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Perio > Pathogenesis Part 1 > Flashcards

Pathogenesis Part 1 Flashcards

1
Q

what type of plaque casues gingivitis

A

supragingival plaque

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2
Q

swelling =

A

edematous

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3
Q

redness =

A

erthema

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4
Q

what type of plaque is involved in periodontitis?

A

subgingival plaque

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5
Q

what type of immunity is non-specific?

A

innate immunity- always there

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6
Q

what stages of periodontal disease does BOP occur

A

bleeding on probing occurs in the early, established and advanced lesion (acute gingivitis, chronic gingivitis and periodontitis)

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7
Q

what stage of periodontal disease does a periodontal pocket form?

A

advanced lesion-periodontitis

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8
Q

what stage of periodontal disease does cytoplasmic alterations of fibroblasts occur?

A

early lesion - acute gingivitis

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9
Q

what stage of periodontal disease do white blood cells migrate into the junctional epithelium and gingival sulcus?

A

initial lesion- clinically healthy

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10
Q

what stage of periodontal disease does the proliferation, apical migration and lateral extension of junctional epithelium occur?

A

established lesion - chronic gingivitis - 2-3wks

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11
Q

when do the basal cells of the junctional epithelium begin to proliferate?

A

early lesion - acute gingivitis - 4-7days

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12
Q

what stage of periodontal disease are immunoglobulins (antibodies) present in the connective tissue and junctional epithelium?

A

established lesion - chronic gingivitis - 2-3wks

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13
Q

what stage of periodontal disease does alveolar bone loss occur?

A

Occurs histologically in the advanced lesion from periodontitis- greater than 3 weeks

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14
Q

what stage of periodontal disease do lymphoid cell accumulate?

A

early lesion - acute gingivitis - 4-7 days

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15
Q

what stage of periodontal disease do plasma cell become cytopathologically altered?

A

advanced lesion- periodontitis

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16
Q

what stage of periodontal disease does the loss of perivascular collagen begin?

A

initial lesion 2-4 days

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17
Q

what stage of periodontal disease is distant bone marrow converted into fibrous connective tissue?

A

advanced lesion - periodontitis

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18
Q

When does fluid begin exudation from the gingival sulcus?

A

initial lesion

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19
Q

what stage of periodontal disease are there periods of quiescence and exacerbation?

A

advanced lesion - periodontitis

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20
Q

what stage of periodontal disease is there a predominance of plasma cells with out bone loss?

A

established lesion- chronic gingivitis

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21
Q

what can be stimulated to destroy collagen and ECM?

A

fibroblasts

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22
Q

what are the 4 types of cells of the innate immune response?

A
  1. mast cells 2. acute phase proteins 3. complement 4. PMN’s
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23
Q

what affect does TNF alpha have?

A

TNF alpha recruits granulocytes to the area of inflammation, induces fever

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24
Q

what affect does histamine have?

A

histamine dilate and increases permeability of blood vessels

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25
Q

what affect do leukotrines have?

A

leukotrines dilate small blood vessels, chemotaxis of leukocytes

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26
Q

what affect do prostaglandins have?

A

prostaglandins increase vascular permeability, regulate the immune response

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27
Q

what is the difference in hyperresponsive, normal, and hyporesponsive groups to periodontitis?

A

Hyperresponsive - NUG/ refractory perio Normal - clinincally obvious perio, gingivitis Hyporesponsive - group doesnt get periodontitis

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28
Q

what type of immunity is adaptice and specific?

A

acquired immunity

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29
Q

What types of cells are involved in the acquired immunity?

A

monocytes/ macrophages lymphocytes

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30
Q

When monocytes/ macrophages are involved what can occur?

A

if unresolved or resolved chronic inflammation can occur

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31
Q

What can occur if the serum compliment is unable to stop the invasion of bacteria?

A

acute inflammation recruit PMN’s

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32
Q

What happens if lymphocytes are able and unable to fight an infection?

A

able - chronic inflammation unable - systemic infection

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33
Q

What type of cell is involved in both the acquired immunity and the innate immunity?

A

monocytes/macrophages

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34
Q

What two types of cells cause acute inflammation?

A

neutrophils and serum complement

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35
Q

what is c-reactive protein? what does is do?

A

C-reactive protein is an acute phase protein. it is produced by the liver and serves to bind lysophosphatidylcholine (on surface of dying bacteria) to activate the complement system. It has a higher affect on heart attacks than LDL!!

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36
Q

What are five types of cells that increase the risk of heart disease?

A
  1. c-reactive protein 2. fibrinogen 3. complement 4. namose binding protein 5. metal binding protein
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37
Q

what activates the serum complement?

A

complement is activated by antigen-antibody interaction

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38
Q

What % of normal proteins in blood is the serum complement?

A

10%

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39
Q

Where is the complement made? and by what?

A

the liver, small intestine made by mononuclear cells

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40
Q

What type(s) of complement cause inflammation? What do they do?

A

C3a and C5a -the release of mast cell mediators = increased permeability of blood vessels and phagocytes can enter tissues

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41
Q

What part of complement forms an antibody coat over the bacteria?

A

C3b - forms antibody coat (opsinization)- helps to internalize the bacteria faster

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42
Q

what is the alternative pathway(non-specific) for complement activation/ cleavage?

A

endotoxins, IgG cleave C3 into C3a and C3b

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43
Q

what is the half life of PMN’s?

A

5-90 hours

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44
Q

How do PMN’s adhere to the endothelium?

A

via selectins, adhesins- ICAM and ELAM

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45
Q

Diapedesis

A

process of squeezing through endothelium

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46
Q

Chemotaxis

A

directed movement to an increase concentration

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47
Q

What affect does NADPH oxidase have? When is it activated?

A

increase in NADPH oxidase activity on surface of cells and granules helps to phagocytize bacteria. Activated in respiratory burst

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48
Q

PMN’s are attracted to what?

A

F-MLP (formyl methionine, leucine, phenylalanine) bacterial cells have this- released as bacteria turn over

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49
Q

What are secondary granules?

A

specific granules -lysosyme, NADPH oxidase, collagenase, lactoferrin

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50
Q

What are primary granules?

A

azurophilic granules -myeloperoxidase, deffensins, elastase, cathepsin

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51
Q

explain the process of rolling

A

PMN’s slow down and roll on membrane, grab onto adhesins / ICAM on endothelium and the leave the blood via diapedesis and undergo chemotexis and then phagocytize bacteria.

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52
Q

epitopes on bacteria cells bind to?

A

the FAB region of antibodies

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53
Q

macrophages are long lived cells that are involved in what type of immunity?

A

both innate and acquired immunity

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54
Q

are PMN’s antigen presenting cells?

A

No but macrophages, dentritic cells, and plasma cells are

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55
Q

the interaction of LPS with macrophages with endotoxins results in the release of what?

A
  1. PGE2 2. TNF alpha 3. IL-1- beta 4. MMP’s
56
Q

what molecules of complement are most typically associated with acute inflammation?

A

C3a and C5a

57
Q

what is true about the IL-1 gene polymorphism?

A

it can be used as a measure of susceptibility for periodontal disease in some patient populations

58
Q

the initial microbial infection is primarily accomplished by what?

A
  1. antigen-antibody response 2. complement 3. mast cells 4. PMN’s
59
Q

c-reactive protein is what type of protein? What part of the immune response is it part of?

A

-acute phase protein -innate immune response

60
Q

chemokinesis

A

movement of cells due to chemical or physical stimulation

61
Q

chemotaxis

A

a specialized type of chemokinesis that is the directed movement of cells towards an increasing chemical gradien

62
Q

the chemotractant that results from the proteolytic breakdown of complement is?

A

C5a

63
Q

c-reactive protein present in the blood is indicative of what?

A

inflammation of the whole body

64
Q

what purpose does c-reactive protein serve in the innate immune system?…. it binds to what?

A

it binds to lysophosphatidylcholine (on surface of dying cells) to activate the complement system

65
Q

what enzyme activates complement?

A

c3 convertase enzyme

66
Q

where is complement produced? by what?

A

the liver and small intestine by mononuclear cells

67
Q

how is complement activated in the alternative pathway?

A

by LPS, endotoxins, aggregated IgG

68
Q

what is a virulence factor that helps bacteria avoid opsonization?

A

hydrophilic bacteria

69
Q

opsonization is activated by what complement product?

A

c3b

70
Q

What does the complement particle C3a bind to and do?

A

C3a binds to the mast cell which releases TNF alpha which causes IL-8 to alter the endothelial surface = vasodilation

71
Q

PMN’s express’s __________ Endothelium express’s ________

A

PMN’s- selectins Endothelium- Adhesions/ ICAM

72
Q

complement causes vasodilation through what?

A

cytokine - IL-8 alters the endothemial surface - caused when C3a binds to a mast cell

73
Q

what is an example of an end cell?

A

PMN

74
Q

tertiary granules

A

cathepsin and gelatinase

75
Q

how does the membrane attack complex in complement work?

A

creates holes in the membrane of bacteria ex- chlorahexadine

76
Q

what are the chemotractants for PMN’s from macrophages/ monocytes?

A

leukotrine B4 IL-8

77
Q

what are the chemotractants for PMN’s from serum/ plasma (proteolytic breakdown of complement)?

A

C5a

78
Q

what are the chemotractants for PMN’s from bacteria?

A

f-met peptides

79
Q

what are the chemotractants for PMN’s from mast cells?

A

neutrophil chemotactic factor

80
Q

what are the chemotractants for PMN’s from the endothelium?

A

endothelial IL-8

81
Q

what are the chemotractants for PMN’s from B-cells and macrophages?

A

IL-1

82
Q

what response is the preferred method of killing for PMN’s?

A

oxidative response via NADPH oxidase

83
Q

what enzymes are involved in the oxidative response of PMN’s?

A
  1. NADPH oxidase 2. cytochrome B 3. myeloperoxidase
84
Q

What are the products of the respiratory burst?

A
  1. HOCL (hypochlorous acid) 2. H2O2 (hydrogen peroxide) 3. O2 -
85
Q

what causes the green color of pus in infections?

A

myeloperoxidase

86
Q

what are proteas inhibitors?

A

stop enzymes when dumped into connective tissue.

87
Q

what causes frustrated phagocytosis?

A

HOCL can neutralize the protease inhibitors - mass tissue destruction

88
Q

what is the inside structure of a plasma cell?

A

rough ER and large golgi apparatus to produce large amounts of antibodies (proteins)

89
Q

what are epitopes? where are they located?

A

antigenic determinants present on the surface of bacteria

90
Q

how do antibodies bind to bacteria?

A

antibodies bind with the FAB region to the Epitope.

91
Q

PMN’s recognize what region of the antibody?

A

FC

92
Q

what antibodies are present in the mouth?

A

IgG and IgA

93
Q

how does IgG get into the mouth?

A

leaked into mouth by gingival crevicular fluid - but it is broken down easily

94
Q

what antibody can cross into the placenta?

A

IgG

95
Q

what are the functions of IgG?

A

opsonization, agglutination, complement fixation

96
Q

what antibody makes up the majority of antibodies in the body?

A

IgG - 80-85%

97
Q

IgA function?

A

protect mucous membranes by preventing the attachment of organisms. ex actively secreted by salivary glands - has the J chain to stabolize

98
Q

functions of IgM?

A

opsonization, agglutination, complement fixation

99
Q

first antibody produced during an immune response?

A

IgM

100
Q

function of IgD?

A

facilitates development and maturation of the antibody response. located on the surface of B-cells

101
Q

IgE function?

A

release granule contents in response to allergic reactions and parasitic infections

102
Q

function of the J-chain in IgA?

A

interacts with the FC fragments of IgG molecules by disulfide bonds to help stabilize it

103
Q

function of the secretor component of IgA?

A

provides protection against degradation enzymes in the digestive system

104
Q

is the host in control in a systemic exposure?

A

no

105
Q

what is the systemic response?

A

B-cell and interlukins

106
Q

what is the monoclonal response?

A

antibodies produced to only 1 bacteria like Aa

107
Q

polyclonal response

A

antibodies produced by B-cells to lots of different antigens

108
Q

is LPS produced from gram (-) or (+) bacteria

A

gram (-) negative

109
Q

the myeloid stem cell gives rise to what 5 things?

A
  1. PMN’s 2. Eosinophils 3. Basophils 4. Mast Cells 5. Monocytes (macrophages)
110
Q

where are mononuclear phagocytes located?

A

all tissues of the body

111
Q

half life of macrophages?

A

months- can reenter tissue and then back into circulation

112
Q

2 roles of macrophages?

A
  1. take up microbacteria and neutralize it 2. scavenger role
113
Q

which can be used multiple times, PMN’s or Macrophages or both?

A

only macrophages, PMN’s are end cells

114
Q

what is the scavenger role of macrophages?

A

search for foreign cells and dead cells and phagocytize it

115
Q

LPS stimulated what receptor of macrophages?

A

CD14 receptor of macrophages

116
Q

the CD14 receptor of macrophages releases _______ which causes extracellular matrix destruction

A

MMP’s

117
Q

fibroblasts can secrete _______ which leads to alveolar bone resorption

A

PGE2

118
Q

what exposes the peptide fragments of the antigen on the macrophage?

A

major histocompatibility complex 2 - presents antigenic peptide on the surface

119
Q

LPS stimulated what receptor of macrophages?

A

CD14 receptor of macrophages

120
Q

the CD14 receptor of macrophages releases _______ which causes alveolar bone resorption

A

PGE2

121
Q

the CD14 receptor of macrophages releases _______ which causes fibroblasts to activate negatively

A

IL-1 beta and TNF alpha

122
Q

the CD14 receptor of macrophages releases _______ which causes extracellular matrix destruction

A

MMP’s

123
Q

fibroblasts can secrete _______ which leads to alveolar bone resorption

A

PGE2

124
Q

what exposes the peptide fragments of the antigen on the macrophage?

A

major histocompatibility complex 2 - presents antigenic peptide on the surface

125
Q

helper T-cells and MHC 2 present the antigenic fragments to what?

A

b-cell - to create more b-cells and to create plasma cells

126
Q

what are conditions that lead to monocyte deregulation?

A

diabetes and smoking

127
Q

what is collagenase and where is it present?

A

present in fibroblasts and it break down tissues

128
Q

what are MMP’s dependent upon?

A

manganese and magnesium ions (divalent cations)

129
Q

what are TIMPS

A

tissue inhibitors or metalloproteases - inhibit MMP’s

130
Q

how long does connective tissue take to repair?

A

6 weeks

131
Q

60 year old patient with untreated periodontitis for whole life, how much attachment loss?

A

60 -20 years (adults dentition) = 40 years thus 4mm of attachment loss ideally

132
Q

what causes macrophages to release lots of collagenases?

A

IL-1 and endotoxins

133
Q

what is collagenase and where is it present?

A

present in fibroblasts and it break down tissues

134
Q

purpose of scaling and root cleaning?

A

remove diseased cementum and restore the junctional epithelium

135
Q

how fast does the epithelium grow?

A

1mm per day ( 0.5 mm per side of the circle)

136
Q

how long does connective tissue take to repair?

A

6 weeks

137
Q

the primary cell involved in the non-pathogenic breakdown of collagen in the gingiva is the _______

A

fibroblast

Perio (5 decks)

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