Dentistry Lecture 1 -- Periodontal Disease and Heart Disease

Question 1

Define periodontal disease

Answer 1

Chronic inflammatory disease that destroys bone and gum tissues that support the teeth.

Question 2

What is the major cause of adult tooth loss

Answer 2

Periodontal disease (affects nearly 75% of Americans)

Question 3

Describe healthy gingiva

Answer 3

Very light coloured tissue with nice architecture hugging teeth
No swelling and obvious inflammatory signs
May have stippling (orange peeling look); fibrous tissue.

Question 4

Why does healthy gingiva have a pink-ish appearance?

Answer 4

Keratinized epithelial layer with blood vessels underneath

Question 5

Healthy bone architecture

Answer 5

Radiograph = 2/3 tooth embedded in bone; 1/3 seen outside

Question 6

What does diseased gingiva look like?

Answer 6

Inflammation (swelling, purulence, edema, probably higher temperature)
Proliferating epithelium.

Question 7

Periodontitis bone architecture

Answer 7

Reduction in bone level ( less than 2/3 tooth embedded in bone)

Question 8

How does periodontitis begin?

Answer 8

Bacteria in plaque causes the gums to become inflamed

Question 9

Define plaque

Answer 9

Sticky, colorless film that constantly forms on your teeth

Question 10

How exactly does plaque cause periodontitis?

Answer 10

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

Question 11

Define gingivitis

Answer 11

The mildest form of periodontal disease = red, swollen gums that bleed easily but usually has little or no discomfort at this stage

Question 12

Periodontitis Symptoms (11)

Answer 12

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

Question 13

Define periodontitis

Answer 13

An infectious and inflammatory disease characterized by:
Increased probing depths
Loss of alveolar bone
Loss of clinical attachment

Question 14

Goal of periodontal therapy

Answer 14

Remove from the tooth and root surfaces all elements – microbiologic or other – that may provoke inflammation and prevent the reestablishment of periodontal health

Question 15

Periodontal treatment examples

Answer 15

Scaling and root planing (surgical or non-surgical)

NOTE: gums may recede post intervention due to hugging the bone, which has been lost

Question 16

Safe pocket depth

Answer 16

1 - 3 mm

Question 17

Caution pocket depth

Answer 17

3 - 5 mm

Question 18

Dangerous pocket depth

Answer 18

5 - 7 mm

Question 19

Risk of coronary artery disease in relation to periodontal disease

Answer 19

People with periodontal disease are almost twice as likely to have coronary artery disease

Question 20

Explain the general logic for claiming that periodontal disease is linked to coronary heart disease

Answer 20

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

Question 21

Virulence factors that are released and disseminated systemically as a response to periodontal disease

Answer 21

Cytotoxins
Proteases
Hemaglutinins
Lipopolysaccharides
Peptidoglycan

Question 22

Explain the systemic response to disseminated virulence factors

Answer 22

Leucocytes, endothelial cells and hepatocytes secrete pro-inflamamtory immunte mediators (cytokines, chemokines, CRP…)

Question 23

Explain the consequence of continued exposure to virulence factors

Answer 23

Soluble antigens react with circulating specific antibody to form immune complexes that further amplify inflammation and sites of deposition

Question 24

Inflammation markers produced locally in the inflamed gingival tissues

Answer 24

IL-1b
IL-6
TNF-a
PGE2

Question 25

Effect of pro-inflammatory cytokines in circulation

Answer 25

Induce leucocytosis and acute-phase proteins

Question 26

Examples of acute-phase reactants (8)

Answer 26

``` CRP Serum amyloid A Protein Fibrinogen Plasminogen activator inhibitor 1 Complement proteins LBP Soluble CD14 ```

Question 27

Potential consequence of gingival inflammatory products spilling into the circulation

Answer 27

Systemic impact, such as induction of endothelial dysfunction

Question 28

TNF-a role in periodontitis

Answer 28

PMN chemoatractant Stimulates macrophages to produce cytokines Stimulates osteoclastic activity

Question 29

TNF-a role in diabetes

Answer 29

Blocks insulin receptprs --> insulin resistance | Mobilize adipocyte lipids

Question 30

TNF-a autocrine role

Answer 30

Regulation of adipose glucose uptake and lipid synthesis

Question 31

IL-1B role in periodontitis

Answer 31

Capillary wall permeability Stimulate collagenase production Stimulate osteoclastic activity

Question 32

IL-1B role in diabetes

Answer 32

Capillary wall permeability Directly cause B-cell death Stimulate liver to produce CRP and complement

Question 33

IL-1B autocrine role

Answer 33

Up-regulate adipocyte COX-2 inflammatory pathway

Question 34

PGE2 role in periodontitis

Answer 34

Small vessel dilation | Stimulate osteoclast differentiation

Question 35

PGE2 role in diabetes

Answer 35

Small vessel dilation Contribute to adipose tissue formation Marker for adipose tissue inflammation

Question 36

PGE2 autocrine role

Answer 36

Regulate osteoblasts in physiologic bone repair Regulate adipocyte lypolysis and leptin release Down-regulate monocyte MMP-1 and MMP-9 production

Question 37

Representative surface area equivalent for the degree of endotoxemia in severe cases of periodontitis

Answer 37

The palm of a hand

Question 38

Most biologically plausible mechanism to explain how periodontal disease is linked to cardiac disease

Answer 38

Chronic oral infection periodontitis leads to entry of bacteria (or their products) into the blood stream

Question 39

Effect of bacteria of oral origin entering the blood stream

Answer 39

Activation of the host inflammatory response by multiple mechanisms --> favors atheroma formation, maturation and exacerbation

Question 40

Define infection in the context of periodontitis

Answer 40

Inflammatory processes induced by a microbial biofilm

Question 41

Define metastatic infection in the context of periodontitis

Answer 41

Simple acts of tooth brushing and eating --> bacteremia disseminating whole bacteria and their products and toxins such as LPS

Question 42

Define inflammation in the context of periodontitis

Answer 42

Infection of the periondontal pocket can lead to systemic inflammatory responses beyond the periodontium

Question 43

Sites of CRP production

Answer 43

Mainly in liver Adipocytes Vascular smooth muscle cells Gingival tissues**

Question 44

When is CRP produced?

Answer 44

In response to a rise in interleukin (IL)-6 and TNF-a

Question 45

Serum levels in CP, aggressive perio, CVD + CP, and post-therapy

Answer 45

CP = increased Aggressive = increased CVD + CP = more than either disease alone Therapy = decrease

Question 46

Effect of periodontal therapy on CRP levels

Answer 46

Reduction of CRP marker to normal or low CVD risk levels following periodontal therapy

Question 47

Define endothelial dysfunction

Answer 47

Impairment of endothelial function and integrity, which occurs during early stage of atherosclerosis and its progression.

Question 48

What can endothelial dysfunction predict?

Answer 48

Adverse CVD events and long-term outcomes

Question 49

Effect of periodontal treatment on endothelial-dependent function

Answer 49

6 months post-therapy, absolute difference of 2.0% | Positive consistent effect in improvement of endothelial-dependent function

Question 50

Circulating pro-inflammatory cytokine concentrations in patients with periodontitis, and CVD + perio

Answer 50

Perio = higher than controls | CVD + perio = significantly higher compared to CVD only

Question 51

Effect of periodontal therapy on cytokine levels in gingival crevicular fluid

Answer 51

Significant reduction in levels of IL-1B and IL-8. However, no other significant effect is observed on serum cytokine levels

Question 52

Serum levels of fibrinogen in CP

Answer 52

Increased

Question 53

Serum levels of fibrinogen with advanced perio disease following full-mouth extraction

Answer 53

Decrease

Question 54

Serum levels of fibrinogen following perio therapy

Answer 54

Decrease (however, limited evidence to support as a biomarker for being effected by perio therapy)

Question 55

Serum levels in patients with CVD + CP

Answer 55

Higher than compared to either condition alone

Question 56

Serum LDL in CP patients

Answer 56

Higher than controls

Question 57

Oxidized LDL in CP patients

Answer 57

Higher than controls

Question 58

Small dense LDL in chronic and aggressive perio patients

Answer 58

Higher than controls

Question 59

What does porphyromonas gingivalis induce in the presence of exogenous LDL?

Answer 59

In vitro foam cell formation

Question 60

Result of trials reviewed comparing serum lipid concentrations after perio therapy

Answer 60

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)

Question 61

Periodontitis and atherosclerotic CVD: consensus report of the joint EFP/AAP workshop on periodontitis and systemic diseases: Moderate evidence shows that periodontal treatment... (3)

Answer 61

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