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

Dentistry Lecture 1 -- Periodontal Disease and Heart Disease Flashcards

1
Q

Define periodontal disease

A

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

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2
Q

What is the major cause of adult tooth loss

A

Periodontal disease (affects nearly 75% of Americans)

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3
Q

Describe healthy gingiva

A

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

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4
Q

Why does healthy gingiva have a pink-ish appearance?

A

Keratinized epithelial layer with blood vessels underneath

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5
Q

Healthy bone architecture

A

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

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6
Q

What does diseased gingiva look like?

A

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

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7
Q

Periodontitis bone architecture

A

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

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8
Q

How does periodontitis begin?

A

Bacteria in plaque causes the gums to become inflamed

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9
Q

Define plaque

A

Sticky, colorless film that constantly forms on your teeth

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10
Q

How exactly does plaque cause periodontitis?

A

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

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11
Q

Define gingivitis

A

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

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12
Q

Periodontitis Symptoms (11)

A 
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
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13
Q

Define periodontitis

A

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

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14
Q

Goal of periodontal therapy

A

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

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15
Q

Periodontal treatment examples

A

Scaling and root planing (surgical or non-surgical)

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

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16
Q

Safe pocket depth

A

1 - 3 mm

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17
Q

Caution pocket depth

A

3 - 5 mm

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18
Q

Dangerous pocket depth

A

5 - 7 mm

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19
Q

Risk of coronary artery disease in relation to periodontal disease

A

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

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20
Q

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

A

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

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21
Q

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

A 
Cytotoxins
Proteases
Hemaglutinins
Lipopolysaccharides
Peptidoglycan
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22
Q

Explain the systemic response to disseminated virulence factors

A

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

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23
Q

Explain the consequence of continued exposure to virulence factors

A

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

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24
Q

Inflammation markers produced locally in the inflamed gingival tissues

A

IL-1b
IL-6
TNF-a
PGE2

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25
Q

Effect of pro-inflammatory cytokines in circulation

A

Induce leucocytosis and acute-phase proteins

26
Q

Examples of acute-phase reactants (8)

A 
CRP
Serum amyloid A
Protein
Fibrinogen
Plasminogen activator inhibitor 1
Complement proteins
LBP
Soluble CD14
27
Q

Potential consequence of gingival inflammatory products spilling into the circulation

A

Systemic impact, such as induction of endothelial dysfunction

28
Q

TNF-a role in periodontitis

A

PMN chemoatractant
Stimulates macrophages to produce cytokines
Stimulates osteoclastic activity

29
Q

TNF-a role in diabetes

A

Blocks insulin receptprs –> insulin resistance

Mobilize adipocyte lipids

30
Q

TNF-a autocrine role

A

Regulation of adipose glucose uptake and lipid synthesis

31
Q

IL-1B role in periodontitis

A

Capillary wall permeability
Stimulate collagenase production
Stimulate osteoclastic activity

32
Q

IL-1B role in diabetes

A

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

33
Q

IL-1B autocrine role

A

Up-regulate adipocyte COX-2 inflammatory pathway

34
Q

PGE2 role in periodontitis

A

Small vessel dilation

Stimulate osteoclast differentiation

35
Q

PGE2 role in diabetes

A

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

36
Q

PGE2 autocrine role

A

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

37
Q

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

A

The palm of a hand

38
Q

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

A

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

39
Q

Effect of bacteria of oral origin entering the blood stream

A

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

40
Q

Define infection in the context of periodontitis

A

Inflammatory processes induced by a microbial biofilm

41
Q

Define metastatic infection in the context of periodontitis

A

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

42
Q

Define inflammation in the context of periodontitis

A

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

43
Q

Sites of CRP production

A

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

44
Q

When is CRP produced?

A

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

45
Q

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

A

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

46
Q

Effect of periodontal therapy on CRP levels

A

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

47
Q

Define endothelial dysfunction

A

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

48
Q

What can endothelial dysfunction predict?

A

Adverse CVD events and long-term outcomes

49
Q

Effect of periodontal treatment on endothelial-dependent function

A

6 months post-therapy, absolute difference of 2.0%

Positive consistent effect in improvement of endothelial-dependent function

50
Q

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

A

Perio = higher than controls

CVD + perio = significantly higher compared to CVD only

51
Q

Effect of periodontal therapy on cytokine levels in gingival crevicular fluid

A

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

52
Q

Serum levels of fibrinogen in CP

A

Increased

53
Q

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

A

Decrease

54
Q

Serum levels of fibrinogen following perio therapy

A

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

55
Q

Serum levels in patients with CVD + CP

A

Higher than compared to either condition alone

56
Q

Serum LDL in CP patients

A

Higher than controls

57
Q

Oxidized LDL in CP patients

A

Higher than controls

58
Q

Small dense LDL in chronic and aggressive perio patients

A

Higher than controls

59
Q

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

A

In vitro foam cell formation

60
Q

Result of trials reviewed comparing serum lipid concentrations after perio therapy

A

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
Q

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

A

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

Block C - Circulation (26 decks)

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