Systemic Risk Factors for Periodontal Disease 3

Question 1

What happens to the periodontal pocket in periodontal disease?

Answer 1

• In periodontal disease the periodontal pocket is filled with a pathogenic anaerobic biofilm resulting in an inflammatory reaction in the adjacent gingival tissues resulting in the pocket wall being ulcerated & leaky.
• The surface area of the exposed ulcerated periodontal pockets can be extensive & has been estimated to be approximately 20 to 30cm2 in a subject with generalised deep periodontal pocketing.
• The inflamed periodontal tissues next to the periodontal pocket contains large numbers of invading bacteria & host inflammatory cells (secreting proinflammatory mediators – IL-1, TNFa, PGE2 , etc).
• The periodontal tissues are very vascular & the blood vessels within the inflamed tissue are very leaky allowing periodontal bacteria (bacteraemia) & the inflammatory mediators to spill over into the systemic bloodstream

Question 2

How could Perio & Systemic disease possibly be linked?

Answer 2

It is the leaking of the pro-inflammatory mediators &/or the periodontal bacteria into the systemic bloodstream accounts for the possible link between periodontal disease & systemic chronic disease either through:

• Rasing systemic inflammation - making any systemic chronic disease already present worse
• Direct effects of the periodontal bacteria
• Or possibly involving both of the above

Question 3

What are some Systemic Diseases possibly linked to Periodontal Disease?

Answer 3

• Diabetes
• Cardiovascular disease (CVD).
• Adverse Pregnancy outcomes

Question 4

The difficulty researching the possible links between most of these chronic conditions & periodontal disease is what?

Answer 4

They have multifactorial aetiologies, often having the same risk factors. Therefore, statistical adjustments are used to rule out the confounding effects of:

• age
• smoking
• hypertension
• diabetes
• stress
• low socio-economic status
• family histories
• triglycerides

Question 5

What are some Possible mechanisms linking CVD & Periodontal Disease?

Answer 5

• The common susceptibility model.
• Direct bacterial effects on platelets.
• Autoimmune responses.
• Invasion/uptake of bacteria into endothelial cells & macrophages.
• Inflammation.
• These pathways are complex & are not fully understood.
• Possible that these pathways may act independently or collectively

Question 6

What is the The Common Susceptibility Model?

Answer 6

• Individuals may inherit a tendency which puts them at a higher risk of developing atherosclerosis & for other chronic diseases.
• One possibility is to inherit a Hyper-inflammatory (over reactive) monocyte phenotype:
• When stimulated these monocytes produce excessive amounts of pro-inflammatory cytokines leading to increased systemic inflammation
• This excessive production of pro-inflammatory mediators exacerbates CVD particularly if other predisposing factors are present:
• Smoking
• hypertenstion
• Triglycerides
• Periodontal disease may be one of a number of chronic diseases that cause the systemic release of excessive quantities of damaging pro-inflammatory mediators which exacerbates CVD.
• Thus, if you successfully treatment the Periodontal disease you do not “cure” the CVD.

Question 7

What is the Direct bacterial effects on platelets?

Answer 7

• Certain surface proteins on some oral bacteria (Streptococcus sanguis & P.gingivalis) mimic the host receptors that trigger thrombus formation within the vascular system.
• Thus, if these oral bacteria enter the blood stream they may trigger inappropriate blood clotting leading to MI and strokes.

Question 8

What is the Autoimmune responses?

Answer 8

• Some periodontal pathogens can cause a cross reaction (molecular mimicry) which causes the host to produce antibodies against itself leading to damage to the host cells.
• Evidence that oral bacteria can cause damage to vessels by this process.

Question 9

What is the Invasion/uptake of bacteria into endothelial cells & macrophages?

Answer 9

• Periodontal pathogens can invade blood vessel walls (vascular endothelial cells) & contribute to atherosclerotic plaque formation.
• Reported that P.gingivalis was detected in 100% of atherosclerotic plaques from carotid endarterectomy samples (Ford PJ et al.2005). F.nucleatum & T.forsythia were found in 80% of samples.

Question 10

What is the Systemic Inflammation?

Answer 10

Periodontal inflammation leads to the systemic release of pro-inflammatory mediators (IL-1, IL-6, TNFα, etc) which causes damage to the vascular tissues leading to atherosclerosis