamont and Jenkinson’s 18 textbook (p55) the potential causal bacteria are briefly mentioned. However, it is said that evidence is yet to be convinced. With regards to the mechanism of the bacterium on the cardiovascular tissues, papers are very limited – the oldest paper to be looked at is 2009. The studies are all very new with no older papers, as the research itself is still new.

The reviews 19, 20, 21, 22, 23 looked at the types of bacteria, which could cause the links between CVD and PD. Asikainen 20 made the valid point that obtaining valid causal research is difficult due to both conditions being chronic and progressively advancing asymptomatically over many years. In addition, there are vast amounts of data, which require to be interpreted; new methods are being looked at to aid this. It is also said that due to the controversial results of studies, doubts of validity have been raised on the relationship. Despite this, there is still a biologically feasible basis and thus research is continued to take place.

The distinct method of the way in which bacteria causes CVD has been very briefly described within a highly recognised textbook by Clerehugh, Tugnait and Genco 3 (p24-25). However, the paper by Saini, Saini and Saini 23 goes into further detail and describes two theories. Number one being that the oral bacteria affects the heart by attaching itself to fatty plaques within the blood stream and this contributes to clot formation. These clots can block the blood flow and thus lead onto heart attack or other problems.

The second theory is that the PD causes inflammation, which increases the plaque build-up which in turn may contribute to the swelling of arteries. Inaba and Amano 20 agree and comment that due to the clear evidence of the association, control of the oral disease is essential for prevention and management of the condition. According to studies 19, 20 this is because as PD progresses, epithelium develops to be ulcerated. This exposes the connective tissues and blood capillaries, thus allowing bacteria from the plaque biofilm to enter the blood stream. To further this, Kerrigan and Cox 21 gave an explanation saying that once this bacteria has entered the blood stream it forms platelet-bacterial aggregates when contact with platelets is made, these bind to heart valves or are involved with atherosclerosis sites.

Saini, Saini and Saini 23 revealed that there are more than 500 bacterial species, which are capable of colonising within the oral environment. Despite this huge number required to be investigated, P. gingivalis is a bacteria that has come to the attention by having an etiological role in the mechanism. Kerrigan and Cox 21 are in agreement with this but investigated Streptococci ssp. and found that along with P. gingivalis these are the two bacteria that are capable of initiating the platelet activation. In addition, a point was made that several bacteria have evolved so that interactions occur at the same time that get the same response. This makes it more difficult to pinpoint the exact bacteria causing the problem, plus most studies to date have been done under static conditions, which may not reflect the same response as in the fluid environment present within the body.

A final review which gives slightly more information 22 finds that it is the bacteria with strains of serotype-k could circulate through the body more freely and thus there is a possibility that serotype-k S. mutans strains are more likely to be associated with the systemic diseases. Having said this, studies are remaining to take place and it is currently an on-going research process. Due to the research, which has been completed so far being sparse and very new, there is a great need for further research to be completed to strengthen the link and validate the findings further.


The results of the review show that there is a link between CVD and PD, with the majority of studies finding conclusive results of a link, even if this link was small. Howell et al. 14 concluded that there was no risk factor between PD and CVD, despite having slightly elevated figures in the results they gathered. This is due to the fact the results are not significant enough to make this a certainty. This is the case that many of the studies presented with non-significant results, due to their only being a slight difference. This makes it difficult to be confident with the results; however, taking into consideration the age and research done since the uncertainty of these few studies it is clear that a link is present. Older papers were required to look at the progression of knowledge.

This topic is difficult to research due to there being many variables which could influence the results; diet, smoking, diabetes, socio-economic class etc. and thus it is difficult to get an appropriate cohort with all aspects the same to be able to complete a fair assessment of the link. This also means that only a correlation can be made as it may not necessarily be the PD which is the cause of CVD it maybe one of the other factors which is common with PD and CVD which influences the disease.

For a cause to be found further studies have to be done. Within the last five years, studies on the exact bacteria, which could be the cause, have commenced. There are, however, hundreds of bacteria to be researched which is a long task to complete and, therefore, further studies are required to look at all the oral bacteria and how they influence PD and CVD. To date it is P. gingivalis and the serotype-k S. mutans strains which have been found to be the potential cause.

There were a variety of studies analysed in this review. There were a total of five cohort studies that are mid-way on the hierarchy of evidence. Four case-controlled studies were analysed in addition and these fall just below cohort studies. Only one randomised controlled trial was included. However, it was a conclusive study that increases its validity upon the hierarchy further. With regards to the bacterium research, it was mainly reviews which were used – this is due to the fact that there is limited research completed to date on this aspect. Reviews are, however, at the top of the hierarchy so they were good sources from which to extract information. Overall, a good variety of research was used, ideally more randomised, controlled trials would have been included, although they are not available to date.

The papers were difficult to compare due to differences within each study design, e.g. exclusion of different variables, the time period that the study ran for, the number of participants, extent of PD, etc. This could be seen as a positive as it means a greater variety of subjects have been analysed with different study designs at each time which reduces bias.

This review has looked at the potential link between PD and CVD and concluded that the link is present and with studies on the causal bacteria in the initial stages the causal factor is closer to being recognised. Although there are still not enough studies that have been completed to pinpoint the exact bacteria or trigger between PD and CVD. Nonetheless the research process is a long process with this topic in particular as there are so many other conditions within the human body, which need to remain the identical within subjects during investigations.

About the Author

Tegan Dowler graduated from the University of the Highlands and Islands in 2015 as a dental hygienist/therapist. She is currently undertaking her vocational training in Forres within Forres Dental Care.

Further reading

Baratt, H. (2009) The hierarchy of research evidence – from well conducted meta-analysis down to small case series, publication bias. Available from (Accessed 1 November 2014).

British Society of Periodontology. (2014) Periodontal Disease and Treatment. Available from (Accessed 18 November 2014).

Hart, C. (1998) Doing a Literature Review: Releasing the Social Science Research Imagination. London: Sage .

NHS choices. (2013) The risks of gum disease. Available from (Accessed 18 November 2014).

Peterson, P, E. and Ogawa, H. (2005) ‘Strengthening the Prevention of Periodontal Disease: The WHO Approach’. Journal of periodontology 76 (12), 2187-2193. Available from (Accessed 18 November 2014).

World Health Organisation. (2013) Cardiovascular diseases (CVDs). Available from 18 November 2014).


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17. Machuca G, Segura-Egea J J, Jimenez-Beato G, Lacalle J R and Bullon P. (2012) ‘Clinical indicators of periodontal disease in patients with coronary heart disease: A 10 years longitudinal study’. Medicina oral, patologia oral y cirugia bucal 17 (4), 569-574 Available from (Accessed 20 October 2014).
18. Lamont, R, J and Jenkinson, H, F. (2010) Oral Microbiology at a Glance. Singapore: Wiley-Blackwell
19. Asikainen S E. (2009) ‘Periodontal bacteria and cardiovascular problems’. Future Microbiology 4 (5), 495-498 Available from (Accessed 20 October 2014).
20. Inaba H and Amano A. (2009) ‘Roles of Oral Bacteria in Cardiovascular Diseases – From Molecular Mechanisms to Clinical Cases: Implication of Periodontal Diseases in Development of Systemic Diseases’. Journal of Pharmacological Sciences 113, 103-109 Available from (Accessed 20 October 2014).
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