Kholy, K., Genco, R., & Van Dyke, T. (2015). Oral infections and cardiovascular disease. Trends In Endocrinology & Metabolism, 26(6), 315-321. doi: 10.1016/j.tem.2015.03.001
There is evidence linking periodontal disease to cardiovascular disease. This review examines the plausibility of the association and how systemic exposure to oral bacteria impacts the initiation and progression of cardiovascular diseases by triggering an inflammatory response.
What is periodontitis?
Periodontitis is an inflammatory disease of the tissues supporting the teeth (gingiva, alveolar bone, periodontal ligament, and cementum) that is induced by bacterial deposits on the teeth (plaque).
What are cardiovascular diseases (CVDs)?
Cardiovascular diseases include: coronary heart disease, stroke and congestive heart failure. They can lead to life threatening acute events such as strokes and myocardial infection.
The high prevalence of both periodontitis and CVD makes it difficult to establish a relationship between these conditions when both occur at once in an individual.
- Periodontitis and CVD share mechanism of inflammation
- The surface area of ulcerated epithelium lining periodontal pockets is around 8-20 cm2
- This provides a portal for bacterial entry into systemic circulation
Do atheromatous plaques contain oral bacteria?
- A series of studies beginning in 2000 reported genomic DNA of several periodontal bacteria
- in human atheromas eg porphyromas gingivalis
- A recent study detected 84 different bacterial taxa in the atheromas and vascular walls of patients with atherosclerotic vascular disease and periodontal disease, versus just 18 taxa in patients with little periodontal disease
How do periodontal bacteria migrate to cardiovascular tissues?
There is evidence for two modes of invasion:
- Bacteraemia-related bacteria invade endothelial layer with production of cytokines
- Transmigrating phagocytes harbouring oral bacteria move through blood stream to contribute to atheroma’s
Some theories for the link:
- Local inflammatory nidus can increase vascular inflammation systemically
- Elevated innate host response of any origin is a risk factor for CVD, as well as for periodontitis, suggesting the inflammatory response as a common susceptibility determinant
- Periodontitis treatment can impact other risk factors for CVD e.g lower c reactive protein levels
- Molecular mimicry- cross reactive autoantibodies to periodontal bacterial lipopolysacchar-ides and heat-shock proteins (HSPs)
Offer an excellent, and easier to control and replicate, alternative to human intervention trials, which are often hard to organize because of logistical or financial constraints
Future research recommendations:
- No studies yet evaluate the impact of treating periodontal disease on primary events – myocardial infarction, only strong evidence for coronary heart disease and strokes
- Most trials are cross sectional by design and so cannot assess impact over a period
- Make a more consistent pool of data with stronger evidence: standardized treatments, measurements, diagnostic criteria
Outstanding questions :
- Are there currently unidentified mechanisms by which bacteria are transported to vascular sites?
- Does the treatment of periodontitis influence the occurrence of myocardial infactions?
- Is there a reverse relationship between periodontitis and CVD? Can the onset of CVD affect periodontal disease?
Chloe Russell-Williams BDS1