Lecture 8 questions Flashcards

1
Q

Acute inflammation or injury increases vascular permeability resulting in

A

redness, edema, and increased gingival crevicular fluid flow

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2
Q

What are the two mechanisms for killing bacteria by neutrophils

A

oxidative and non-oxidative

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3
Q

what does the oxidative mechanism for killing bacterial involve

A

reactive oxygen radicals and electron transfer reactions

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4
Q

What does the non-oxidative mechanism for killing bacteria involve

A

enzymes that cleave

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5
Q

how does a neutrophil protect the host

A

sends out cytoplasmic projections around bacteria creating a phagolysosome, which when completely surrounding the bacteria, is less damaging for the host

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6
Q

what is the main difference between innate and adaptive/acquired immunity?

A

innate is based on inherent biological response, while adaptive/acquired is based on recognition of antigens, immune memory and clonal expansion

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7
Q

what are the 3 major cells in chronic periodontitis?

A

plasma cells > b lymphocytes > t lymphocytes

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8
Q

what do Th1 cells do?

A

interact with cancer cells or cells that have been infected

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9
Q

what do Th2 cells do

A

produce antibodies

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10
Q

what do b lymphocytes differentiate into

A

plasma cells, when acted upon by IL-10

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11
Q

what compounds can serve as antigens?

A

LPS, bacterial proteins, etc

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12
Q

what can function as antigen presenting cells (APC)

A

macrophages and langerhans cells

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13
Q

what do the alpha and beta chains in T-cell receptors determine

A

the type of immune response

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14
Q

what are the cytokines associated with Th1

A

IL-1, IFN-gamma, TFN-alpha

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15
Q

what are the cytokines associated with Th2

A

IL-4, IL-5, IL-6, IL-10, IL-13

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16
Q

how are Th1 and Th2 balanced

A

they are suppressed by IL-10 which has a general anti-inflammatory properties. a lot of IL-10 means that the are is pretty stable

17
Q

explain the t-cell response

A

Tc activated by cytokines -> Tc response to intracellular pathogens –> Tc recognize antigen presentation and destroy infected cells

18
Q

are there many Tc found in periodontitis

A

no, suggesting that viruses and invasive bacteria are not major players

19
Q

explain the b-cell response

A

Ab mediated humoral immunity triggered in response to soluble antigens -> Ag-Ab complex activated complement -> Ag-Ab complex facilitates opsonization -> Th2 activate B cells to plasma cells

20
Q

what are the 2 types of B cells

A

conventional: produce Ab against bacteria, they decrease in healthy or treated sites
auto reactive: produce auto-Ab, they don’t decrease after treatment

21
Q

explain Ab-medidated protection

A

Ab blocks entry of toxins/viruses (IgM, IgG, IgA) -> immobilizes bacteria (IgM>IgG) –> agglutinates bacteria (IgM, IgG)

22
Q

explain Ab plus complement-mediated protection

A

lysing bacteria (IgM, IgG)

23
Q

explain Ab plus cells-mediated protection

A

opsonizes bacteria/fungi for phagocytosis (IgG) -> activates extracellular killing (IgG)

24
Q

what is avidity?

A

Ag-binding differs among antibody subclasses, not all are capable of effective opsonization or complement activation

25
Q

how are IgG1 and IgG2 differ in periodontitis

A

IgG1 > IgG2 in chronic periodontitis but IgG1 < IgG2 in aggressive periodontitis

26
Q

explain antigen recognition in B-cell response

A

IgG2 recognizes LPS while other subclasses mainly recognize protein Ag

27
Q

what is the systemic humoral immune response to plaque antigens in the gingival crevice

A

1) plaque antigens diffuse through the junctional epithelium
2) langerhans cells within the epithelium capture and process the antigens
3) antigen-presenting cells (macrophages and langerhans cells) leave the gingiva in the lymphatics
4) antigen-presenting cells reach the lymph node and begin to stimulate lymphocytes to produce a specific immune response
5) periodontal microbe specific antibodies are produced any plasmas cells within the lymph nodes and travel back to the gingiva via blood vessels
6) antibodies leave the circulation and are carried to the crevice in the transudate from the inflamed and dilated blood vessels
7) antibody action on microbes in the crevice can result in killing, aggregation, precipitation, detoxification, opsonization and phagocytosis of bacteria

28
Q

what is the local cellular immune response to plaque antigens in the gingival crevice?

A

1) plaque antigens diffuse through the junctional epithelium
2) langerhans cells within the epithelium capture and process the antigens
3) antigen-presenting cells (macrophages and langerhans cells) leave the gingiva in the lymphatics
4) antigen-presenting cells reach the lymph node and begin to stimulate lymphocytes to produce a specific immune response
5) periodontally specific B cells (pre-plasma cells) and T cells proliferate within the lymph nodes and enter the blood stream
6) periodontally specific lymphocytes “home” back to the periodontist and locate within the tissues where they begin their humoral and cell-mediated immune functions
7) antibodies are produced located by plasma cells which are controlled by type 2 T-helper cells (TH2). cell-mediated immune activity is regulated by type 1 T-helper cells (TH1)

29
Q

Here are some other points we have to know

A

1) homing of relevant immune cells takes place in periodontal lesion
2) Th2>Th1 cells in chronic periodontal lesions
3) plasma cells are among the most predominate and active secretory cells in advanced periodontal lesions
4) the ratio of IgG subclasses are similar in serum and GCF
6) a person’s ability to mount a specific Ab response to bacteria in the subgingival biofilm may indicate a patient’s susceptibility to the disease and ability to respond to treatment