Dentistry Lecture 1 -- Periodontal Disease and Heart Disease Flashcards
Define periodontal disease
Chronic inflammatory disease that destroys bone and gum tissues that support the teeth.
What is the major cause of adult tooth loss
Periodontal disease (affects nearly 75% of Americans)
Describe healthy gingiva
Very light coloured tissue with nice architecture hugging teeth
No swelling and obvious inflammatory signs
May have stippling (orange peeling look); fibrous tissue.
Why does healthy gingiva have a pink-ish appearance?
Keratinized epithelial layer with blood vessels underneath
Healthy bone architecture
Radiograph = 2/3 tooth embedded in bone; 1/3 seen outside
What does diseased gingiva look like?
Inflammation (swelling, purulence, edema, probably higher temperature)
Proliferating epithelium.
Periodontitis bone architecture
Reduction in bone level ( less than 2/3 tooth embedded in bone)
How does periodontitis begin?
Bacteria in plaque causes the gums to become inflamed
Define plaque
Sticky, colorless film that constantly forms on your teeth
How exactly does plaque cause periodontitis?
Plaque is usually blocked by epithelial cells, but inside sulcus, no keratin (no more than 2 or 3 cell layers at best) so not a great barrier –> ulceration due to inflammation –> penetration into connective tissue (rely on inflammatory process to counter, but attack is happening ALL THE TIME) –> loss of connective tissue and bone
Define gingivitis
The mildest form of periodontal disease = red, swollen gums that bleed easily but usually has little or no discomfort at this stage
Periodontitis Symptoms (11)
Periodontal pocket formation Destruction of alveolar bone and periodontal ligament Tissue recession Tooth mobility and drifting Halitosis Tooth loss Edema (shiny gums) Suppuration Bleeding on probing Surface ulceration
Define periodontitis
An infectious and inflammatory disease characterized by:
Increased probing depths
Loss of alveolar bone
Loss of clinical attachment
Goal of periodontal therapy
Remove from the tooth and root surfaces all elements – microbiologic or other – that may provoke inflammation and prevent the reestablishment of periodontal health
Periodontal treatment examples
Scaling and root planing (surgical or non-surgical)
NOTE: gums may recede post intervention due to hugging the bone, which has been lost
Safe pocket depth
1 - 3 mm
Caution pocket depth
3 - 5 mm
Dangerous pocket depth
5 - 7 mm
Risk of coronary artery disease in relation to periodontal disease
People with periodontal disease are almost twice as likely to have coronary artery disease
Explain the general logic for claiming that periodontal disease is linked to coronary heart disease
Microbes + genetic susceptibility, smoking and other factors lead to coronary heart disease and CVD AND periodontal disease and dental caries.
Dental disease leads to tooth loss –> poor chewing ability and therefore compromised diet and nutritional status, which contributes to becteremia and systemic inflammation. This ALSO leads to atherosclerosis/thrombosis –> coronary heart disease and CVD
Virulence factors that are released and disseminated systemically as a response to periodontal disease
Cytotoxins Proteases Hemaglutinins Lipopolysaccharides Peptidoglycan
Explain the systemic response to disseminated virulence factors
Leucocytes, endothelial cells and hepatocytes secrete pro-inflamamtory immunte mediators (cytokines, chemokines, CRP…)
Explain the consequence of continued exposure to virulence factors
Soluble antigens react with circulating specific antibody to form immune complexes that further amplify inflammation and sites of deposition
Inflammation markers produced locally in the inflamed gingival tissues
IL-1b
IL-6
TNF-a
PGE2
Effect of pro-inflammatory cytokines in circulation
Induce leucocytosis and acute-phase proteins
Examples of acute-phase reactants (8)
CRP Serum amyloid A Protein Fibrinogen Plasminogen activator inhibitor 1 Complement proteins LBP Soluble CD14
Potential consequence of gingival inflammatory products spilling into the circulation
Systemic impact, such as induction of endothelial dysfunction
TNF-a role in periodontitis
PMN chemoatractant
Stimulates macrophages to produce cytokines
Stimulates osteoclastic activity
TNF-a role in diabetes
Blocks insulin receptprs –> insulin resistance
Mobilize adipocyte lipids
TNF-a autocrine role
Regulation of adipose glucose uptake and lipid synthesis
IL-1B role in periodontitis
Capillary wall permeability
Stimulate collagenase production
Stimulate osteoclastic activity
IL-1B role in diabetes
Capillary wall permeability
Directly cause B-cell death
Stimulate liver to produce CRP and complement
IL-1B autocrine role
Up-regulate adipocyte COX-2 inflammatory pathway
PGE2 role in periodontitis
Small vessel dilation
Stimulate osteoclast differentiation
PGE2 role in diabetes
Small vessel dilation
Contribute to adipose tissue formation
Marker for adipose tissue inflammation
PGE2 autocrine role
Regulate osteoblasts in physiologic bone repair
Regulate adipocyte lypolysis and leptin release
Down-regulate monocyte MMP-1 and MMP-9 production
Representative surface area equivalent for the degree of endotoxemia in severe cases of periodontitis
The palm of a hand
Most biologically plausible mechanism to explain how periodontal disease is linked to cardiac disease
Chronic oral infection periodontitis leads to entry of bacteria (or their products) into the blood stream
Effect of bacteria of oral origin entering the blood stream
Activation of the host inflammatory response by multiple mechanisms –> favors atheroma formation, maturation and exacerbation
Define infection in the context of periodontitis
Inflammatory processes induced by a microbial biofilm
Define metastatic infection in the context of periodontitis
Simple acts of tooth brushing and eating –> bacteremia disseminating whole bacteria and their products and toxins such as LPS
Define inflammation in the context of periodontitis
Infection of the periondontal pocket can lead to systemic inflammatory responses beyond the periodontium
Sites of CRP production
Mainly in liver
Adipocytes
Vascular smooth muscle cells
Gingival tissues**
When is CRP produced?
In response to a rise in interleukin (IL)-6 and TNF-a
Serum levels in CP, aggressive perio, CVD + CP, and post-therapy
CP = increased
Aggressive = increased
CVD + CP = more than either disease alone
Therapy = decrease
Effect of periodontal therapy on CRP levels
Reduction of CRP marker to normal or low CVD risk levels following periodontal therapy
Define endothelial dysfunction
Impairment of endothelial function and integrity, which occurs during early stage of atherosclerosis and its progression.
What can endothelial dysfunction predict?
Adverse CVD events and long-term outcomes
Effect of periodontal treatment on endothelial-dependent function
6 months post-therapy, absolute difference of 2.0%
Positive consistent effect in improvement of endothelial-dependent function
Circulating pro-inflammatory cytokine concentrations in patients with periodontitis, and CVD + perio
Perio = higher than controls
CVD + perio = significantly higher compared to CVD only
Effect of periodontal therapy on cytokine levels in gingival crevicular fluid
Significant reduction in levels of IL-1B and IL-8. However, no other significant effect is observed on serum cytokine levels
Serum levels of fibrinogen in CP
Increased
Serum levels of fibrinogen with advanced perio disease following full-mouth extraction
Decrease
Serum levels of fibrinogen following perio therapy
Decrease (however, limited evidence to support as a biomarker for being effected by perio therapy)
Serum levels in patients with CVD + CP
Higher than compared to either condition alone
Serum LDL in CP patients
Higher than controls
Oxidized LDL in CP patients
Higher than controls
Small dense LDL in chronic and aggressive perio patients
Higher than controls
What does porphyromonas gingivalis induce in the presence of exogenous LDL?
In vitro foam cell formation
Result of trials reviewed comparing serum lipid concentrations after perio therapy
More than one-third of trials reported an improvement in serum lipid concentrations post-therapy (reduction in TC in some, increase in HDL levels in others)
Periodontitis and atherosclerotic CVD: consensus report of the joint EFP/AAP workshop on periodontitis and systemic diseases: Moderate evidence shows that periodontal treatment… (3)
1) Reduces systemic inflammation as evidenced by reduction in CRP and improvement of both clinical and surrogate measures of endothelial function
2) No effect on lipid profiles
3) Limited evidence = improvements in coagulation, biomarkers or endothelial cell activation, arterial BP and subclinical atherosclerosis
