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DENT 318 - Periodontology > Etiology, Contributing Factors and Link to Systemic Disease > Flashcards

Etiology, Contributing Factors and Link to Systemic Disease Flashcards

1
Q

Define risk factor

A

A characteristic that places and individual at increased risk of contracting a disease

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2
Q

Define risk indicator

A

A probable or putative risk factor that has been identified in cross-sectional correlation studies but not confirmed through longitudinal studies

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3
Q

4 risk factors for periodontitis

A
  • Diabetes
  • Inadequate oral hygiene
  • Genetics
  • Smoking
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4
Q

8 risk indicators for periodontitis

A
  • Socio-economic status
  • Obesity
  • Stress
  • Age
  • Contraceptives
  • Alcohol
  • Race
  • Sex
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5
Q

Define etiology

A

The study or theory of the causation of a disease

A single or a cluster of factors that contribute to disease

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6
Q

Role of bacterial plaque in periodontal disease

A

Necessary but not sufficient to cause disease

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7
Q

Primary etiologic factor of periodontitis

A

Microbial plaque

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8
Q

Secondary etiologic factor of periodontitis

A

Calculus (most significant local contributing factor)

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9
Q

3 characteristics of bacteria related to health

A
  • Gram positive
  • Facultatives anaerobes
  • Generally non motile

i.e. streptococcus anguis and mitus, actinomyces viscosus, israelli and naeslundi

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10
Q

3 characteristics of bacteria related to disease

A
  • Gram negative
  • Strict anaerobes
  • Motile & non-motile forms
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11
Q

What is the pathogenic potential of calculus?

A
  • Plaque retention
  • Production of an inflammatory reaction in the tissue
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12
Q

3 bacterial species in the red category

A
  • P. gingivalis
  • T. forsythensis
  • T. denticola
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13
Q

11 local and anatomical factors contributing to periodontal disease

A
  • Root morphology
  • Furcation
  • Cervico-enamel projections (CEP)
  • Enamel pearls
  • Palatogingival grooves
  • Root proximity
  • Food impaction/open contacts
  • Marginal ridge discrepancy (plunger cusp)
  • Restorations (quality of restorative margins, contours, curvatures, etc)
  • Position of tooth
  • Caries
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14
Q

Anatomic variation of furcation that creates a protected environment for plaque and calculus collection

A

Internal intra-radicular root concavities

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15
Q

Significance of accessory canals for periodontal disease

A

Communication between the pulp and the furcation

Endo-perio or perio-endo lesions

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16
Q

How do cervico-enamel projections contribute to periodontal disease?

A

Acts like a pathway for transferring the plaque to the furcation

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17
Q

Define enamel pearls

A

Localized masses of enamel that develop ectopically, typically over the root surfaces in close proximity to the CEJ

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18
Q

How do open contacts contribute to periodontal disease?

A

Food impaction

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19
Q

Define palato-gingival groove

A

Groove in the enamel of the tooth leading into the gingiva. Site of bacterial and plaque accumulation.

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20
Q

7 systemic factors contributing to periodontal disease

A
  • Smoking
  • Stress
  • Medical conditions
  • Medications
  • Genetics
  • Age
  • Sex
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21
Q

4 effects of smoking on periodontium

A
  • Increases the prevalence and severity of destruction
  • Increase in PD, CAL and bone loss
  • Increased rate of destruction
  • Increased number of tooth loss

NOTE: These negative effects are cumulative over time with increased smoking. However, these same effects will decrease with cessation

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22
Q

Mechanism of periodontitis associated with diabetes

A
  • Altered neutrophil response
  • Upregulation of monocutes –> hyper-inflammatory response
  • AGE-RAGE interaction may lead to increased production of inflammatory cytokines in the diabetic patient
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23
Q

Earlier theory of etiology of periodontal disease (5 points)

A
  • All individuals are equally susceptible to periodontitis
  • Always starts with gingivitis and if not treated will progress to periodontitis
  • As people age the chances of getting periodontitis goes higher
  • Plaque, calculus and other local factors are the only contributors to periodontal disease
  • NO ROLE OF HOST SUSCEPTIBILITY
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24
Q

Today’s theory of etiology of periodontal disease

A
  • Not all individuals are equally susceptible to periodontal disease
  • Gingivities doesn’t always progress to periodontitis
  • Prevalence and severity of periodontal disease increased with age but susceptibility to future periodontal disease is not dependent upon age
  • Systemic and environmental factors play a role in progression of the disease
  • BUT HOST SUSCEPTIBILITY PLAYS A MAJOR ROLE
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25
Q

Define the non-specific plaque hypothesis

A

Periodontal disease results from the “elaboration of noxious products by the entire plaque flora”. If small amounts of plaque are present, the noxious products are neutralized by the host. But if large amounts are present, this overwhelms the host’s defenses.

The control of periodontal disease depends on control of the amount of plaque accumulation

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26
Q

Define the specific plaque hypothesis

A
  • Only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganisms
  • Acceptance of this hypothesis was spurred by the recognition of a.a. as a pathogen in localized aggressive periodontitis
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27
Q

Define biofilm

A

Multi-species community of microorganisms that adhere to each other and a surface, and are encased in an extracellular matrix

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28
Q

Define virulence factor

A

The unique properties which permit a bacterial species to colonize a target organ, defend itself from the host and cause tissue damage

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29
Q

2 categories of virulence factors

A
  1. Factors favoring bacterial adherence and colonization
  2. Factors which mediate host tissue destruction
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30
Q

Adherence factors of subgingival species

A

Adhesions including fimbriae and cell-associated proteins

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31
Q

Define lipopolysaccharides

A

Large molecules composed of a lipid component (lipid A) and a polysaccharide component. They are found in the outer membrane of gram-negative bacteria. Act as andotoxins and elicit strong immune responses.

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32
Q

5 host defense mechanisms that must be overcome to induce periodontitis

A
  • Salivary and gingival crevicular fluid flow
  • Mechanical displacement (i.e. tissue desquamation)
  • Specific antibodies
  • Host products (i.e. glycoproteins that block bacterial cell binding)
  • Cells of the immune system
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33
Q

2 bacterial mechanisms that may mediate host tissue damage

A
  • Invasion of the tissue by pathogens
  • Diffusion of bacterial byproducts from the crevice into the gingival tissues
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34
Q

4 examples of bacterial byproducts that may diffuse from the crvice into the gingival tissues to mediate host tissue damage

A
  • Ammonia (NH)
  • Hydrogen sulfide (HS)
  • Short-chain carboxylic acids (i.e. butyric acid and propionic acid)
  • Proteases
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35
Q

Define yellow complex bacteria

A

Early colonizers; most associated with caries formation

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36
Q

Complexes that include microorganisms primarily considered to be secondary colonizers

A

Green, orange or red

37
Q

Complex associated with bleeding probing

A

Red complex

38
Q

Describe the bacterial properties of P. gingivalis

A

Gram negative, rod-shaped, anaerobic

39
Q

5 virulence factors of P. gingivalis that make it an aggressive periodontal pathogen

A
  • Fimbriae –> adhesion
  • Capsule –> protection against phagocytic cells
  • Proteases
  • Hemolysin
  • Collagenase
40
Q

Describe how P. gingivalis is virulent

A

Can inhibit the migration of PMN’s across an epithelial barrier and affects production or degradation of cytokines by mammalian cells. Has the capacity to invade soft tissues

41
Q

Describe the bacterial properties of T. Forsythia

A

Anaerobic, gram-negative nonmotile, spindle-shaped pathogen

42
Q

2 virulence factors of T. forsythia

A
  • Proteolytic enzymes that destroy immunoglobulins and factors of the complement system
  • Induces apoptotic cell death
43
Q

Describe the bacterial properties of T. denticula

A
  • Gram-negative
  • Obligate anaerobe
  • Motile
  • Highly protelytic spichete bacterium
44
Q

4 virulence factors of T. denticula

A
  • Produces proteolytic enzymes that can destroy Ig’s (IgA, IgM, IgG) or complement factors
  • Has capacity to destroy collagen
  • Has ability to travel through viscous media and tissue
  • Can pass through GCF and penetrate gingival epithelium and connective tissue
45
Q

Describe the bacterial properties of aggregatibacter actinomycetemcomitans

A
  • Gram-negative
  • Facultative nonmotile
  • Rod-shaped
46
Q

5 virulence factors of aggregatibacter actinomycetemcomitans

A
  • Very tissue invasive
  • Lipopolysaccharide cell wall: endotoxin
  • Leukotoxin
  • Collagenase
  • Proteases that destroy IgG
47
Q

Define leukotoxin

A

Toxin which creates micro-pores in PMNs, monocytes and some lymphocytes and causes their cell deaths

48
Q

What does the majority of the tissue damage in periodontitis derive from?

A

The excessive and dysregulated production of a variet of inflammatory mediators and destructive enzymes in response to the presnece of the subgingival plaque bacteria

49
Q

3 key types of mediators of tissue destruction in periodontitis

A
  • Cytokines
  • Prostanoids
  • Matrix metalloproteinases (MMPs)
50
Q

2 cytokines that play a key role in the initiation, regulation and perpetuation of innate immune responses in the periodontium

A

IL-1B

TNF-a

51
Q

3 prostanoids

A
  • PGs
  • Thromboxanes
  • Prostacyclins
52
Q

Effect of PGE2

A

Vasodilation and induction of cytokine production by a variety of cel types

53
Q

3 upregulators of COX-2

A

IL-1B

TNF-a

Bacterial LPS

54
Q

Result of upregulation of COX-2

A

Increased production of PGE2 in inflamed tissues

55
Q

2 cell types that produce PGE2 in the periodontium

A

Macrophages

Fibroblasts

56
Q

Effect of PGE2 production

A

Induction of MMPs and osteoclastic bone resorption. Major role in contributing ot the tissue damage that characterizes periodontitis

57
Q

Define MMPs

A

A family of proteolytic enzymes that degrade extracellular matrix molecules such as collagen, gelatin, and elastin

58
Q

6 cell types that produce MMPs

A
  • Neutrophils
  • Macrophages
  • Fibroblasts
  • Epithelial cells
  • Osteoblasts
  • Osteoclasts
59
Q

4 histologic stages of gingivitis and periodontitis

A
  • Initial lesion
  • Early lesion
  • Established lesion
  • Advanced lesion
60
Q

3 characteristics of the initial lesion

A

Clinically healthy gingival tissue:

  • Slightly elevated vascular permeability and vasodilation
  • GCF flows out of the sulcus
  • Migration of leukocytes, primarily neutrophils, in relatively small numbers through the gingival connective tissue, accross the junctional epithelum and into the sulcus
61
Q

5 characteristics of the early lesion

A

Corresponds to early gingivitis that is evident clinically:

  • Increased vascular permeability, vasodilation, and GCF flow
  • Large numbers of infiltrating leukocytes
  • Degeneration of fibroblasts
  • Collagen destruction –> collagen depleted areas of connective tissue
  • Proliferation of the junctional and sulcular epithelium into collagen-depleted areas
62
Q

2 main leukocytes present in early lesion

A

Neutrophils and lymphocytes

63
Q

5 characteristics of established lesion

A

Corresponds to established, chronic gingivitis

  • Dense inflammatory cell infiltrate
  • Accumulation of inflammatory cells in the connective tissues
  • Elevated release of MMPs and lysosomal contents from neutrophils
  • Significant collagen depletion and proliferation of epithelium
  • Formation of pocket epithelium containing large numbers of neutrophils
64
Q

3 cell types in the inflammatory cell infiltrate of the established lesion

A

Plasma cells, lymphocytes and neutrophils

65
Q

5 characteristics of the advanced lesion

A

Marks the transition from gingivitis to periodontitis

  • Predominance of neutrophils in the pocket epithelium and in the pocket
  • Dense inflammatory cell infiltrate in the connective tissues
  • Apical migration of junctional epithelium to preserve intact epithelial barrier
  • Continued collagen breakdown –> large areas of collagen depleted connective tissue
  • Osteoclastic resorption of alveolar bone
66
Q

Primary cell type in inflammatory cell infiltrate of the advanced lesion

A

Plasma cells

67
Q

Body’s first response to injury

A

Inflammation

68
Q

5 characteristics of acute inflammation

A
  • Redness
  • Swelling
  • Heat
  • Altered function
  • Self-perpetuating
69
Q

One important inflammation marker found in the blood

A

C-reactive protein (CRP)

70
Q

Significance of elevated CRP

A

It’s a risk factor for several chronic inflammatory diseases

71
Q

3 diseases of aging for which inflammation appears to be a common link

A

Heart disease

Arthritis

Periodontitis

72
Q

Purpose of inflammation

A

To contain the injury to the local site in an immediate reaction in order to protect the body from further damage

73
Q

When does chronic inflammation occur?

A

When there is sustained infection (i.e. periodontitis)

74
Q

How does periodontitis affect your general systemic health?

A

It is a significant contributor to the total inflammatory burden on your body and can adversely affect your systemic health. It shares common inflammatory processes similar to diabetes, CVD and stroke

75
Q

What is the link between periodontitis and cardiovascular disease?

A
  • Inflammation contributes to heart attacks as much as or more than cholesterol
  • Artherosclerosis always begins with injury to the endothelium of blood vessels
  • Periodontal pathogens have been found in atherosclerotic lesions
76
Q

3 distinct pathways through which gingival inflammation may influence atherosclerosis

A
  • Local inflammation processes from periodontal pockets produce micro-ulcerations through the pocket epithelium, promoting risks for distant-site infection and transient bacteremia
  • Bacteria release biologically active molecuels (i.e. LPS, endotoxins, chemotactic peptides, proteins, organic acids) that may enter the systemic circulation
  • These products can trigger the host inflammatory response and elevate serum concentrations of acute-phase reactants and inflammatory mediators
77
Q

7 inflammatory mediators that may be elevated when periodontal bacteria release biologically active molecules

A
  • CRP
  • Serum amyloid A
  • Fibrinogen
  • Haptoglobin
  • TNF-a
  • IL-6
  • IL-8
78
Q

5 inflammatory diseases with which periodontal disease has a relationship

A
  • CVD
  • Arthritis
  • Alzheimer’s Disease
  • Diabetes
  • Cancers
79
Q

Effect of chronic periodontal disease exposure on risk of developing Alzheimer’s disease

A

It quadruples the individual’s risk

80
Q

Effect of hyperglycemia on inflammation

A

Inhibition of resolution of inflammation

81
Q

Effect of CRP on insulin resistance

A

High CRP promotes insulin resistance

82
Q

Link between diabetes and likelihood of having periodontal disease

A

Patients with diabetes are 3 times more likely to have periodontal disease

83
Q

Specific interaction in diabetes that leads to the exaggerated inflammatory response and periodontal tissue destruction

A

AGE-RAGE interaction

NOTE: AGEs directly and indirectly promote inflammation

84
Q

2 cancers with a positive correlation between risk of development and presence of periodontal disease

A

Pancreatic cancer

Head and neck cancers

85
Q

Link of obesity to periodontitis

A
  • Patients with higher BMI tend to have higher levels of CRP
  • Calorie reduction –> decreased gingival bleeding and rate of periodontal disease progression
86
Q

4 inflammatory mediators associated with adverse pregnancy outcomes

A
  • IL-1
  • IL-6
  • TNF-a
  • PGE2
87
Q

3 types of systemic risk factors for periodontal disease

A
  • Biologic
  • Genetic
  • Behavioral
88
Q

3 ways genetic risk factors can be minimized

A
  • Proper diet
  • Exercise
  • Oral hygiene
89
Q

5 behavioral risk factors for periodontal disease

A
  • Poor oral hygiene
  • Smoking (specifically, nictine intake)
  • Stress
  • Sleep deprivation
  • Poor diet

DENT 318 - Periodontology (4 decks)

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