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23 Periodontology > 5 - Periodontal Pathogenesis > Flashcards

5 - Periodontal Pathogenesis Flashcards

1
Q

what is the origination and development of a disease

A

pathogenesis

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2
Q

what is the host respose to a CHALLENGE (insult or injury)

A

inflammation

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3
Q

inflammation is linked to most chronic diseases of aging and premature births such as what

A

RVD, RA, alzheimer’s, pancreatic cancer, obesity, pre-term low-bith weight infants, periodontitis

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4
Q

inflammation leads to what remodeling

A

soft and hard tissue

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5
Q

inflammation is part of what repair process

A

wound healing repair process

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6
Q

what plays a key role in pathogenesis of periodontal disease

A

inflammation

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7
Q

what happened in Sri Lankan study

A

8%: Rapid progression of periodontal disease
81%: Moderate disease progression
11%: No disease progression beyond gingivitis
ALL patients had abundant plaque and calculus.

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8
Q

what causes the different expressions of periodontal disease in all patients in the Sri Lankan study?

A

the host inflammatory response is different in all patients

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9
Q

what is the etiologic role of bacterial plaque

A

initiate and perpetuate inflammatory responses in gingival tissues

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10
Q

___ responses determines susceptibility to disease

A

immune-inflammatory

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11
Q

what is the primary etiology to perio disease

A

biofilm

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12
Q

what is the paradox to the role of inflamamtion

A

Host defense processes to prevent
ingress of bacteria result in most of
the tissue damage leading to clinical
manifestations of disease.

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13
Q

unique features of perio disease

A
  1. Not caused by a single organism
  2. Bacteria that colonize the subgingival sulcus are effectively OUTSIDE the body
  3. Yet, the inflammatory response develops INSIDE the body.
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14
Q

what are present in clinically healthy gingiva

A
  1. PMN leukocytes
  2. lymphocytes
  3. macrophages
  4. outflow of GCF
  5. steady state equilibrium between low-grade inflammation and subgingival microflora
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15
Q

what migrates thru CT thru JE into sulcus

A

PMN leukocytes

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16
Q

what is attracted by chemotactic stimuli created by bacterial products

A

macrophages

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17
Q

what disease occurs prior to periodontitis

A

gingivitis

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18
Q

T/F: all gingivitis progresses to periodontits

A

FALSE! not all gingivitis progresses to perio

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19
Q

gingivitis is dependent on what

A

host inflammatory response and susceptibility to disease

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20
Q

what are the different stages of lesions in the histopathology of of gingivitis and periodontitis

A
  1. intial lesion
  2. early lesion
  3. established lesion
  4. advanced lesion
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21
Q

what lesion:

Develops within 2-4 days of plaque accumulation
Slightly elevated vascular permeability
GCF flow
PMN

A

initial lesion

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22
Q

what lesions corresponds to “clinical gingival health”

A

initial lesion

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23
Q

what lesion:

Increased vascular permeability, vasodilation, GCF flow
PMN
Lymphocytes
Collagen destruction: apical and lateral to JE and sulcular epithelium
60% of collagen destruction occurs
proliferation of JE

A

early lesion

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24
Q

what lesion corresponds to EARLY GINGIVITIS

A

early lesion

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25
Q

what lesion

Plasma cells
Lymphocytes
PMN
Elevated release of MMPs and lysosomal contents
from PMN
Significant collagen destruction

A

established lesionw

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26
Q

what lesion corresponds to ESTABLISHED GINGIVITIS

A

established lesion

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27
Q

what lesion

Plasma cells in CT
PMN in pocket epithelium
Apical migration of JE
Collagen destruction extends into PDL and bone
Osteoclastic bone resorption

A

advanced lesion

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28
Q

what lesion correspons to PERIODONTITIS

A

advanced lesion

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29
Q

what are the inflammatory responses in periodontium

A
  1. molecules signal tissue damage
  2. majority of tissue destruction results from host inflammatory process
  3. bacteria drive and perpetuate the inflammation
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30
Q

how do molecules signal tissue damage?

A
  1. microbial virulence factors
  2. host immune-inflammatory response
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31
Q

how does tissue destruction occurs from host inflammatory processes

A

excessive, dysregulated production of inflammatory mediators, enzymes

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32
Q

T/F: bacteria drive and perpetuation to inflammation contributes to a LARGE proportion of tissue damage

A

FALSE! contributes to SMALL proportion of tissue damage

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33
Q

lipopolysaccharide (LPS) is recognized by what TLR

A

TLR-4

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34
Q

what is a cell surface receptor that recognizes microbe associated molceular patterns and is found on innate immune cells

A

TLR-4

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35
Q

what is:

Lipid A component
Polysaccharide component
Found in outer membrane of gram-negative
bacteria
Endotoxin
Elicits strong immune response
Recognized by host Toll-like receptor (TLR)

A

LPS

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36
Q

porphyromonas gingivalis has an atypical LPS that is recognized by what

A

TLR-2 and TLR-4

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37
Q

the host response to LPS results in what

A
  1. increased production of cytokines
  2. differentiation of immune cells
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38
Q

what stimulates immune response less potently than LPS and is made of gram+ cell walls

A

lipoteichoic acid (LTA)

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39
Q

what recognizes LTA

A

TLR-2

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40
Q

what are bacterial enzymes and noxious products

A
  1. ammonia
  2. hydrogen sulfide
  3. butyric acid
  4. bacterial proteases
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41
Q

butyric acid leads to apoptosis of what cells

A

T-cells, B-cells, and fibroblasts

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42
Q

what digest proteins and provide nutrition for bacteria

A

bacterial proteases

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43
Q

T/F: bacterial proteases increase tissue breakdown

A

TRUE

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44
Q

what are gingipains?

A

bacterial enzymes produced by P, gingivalis

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45
Q

what are examples of microbial invasion

A
  1. A.a. and P. gingivalis invade gingival epi and CT
  2. fusobacterium nucleatum invades oral epi cells
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46
Q

what is the clinical significance of microbial virulence factors

A
  • bacteria in tissue is not removed by scaling and root planing
  • sheltered from host defense
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47
Q

what are host derived inflammatoyr mediators

A
  1. cytokines
  2. prostaglandins
  3. matrix metalloproteinases (MMPs)
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48
Q

what are:

Soluble proteins
Messengers- transmit cell-cell signaling
Produced in tissues, act locally in tissues

A

cytokinesw

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49
Q

what are cytokines produced by

A

PMN
Macrophage
Lymphocytes
Fibroblasts
Epithelial cells

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50
Q

what cell

Elevated in gingivitis and periodontitis
Correlates with disease severity
Exacerbates inflammation, bone resorption
Stimulates production of PGE2, NO, MMPs
Mainly produced by monocyte, macrophage, PMN

A

IL-1beta (cytokine)

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51
Q

what cell

Stimulated by IL-1B and TNF-a
Produced by T-cell, B-cell, macrophage, dendritic
cells, fibroblasts, osteoblast
Stimulates development of osteoclasts
Stimulates bone resorption

A

IL-6 (cytokine)

52
Q

what is this:

Secreted by macrophages in response to LPS
Increased levels in periodontitis
Stimulates development of osteoclasts
Apoptosis of fibroblasts (limits tissue repair)
Upregulation of MMPs

A

TNF-alpha (cytokine)

53
Q

prostaglandins are derived from what

A

arachidonic acid

54
Q

arachidonic acid is metabolized by ___ and ___

A

COX-1 and COX-2

55
Q

what is PGE-2 responsible for

A

Vasodilation
Induces cytokine production
Produced by macrophages, fibroblasts
Induces MMPs production
Induces osteoclastic bone resorption
Inhibited by NSAIDs

56
Q

what is a family of proteolytic enzymes and degrades collagen, gelatin, and elastin

A

MMP

57
Q

what are PMN MMP produced by

A

PMN, macrophages, fibroblasts, epithelial cells, osteoblasts, osteoclasts

58
Q

what MMP degrade Type I collagen found in PDL

A

MMP-8 and MMP-8 (PMNs)

59
Q

what MMP affect collagenase-1

A

MMP-1 (fibroblast)

60
Q

what is MMP inhibited by

A

TIMP (specifically TIMP-1) and tetracycline

61
Q

what does TIMP stand for

A

tissue inhibitor of metalloproteinases

62
Q

TIMP-1 is produced by what

A

fibroblast, macrophage, and endothelial cells

63
Q

osteoclastic boen resorption occurs at ___ approaches the bone

A

tissue inflamamtion

64
Q

what is a protective mech to prevent bacterial invasion of bone and leads to tooth mobility, tooth loss

A

osteoclastic bone reorption

65
Q

inflammatory mediators must be ___ mm from bone to stimulate bone reosorption. this is the critical distance

A

<2.5 mm

66
Q

what prevents binding of RANKL to RANK

A

osteoprotegerin (decoy to prevent resorption)

67
Q

sites with periodontitis have [increased or diecreased] RANKL and [increased or decreased] OPG

A

increase RANKL, decrease OPG

68
Q

what can be used as a therapeutic role to “switch off” inflammation

A

lipoxin, resolvins, and protextins, and antiinflammatory cytokines

69
Q

what are anti-inflammatory cytokines

A

IL-10 and TGF-beta

70
Q

in innate immune response, is the response improved as a result of previous exposure to pathogen

A

innate immune response

71
Q

T/F: cells of innate immune response kill many different pathogens rather than one specific pathogen

A

TRUE

72
Q

what are the cells of innate immune response

A

Monocytes
Macrophages
Neutrophils
Peripheral dendritic cell
Eosinophil
Basophil
Mast cell
NK cells

73
Q

what cell of innate immune response:

Resides in epithelium
Ingests antigen and transports it to lymph nodes

A

peripheral dendritic cell

74
Q

what cell of innate immune response:

Phagocytic leukocyte
Layer of PMNs in junctional epithelium: host defense
barrier

A

neutrophil (PMN)

75
Q

monocyte vs. macrophage

A

Phagocytic leukocyte
Monocyte: circulating in blood
Macrophage: differentiate and live in the tissue
Macrophages present antigen to T cells

76
Q

what cells orchestrate the CHRONIC immune response

A

macrophages and lymphocytes

77
Q

what are large granular cytotoxic lymphocytes

A

NK cells

78
Q

what recognizes and kills tumor cells and virally infected cells in innate immunity

A

NK cells

79
Q

what Recognizes changes in Major Histocompatibility
Complex (MHC) Class I molecule (found on all
cells)

A

NK cells

80
Q

are normal cells killed by NK cells

A

no

81
Q

alterations in antigen presented in MHC class I molecule of tumor-infected cells result in what

A

NK killing of infected cell

82
Q

what increases after exposure to pathogen and maintains higher levels of immunity for years

A

adaptive immune response

83
Q

what are the different lyphocytes

A

T cells (helper CD4, cytotoxic CD8) and B cells

84
Q

what cells are in stable perio

A

t cells

85
Q

what cells are in active perio

A

B-cells, plasma cells, progression of disease

86
Q

do lymphocytes generate progeny that recognize same antigen

A

yes

87
Q

what enables the immune system to respond more rapidly when re-exposed to same pathogen

A

lymphocytes

88
Q

what are the T cells of adaptive immune response

A

lyphocytes, TCR, CD4+, Th1, Th2, CD8

89
Q

what recognizes antigens on surface of antigen presenting cells

A

T-cell antigen receptor

90
Q

what helps immune response by providing proliferation and differenation signals thru cytokine secretion

A

CD4+

91
Q

what secretes IFN-gamma, activates cell-mediated immunity

A

Th1

92
Q

what secretes IL-4, IL-5, IL-13 and regulates humoral (antibody) mediated immunity

A

Th2

93
Q

what controls intra-cellular antigens (bacteria, fungi, viruses)

A

CD8+ cytotoxic T cells

94
Q

in absence of T cell, what do B cells do

A

differentiate to form PLASMA CELLS that secrete IgM antibody (primary response immunoglobulins)

95
Q

in presence of T cell, what do B cells do

A

differentiate to MEMORY B cells

96
Q

what cells give rise to plasma cells that secrete IgG, IgA, IgE antibody

A

memory B cells

97
Q

due to memory, secondary response is what?

A

rapid onset, longer duration, greater in strength, greater specificity against antigen

98
Q

what are antigen presenting cells

A
  1. peripheral dentritic cells
  2. langerhans cells
  3. macrophages
  4. B cells
99
Q

what are the function of antigen presenting cells

A
  1. express MHC Class II molecules
  2. present antigen to CD4+ T cells, which control proliferation of other T and B cells
100
Q

what is a network of membrane associated cell receptors and soluble serum glycoproteins

A

complements

101
Q

where are complements produced

A

liver and macrophages

102
Q

what enables leukocytes to recognize and bind foreign substances for which they lack receptors

A

complement

103
Q

does complement promotes inflammation

A

YES

104
Q

do complements exert negative regulation on T-cell immunity

A

yes

105
Q

does complement promote immune homeostasis

A

yes

106
Q

are complements activated within the cell (in addition to circulation and cell surface)

A

yes

107
Q

do complements participate in basic cellular processes

A

yes

108
Q

what is an intracellular effector system and plays a critical role in induction and control of T cell responses

A

complement

109
Q

what complement:

increases vascular permeability and dilation

A

C2a

110
Q

what complement:

Anaphylotoxins
Induce mast cell secretion
Chemotaxin
Attracts leukocytes

A

C3a, C5a

111
Q

what complement:

Opsonin
Coats molecules to enable phagocytes to ingest
them

A

C3b

112
Q

what complement:

C5b, C6, C7, C8, C9
Lyses bacteria and fungi by forming a large pore
in the target cell membrane

A

membrane attack complex

113
Q

what is directed movement of leukocytes from blood into local tissues

A

transendothelial migration

114
Q

defects in transendothelial migration are associated with what

A

periodontits as a manifestation of systemic disease

115
Q

steps of transendothelial migration

A
  1. rolling
  2. insult
  3. signaling endo
  4. increased rolling
  5. rolling arrest
  6. strong adhesion
  7. zipper phase
  8. basement membrane degradation
  9. chemotaxis
116
Q

what are the leukocyte functions

A
  1. chemotaxis
  2. phagocytosis
  3. killing
  4. antigen presentation
117
Q

mast cells in tissue chemotaxis release what

A

neutrophil chemotactic factor

118
Q

in chemotaxis C5a attracts what

A

nutrophils

119
Q

localized aggressive periodontitis (1999) has been renamed to what in 2018

A

Stage III-IV, Grade C

120
Q

what causes localized aggressive perio/stage III-IV, Grade C

A

decrease in chemotactic response to C5a due to dysfunctional neutrophils

121
Q

what is a defect in neutrophil transendothelial migration

A

leukocyte adhesion deficiency

122
Q

what has a lack of extravascular neutrophils in perio tissues and affects primary and perm dentitions

A

leukocyte adhesion deficiency

123
Q

what deficiency causes bacteria destroy host tissue unimpeded by normal host immune response

A

leukocyte adhesion deficiency

124
Q

what is a cyclic reduction in circulating neutrophils

A

cyclic neutropenia

125
Q

what is a tetracycline used in SUB-antimicrobial doe as an adjuct to treat periodontitis

A

doxycycline

126
Q

what is doxycycline and example of

A

tetracycline

127
Q

what enzymes is doxycyline inhibitins

A

MMPs (know it as collagenase that breaks down bone)

23 Periodontology (13 decks)

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