Host Response to Periodontal Bacteria Flashcards by John Fixari

How doe bacteria induce damage to periodontal tissues?

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

Bacteria activating the host’s own inflammatory and immune system

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What are the different types of major microbial virulence factors?

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

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What are the mechanisms of periodontal defense?

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

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How does the periodontium prevent bacterial entry?

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

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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What are the different types of innate immune responses?

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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Adaptive or acquired immunity

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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How does clonal expansion aid in adaptive/acquired immunity?

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

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What is the host defense hierarchy?

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

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

Salivary glands
Mucosa
Tongue
Crevice

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Salivary gland contribution to innate immunity

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

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Mucosa contribution to innate immunity of the oral cavity?

TLR receptors - detect features of bacteria

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TLR receptors

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

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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What are the 2 ways to activate the complement system?

1) Classic - contact antibody labeled microbe

2) Alternate - contact bacterial cell walls

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What is the role of C3b in the complement system?

Enhances the efficiency of phagocytosis

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

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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Membrane attack complex

Forms during the complement pathway

Creates pores in a microbe so it lyses itself

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

Involved in the coordination of inflammatory and immune resonses

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What cytokine(s) provide pro-inflammatory activity?

IL-1

TNF-a

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What cytokine(s) provide chemotactic activity

IL-8

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What is the role of prostaglandins in innate immunity?

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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Where do prostaglandins come from?

Study These Flashcards

Derived from arachidonic acid

Produced by activated macrophages and other cells

What is the role of matrix metalloproteinases in innate immunity?

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)

What is the role of Proteinase inhibitors in innate immunity?

Antagonize inflammation | Inhibit degradation of matrix proteins

What are the two major proteinase inhibitors?

Alpha-2 macroglobulin (broad spectrum proteinase inhibitor) | Alpha-1 antitrypsin (broad spectrum proteinase inhibitor and potent inhibitor of PMN collagenase)

What are the major antimicrobial peptides?

Defensins | Calprotectin

Defensins

Inhibit bacteria and fungi | Produced by salivary gland epithelium

Calprotectin

Inhibit bacteria and fungi by chelating zinc | Produced by epithelium, PMNs, Monocytes, and Macrophages

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

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

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

Secretion Respiratory burst Phagocytois Lysis apoptosis

How are PMNs recruited to the gingival crevice?

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

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

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

In periodontitis, how do the number of cells compare?

Plasma cells > B lymphocytes > T lymphocytes

Th1 cells responsibility

Regulate cell-mediated immunity | Release cytokines to recruit cytotoxic t-cells

Th2 cells responsibility

Release cytokines that activate B cells

B2 cells

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

B1 cells

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

T cell receptor structure

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

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

True - this leads to a different type of immune response

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

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

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

Their cytokine profiles are different

Which cytokines communicate with Th1?

IL-2 INF-gamma TNF-alpha

Which cytokines communicate with Th2?

``` IL-4 IL-5 IL-6 IL-10 IL-13 ```

What is IL-10 an indicator of?

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

T cell response

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

Cytotoxic T-cell contribution to periodontitis

There aren't many Tc cells found in periodontitis | This suggest that viruses and invasive bacteria are not major players

B cell response

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

How can antibody alone protect cells?

Block entry of toxins Immobilize bacteria Agglutinate bacteria

How can an antibody plus its compliment protect cells?

Lyses bacteria

How can an antibody plus a cell protect cells?

Opsonizes bacteria, fungi for phagocytosis | Activates extracellular killing

Avidity

Ag-binding differs among antibody subclasses | Not all are capable of effective opsonization

How do IgG2 and IgG1 numbers differ in periodontitis?

IgG2 > IgG1 in aggressive periodontitis | BUT IdG1 > IgG2 in chronic periodontitis

Where does the homing of relevant immune cells take place?

Within the periodontal lesion

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

Th2 > Th1

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

Plasma cells

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

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

Host Response to Periodontal Bacteria Flashcards

(58 cards)