Dentistry Lecture 1 -- Periodontal Disease and Heart Disease Flashcards Preview

Block C - Circulation > Dentistry Lecture 1 -- Periodontal Disease and Heart Disease > Flashcards

Flashcards in Dentistry Lecture 1 -- Periodontal Disease and Heart Disease Deck (61):
1

Define periodontal disease

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

2

What is the major cause of adult tooth loss

Periodontal disease (affects nearly 75% of Americans)

3

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.

4

Why does healthy gingiva have a pink-ish appearance?

Keratinized epithelial layer with blood vessels underneath

5

Healthy bone architecture

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

6

What does diseased gingiva look like?

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

7

Periodontitis bone architecture

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

8

How does periodontitis begin?

Bacteria in plaque causes the gums to become inflamed

9

Define plaque

Sticky, colorless film that constantly forms on your teeth

10

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

11

Define gingivitis

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

12

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

13

Define periodontitis

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

14

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

15

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

16

Safe pocket depth

1 - 3 mm

17

Caution pocket depth

3 - 5 mm

18

Dangerous pocket depth

5 - 7 mm

19

Risk of coronary artery disease in relation to periodontal disease

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

20

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

21

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

Cytotoxins
Proteases
Hemaglutinins
Lipopolysaccharides
Peptidoglycan

22

Explain the systemic response to disseminated virulence factors

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

23

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

24

Inflammation markers produced locally in the inflamed gingival tissues

IL-1b
IL-6
TNF-a
PGE2

25

Effect of pro-inflammatory cytokines in circulation

Induce leucocytosis and acute-phase proteins

26

Examples of acute-phase reactants (8)

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

27

Potential consequence of gingival inflammatory products spilling into the circulation

Systemic impact, such as induction of endothelial dysfunction

28

TNF-a role in periodontitis

PMN chemoatractant
Stimulates macrophages to produce cytokines
Stimulates osteoclastic activity

29

TNF-a role in diabetes

Blocks insulin receptprs --> insulin resistance
Mobilize adipocyte lipids

30

TNF-a autocrine role

Regulation of adipose glucose uptake and lipid synthesis

31

IL-1B role in periodontitis

Capillary wall permeability
Stimulate collagenase production
Stimulate osteoclastic activity

32

IL-1B role in diabetes

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

33

IL-1B autocrine role

Up-regulate adipocyte COX-2 inflammatory pathway

34

PGE2 role in periodontitis

Small vessel dilation
Stimulate osteoclast differentiation

35

PGE2 role in diabetes

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

36

PGE2 autocrine role

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

37

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

The palm of a hand

38

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

39

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

40

Define infection in the context of periodontitis

Inflammatory processes induced by a microbial biofilm

41

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

42

Define inflammation in the context of periodontitis

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

43

Sites of CRP production

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

44

When is CRP produced?

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

45

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

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

46

Effect of periodontal therapy on CRP levels

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

47

Define endothelial dysfunction

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

48

What can endothelial dysfunction predict?

Adverse CVD events and long-term outcomes

49

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

50

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

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

51

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

52

Serum levels of fibrinogen in CP

Increased

53

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

Decrease

54

Serum levels of fibrinogen following perio therapy

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

55

Serum levels in patients with CVD + CP

Higher than compared to either condition alone

56

Serum LDL in CP patients

Higher than controls

57

Oxidized LDL in CP patients

Higher than controls

58

Small dense LDL in chronic and aggressive perio patients

Higher than controls

59

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

In vitro foam cell formation

60

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)

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)

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