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AU 15 - Periodontology > Host Response to Periodontal Bacteria > Flashcards

Host Response to Periodontal Bacteria Flashcards

1
Q

How doe bacteria induce damage to periodontal tissues?

A

Attach, colonize the crevice, and sometimes invade
Release substances that directly damage host
Activate the host’s own inflammatory and immune systems leading to host damage

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2
Q

Which method of bacteria-induced damage does the most damage?

A

Bacteria activating the host’s own inflammatory and immune system

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3
Q

What are the different types of major microbial virulence factors?

A

Ability to invade periodontal epithelium
Metabolic waste products that have direct cytotoxic effects
Damaging bacterial enzymes
Immunostimulatory molecules

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4
Q

What are the mechanisms of periodontal defense?

A

Prevention of bacterial entry (passive)
Innate immune response
Acquired immune response

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5
Q

How does the periodontium prevent bacterial entry?

A

Shedding of epithelial cells into the oral cavity - inhibits colonization
Intact epithelial barrier that is hard to penetrate
Positive fluid flow into the gingival crevice (has the capability to shed bacterial and discourages penetration)

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6
Q

What is the structure of the endothelium and what occurs during inflammation?

A

When endothelial cells are growing, they grow until the contact another cell, and there’s a protein that maintains a tight connection
During inflammation, those proteins are lost and small gaps form increasing permeability
Fluid escapes and can clear bacteria in the epithelium

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7
Q

What are the different types of innate immune responses?

A

Complement system
Oral mucosa produces anti-microbial peptides (defensins)
Oral epithelium produces pro-inflammatory cytokines
Antimicrobial effect of antibodies, lactoferrin, lysozyme
Phagocytic function of neutrophils and macrophages

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8
Q

Adaptive or acquired immunity

A

Second line of defense
Specific response to bacterial antigens
Ag recognition, immune memory, and clonal expansion are all hallmarks of adaptive immunity

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9
Q

How does clonal expansion aid in adaptive/acquired immunity?

A

Provides the capability to produce a wide-scale release of a specific antibody

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10
Q

What is the host defense hierarchy?

A 
Serum compliment
Neutrophil
Monocyte/Macrophage
Lymphocyte
If none of these can resolve it, then you get a systemic infection
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11
Q

What parts of the mouth play a major role in innate immunity?

A

Salivary glands
Mucosa
Tongue
Crevice

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12
Q

Salivary gland contribution to innate immunity

A

Saliva has a bunch of compounds that play defensive roles, such as sIgA, Mucins, Agglutinin

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13
Q

Mucosa contribution to innate immunity of the oral cavity?

A

TLR receptors - detect features of bacteria

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14
Q

TLR receptors

A

Recognize conserved microbial-associated molecular patterns
Expressed by all cells
Signals for cells to produce cytokines, chemokines, antimicrobial peptides, nitric oxide, and eicosanoids
Essentially how the body recognizes there is an attack

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15
Q

What are the biological activities of Lipopolysaccharides (LPS - endotoxin)

A 
Complement activation
PMN activation
Macrophage activation
B-cell mitogen activity
Pyrogenicity
Stimulation of bone resorption
Stimulation of prostaglandin synthesis
Induction of Tumor necrosis factor (TNF-a)
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16
Q

What are the 2 ways to activate the complement system?

A

1) Classic - contact antibody labeled microbe

2) Alternate - contact bacterial cell walls

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17
Q

What is the role of C3b in the complement system?

A

Enhances the efficiency of phagocytosis

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18
Q

What is the role of C3a and C5a in the complement system?

A

Enhance mast cell degeneration and inflammation

Mast cells release histamine, TNF-a, nitric oxide, and IL-1 - and these things make the endothelium more leaky

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19
Q

Membrane attack complex

A

Forms during the complement pathway

Creates pores in a microbe so it lyses itself

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20
Q

What is the role of cytokines in the innate immune system?

A

Involved in the coordination of inflammatory and immune resonses

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21
Q

What cytokine(s) provide pro-inflammatory activity?

A

IL-1

TNF-a

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22
Q

What cytokine(s) provide chemotactic activity

A

IL-8

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23
Q

What is the role of prostaglandins in innate immunity?

A

Induce vasodilation and cytokine production - makes vessels leakier
PGE2 induces production of matrix metalloproteinases by fibroblasts and osteoclasts, which damage periodontal tissue

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24
Q

Where do prostaglandins come from?

A

Derived from arachidonic acid

Produced by activated macrophages and other cells

25
Q

What is the role of matrix metalloproteinases in innate immunity?

A

Degrade extracellular matrix
If the host can breakdown ECM, it can give neutrophils and macrophages better access to bacteria
Concentrations are higher in inflamed gingiva
An example is PMN collagenase (which degrades the major structural protein in the gingiva)

26
Q

What is the role of Proteinase inhibitors in innate immunity?

A

Antagonize inflammation

Inhibit degradation of matrix proteins

27
Q

What are the two major proteinase inhibitors?

A

Alpha-2 macroglobulin (broad spectrum proteinase inhibitor)

Alpha-1 antitrypsin (broad spectrum proteinase inhibitor and potent inhibitor of PMN collagenase)

28
Q

What are the major antimicrobial peptides?

A

Defensins

Calprotectin

29
Q

Defensins

A

Inhibit bacteria and fungi

Produced by salivary gland epithelium

30
Q

Calprotectin

A

Inhibit bacteria and fungi by chelating zinc

Produced by epithelium, PMNs, Monocytes, and Macrophages

31
Q

What are the cellular elements of innate immunity, and where are they found?

A

Neutrophils - deployed from the blood
Macrophages - found in organs and tissues
Mast cells - found throughout the body, especially CT subadjacent to mucosal surfaces

32
Q

What are the ways PMNs deliver antimicrobial substances to bacteria in the early stages of an infection?

A

Secretion
Respiratory burst
Phagocytois
Lysis apoptosis

33
Q

How are PMNs recruited to the gingival crevice?

A

PMNs start in circulation
Presence of plaque can be communicated to the CT by proteases, LPS, f-Met-Leu-Phe
Those things talk to macrophages, which release cytokines (TNF, IL-1)
This increases adhesion molecule expression - and these can bind to neutrophils, which then go to the site

34
Q

What is the difference between innate immunity and adaptive immunity, when it comes to pathogen specificity?

A

Innate: inherent biological responses
Adaptive: based on recognition of antigens, immune memory, and clonal expression

35
Q

In periodontitis, how do the number of cells compare?

A

Plasma cells > B lymphocytes > T lymphocytes

36
Q

Th1 cells responsibility

A

Regulate cell-mediated immunity

Release cytokines to recruit cytotoxic t-cells

37
Q

Th2 cells responsibility

A

Release cytokines that activate B cells

38
Q

B2 cells

A

Conventional
Make antibodies to respond to invaders/bacteria
Decrease in healthy and treated sites

39
Q

B1 cells

A

Autoreactive
Make antibodies to respond to host tissue
Numbers do not decrease after treatment (this allows the response to amplify if seen again)

40
Q

T cell receptor structure

A

Receptor has 2 glycoprotein chains (a and B) with variable segments
Variable segments determine the type of immunity response

41
Q

T/F - TCR in periodontitis are different before and after therapy

A

True - this leads to a different type of immune response

42
Q

T/F - TCR is the same between chronic and aggressive periodontitis

A

False - TCR is DIFFERENT between chronic and aggressive periodontitis - leading to a different type of immune response

43
Q

What makes the 2 types of t-helper cells different?

A

Their cytokine profiles are different

44
Q

Which cytokines communicate with Th1?

A

IL-2
INF-gamma
TNF-alpha

45
Q

Which cytokines communicate with Th2?

A 
IL-4
IL-5
IL-6
IL-10
IL-13
46
Q

What is IL-10 an indicator of?

A

It can contribute to both Th1 and Th2
It normally knocks down cell-mediated response, and increases humoral response
Lots of IL-10 = stabilized perio lesion
Little IL-10 = lesion can be progressing

47
Q

T cell response

A

Cytotoxic t cells (Tc) are activated by cytokines
Respond to intracellular pathogens
Antigens from these pathogens bind MHC-1 molecules
Tc recognize this antigen presentation and destroy infected cells

48
Q

Cytotoxic T-cell contribution to periodontitis

A

There aren’t many Tc cells found in periodontitis

This suggest that viruses and invasive bacteria are not major players

49
Q

B cell response

A

Hummoral immunity (antibody mediated) is triggered in response to soluble antigens
Ag-Ab complex activates complement
Ag-Ab complex facilitates opsonization
Th-2 cytokines activate B cells to plasma cells

50
Q

How can antibody alone protect cells?

A

Block entry of toxins
Immobilize bacteria
Agglutinate bacteria

51
Q

How can an antibody plus its compliment protect cells?

A

Lyses bacteria

52
Q

How can an antibody plus a cell protect cells?

A

Opsonizes bacteria, fungi for phagocytosis

Activates extracellular killing

53
Q

Avidity

A

Ag-binding differs among antibody subclasses

Not all are capable of effective opsonization

54
Q

How do IgG2 and IgG1 numbers differ in periodontitis?

A

IgG2 > IgG1 in aggressive periodontitis

BUT IdG1 > IgG2 in chronic periodontitis

55
Q

Where does the homing of relevant immune cells take place?

A

Within the periodontal lesion

56
Q

Which T-helper cell outnumbers the other in chronic periodontal lesions?

A

Th2 > Th1

57
Q

What is the most predominant and active secretory cell in advanced perio lesions?

A

Plasma cells

58
Q

An individual’s ability to mount a specific Ab response to bacteria in the subgingival biofilm may indicate what?

A

Their susceptibility to the disease and the ability to respond to treatment

AU 15 - Periodontology (8 decks)

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