Tutorial Answers Flashcards

1
Q

what is provisional diagnosis based on

A

symptoms
signs
history

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2
Q

how does a surgical seive aid in diagnosis

A

helps in the narrowing down of disease responsible.
oral clues may also provide evidence of other underlying diseases whcih in turn may lead to manifestations in the oral cavity.

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3
Q

what can be done to aid in patient diagnosis following a provisional diagnosis

A

refer to a specialist, order a biospy or other clinical tests

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4
Q

what biological process causes the redness of gingiva

A

inflammation

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5
Q

what are the basic stages of inflammation

A
  • initiation of reaction (response to harmful agents)
  • progression (containment of harmful agents)
  • amplification (modulation of immune response)
  • resolution (favourable outcome leading to healing)
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6
Q

how does the oral epithelium and saliva protect against infection by pathogenic bacteria that may be present in the dental plaque

A

gum tissue acts principally as a physical barrier, a number of antimicrobial products are produced by cells and also in the gingiva to protect the tissue

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7
Q

what are some key molecules found in the saliva that aid in the protection of the mouth

A
  • lactoferrin
  • lysozyme
  • peroxidase
  • antimicrobial peptides
  • immunoglobins
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8
Q

what is the function of lactoferrin

A

glycoprotein that transports ions but has antimicrobial activity
present in the saliva and produced by neutrophils

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9
Q

what is the function of lysosyme

A

present in the saliva and produced by macrophages and neutrophils
targets cell walls of bacteria

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10
Q

what is the function of cystatins

A

anti protease activity and supports remineralisation of the teeth

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11
Q

what are the major families of antimicrobial peptides found in the saliva

A

b defensins
human neutrophil peptides
cathelicidins

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12
Q

how does the body identify potentially harmful organisms in dental plaque, what types of receptors are involved, and what do they recognise?

A

pattern recognition receptors like toll like receptors and pathogen associated molecular patterns, activation leads to change in cell phenotype and the production of inflammatory mediators

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13
Q

wha tis the basic function of neutrophils

A

produce NETs

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14
Q

what is the main function of macrophages

A

phagocytosis and antigen presentation

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15
Q

what is the main function of dendritic cells

A

phagocytose and present antigen

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16
Q

what is the main function of mast cells

A

degranulate to release histamine and antimicrobial agents

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17
Q

what is the main function of b cells

A

produce antibodies

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18
Q

what is the main function of t cells

A

to drive cell mediated responses

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19
Q

can you describe how the immune cell populations within the gingival tissues differ during the early inflammatory response compared to a later chronic inflammatory response

A

early inflammation is mainly macrophages and neutrophils
later there are more b cells and t cells

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20
Q

how do both myeloid and lymphoid cells originate

A

both lineages from common stem cell precursors form myleoid and lymphoid stem cell progenitors in the bone marrow

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21
Q

what roles do the thymus, lymph nodes and spleen play in immune cell function

A

these are organs of the immune system
the thymus is where t cells mature
the lymph nodes and spleen are reservoirs of immune cells

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22
Q

what are Il6 and Il1beta

A

cytokines, signalling molecuels that coordinate immune response

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23
Q

what are the families of cytokines

A

interleukins
tnf family
interferons

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24
Q

why can interleukin levels in a periodontitis patient be raised

A

there is elevated localised production of interleukins at the inflammatory site that enter their way into the circulation. give information to dictate immune response, and cytokine production can be related to the type of threat and tell the body how to respond

25
Q

explain the processes involved in the activation of complement

A

there are three pathways determined by the initiating factor
- classical complement pathway binds via the antibody IgG or IgM coating the bacterial surface
- alternative complement pathway is when C3b binds directly to the cell wall of a microbial cell
- lectin pathway is when complement proteins bind to the mannose binding lectin on the cell surface

26
Q

what is mannose

A

a carbohydrate on the surface of microbial cells

27
Q

what is the process of complement activation

A

involves proteins enzymes and subsequent fragments following enzymatic degradation eg C3 splits into C3a and C3b and C5 splits into C5a and C5b
C3/5a are anaphylatoxins with multiple functions within the immune system such as increasing vascular permeability and increasing cellular migration

28
Q

what is the result of complement activation

A

formation of the membrane attack complex
form pores on the surface of the bacteria which drives lysis of the cell
anaphylatoxin production

29
Q

explain the process by which circulating neutrophils are recruited to the site of infection

A

cell adhesion molecules control interactions between immune cells like neutrophils and endothelial cells which move against the chemokine gradient and undergo diapedesis through interactions between receptors on immune cells and receptors on endothelial cells

30
Q

what are the three main families of cell adhesion molecules

A

selectins
integrins
immunoglobin superfamily

31
Q

describe the production of chemokine gradients during inflammation

A

chemokines are released by cells at the site of infection
due to endocrine nature they will enter the circulation and create a gradient so there is high interleukin concentration in the tissue and low in the blood and the cells will move toward the higher concentration

32
Q

what are the other effector functions of neutrophils aside from engulfing and destroying invading pathogens by phagocytosis

A
  • degranulation due to granules in cell vesicles containing numerous antimicrobial peptides and enzymes that are released upon activation of receptors
  • production of neutrophil nets - the activation of neutrophils releases proteins and some genetic material to form extracellular fibril matrix
  • these trap pathogens whilst granule release leads to antimicrobial activity
33
Q

what is an antigen

A

a substance which triggers a specific immune response

34
Q

what is an antigen presenting cell

A

cells which present antigens to the adaptive immune response

35
Q

how do antigen presenting cells process antigens

A

they are constantly processing them in tissues in both health and diseased states
they are loaded onto either MHC1 if they are endogenous or II if they are exogenous

36
Q

which t cells get antigens from MHC1

A

CD8

37
Q

which t cells get antigens from MHC2

A

CD4

38
Q

how do dendritic cells activate naive t cells to initiate a primary adaptive immune response

A

dendritic cells take up and process the antigen at the mucosal barrier surface
once they have taken up the antigen they migrate to lymph nodes and mature en route
dendritic cells have co stimulatory activity and can prime naive t cells in specific regions of the lymph node

39
Q

what is t cell priming

A

this is when a naive t cell, after undergoing education in the thymus, residingin the lymph nodes, interacts with dendritic cells.
three signals are critical for activation and differentiation into subsets

40
Q

what is signal one of t cell priming

A

activation of the t cell via MHC-TCR interactions

41
Q

what is signal two of t cell priming

A

survival and clonal expansion of t cells driven by co stimulatory molecules

42
Q

what is signal three of t cell priming

A

differentiation into subsets for CD4 cells.
for CD8 cells, the third signal is an effector function of destruction of infected cells, and all nucleated cell types have an ability to present an antigen via the MHC1

43
Q

which t cell subsets can initiate the adaptive immune response

A

CD4

44
Q

explain how a t cell with a receptor specific for the clostridium tetani antigen is developed from a pre thymic t cell in the thymus

A

t cells will interact with thymic cortical epithelial cells in the thymus
needs to be of a level of moderate binding so the t cell receptor recognises the MHC molecule
in positive selection, if there is no recognition at all the cells are destroyed via apoptosis
in negative selection, if the TCR binds too strongly to the self peptide then the t cell is also removed via apoptosis
t cell receptors are generated through the process of somatic recombination

45
Q

what are the basic principles of vaccination

A

used to elicit a primary response to a pathogen to form immunological memory in the form of memory b cells which will protect the host upon re encounter with the antigen
it involves class switching of IgM to IgG antibody in the memory b cells to produce a more effective, stronger response upon re exposure

46
Q

explain how vaccination activates a specific b cell response and generates immunological memory

A

b cells can take up antigens in a similar manner to other APCs which are presented to t cells via MHC
these t cells will already have receptors specific for that antigen and therefore will drive production of memory b cells and plasma b cells

47
Q

explain the basic principles of central tolerance

A

checkpoints are in place for both t and b cells
t cells interact with thymic cortical epithelial cells in the thymus and undergo positive and negative selection. if they self react, they die

48
Q

explain the basic principles of peripheral tolerance

A

some self reactive b and t cells bypass the central tolerance mechanism and peripheral tolerance will prevent their activation
self reactive t cells do not get all three signals from the dendritic cells for activation and differentiation, so if there is loss of signal 2 or 3 then there are anergic t cells or cells targeted for deletion via apoptosis

49
Q

explain the role of plasma factors in the clotting process

A

the coagulation pathway leads to the production of fibrin, which is the main component of clot formation.

the fibrinolytic system uses plasmin to control degradation of fibrin clots

balance between these two systems is important

50
Q

in addition to coagulation, what are the other plasma factor cascades and how are they interlinked to support the healing processes and inflammatory responses

A

kinin
fibrinolytic
complement
coagulation

51
Q

what is the plasma factor that activates all four enzymatic cascades that support healing and inflammation

A

coagulation factor XII - hagement factor

52
Q

what are the different roles of macrophages in chronic inflammation

A

M1 macrophages are activated when there is tissue injury by driving an inflammatory response
M2 macrophages are involved in tissue repair through suppression of inflammatory responses

53
Q

how can chronic inflammation cause soft tissue destruction

A
  • tissue injury involves activation of coagulation, recruitment of immune cells, production or arachidonic acid metabolites like prostaglandins
  • tissue repair involves fibrosis, using growth factors to drive cellular recruitment and angiogenesis
54
Q

what molecule functions in reconstructing soft tissue

A

matrix metalloproteinases

55
Q

describe the phases involved in formation of granulation tissue

A

first is vascular granulation tissue
- proliferating capillaries, fibroblasts and immune cells
- new capillaries are leaky which allows cells and fluid to leak into the tissue

second is fibrous granulation tissue
- capillaries regress and immune cells return to the blood
- mature fibroblasts which lay down collagen
- collagen is remodelled to an early fibrous scar

56
Q

what are the major causes of cell injury

A

microbial infection
physical agents
irritants and corrosive chemicals
tissue necrosis

57
Q

how does uv radiation lead to cell injury

A

dna damage resulting from uv exposure leads to apoptosis via activation of p53
if larger doses of the same injurious agent affect the cell, then necrosis may be the cause of cell death due to coagulation of cellular proteins, disruption of cell membranes and changes to the nucleus

58
Q

what is the principle mechanism of type 1 hypersensitivity, and what are the cells and mediators involved

A
  • allergens processed by APCs
  • presented to t helper cells
  • plasma b cells produce IgE
  • allergen react with IgE and the complexes bind to mast cells and basophils
  • histamine release
59
Q

what treatments are available for hay fever and how do they work biologically

A

IgE responses drive mast cells to release histamine, so antihistamines are the logical choice of therapy
antagonistic in their actions, block the binding of histamine to the receptors on mast cells and basophils