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periodontal pathogens Flashcards

1
Q

what is the non-specific plaque hypothesis

A

All plaque bacteria is considered to be bad and any accumulation of micro-organisms at or below the gingival margin causes inflammation

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2
Q

treating periodontum in the non-specific palque hypothesis

A

Plaque control is important in perio treatment

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3
Q

what is the specific plaque hypothesis

A

Specific organisms in dental palque are etiological agents

- microbio comp of disease sites different from healthy

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4
Q

how do you control LAP in the specific plaque hypothesis

A

Local debridement and systemic antibiotics

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5
Q

what is the ecological laque hypothesis

A

That a change in environment, leads to a change in the palque that causes it to become bad

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6
Q

what kind of environment is found in periodontitis

A

an anaerobic envinroment, with lots of anaerobic pathogens

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7
Q

what is Oral Dysbiosis

A

Bacteria capable of causing tissue damage directly, may depend on the presence of other cells for nutrients or attachment

  • both my also rely on other organisms
  • community needed for perio disease
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8
Q

roll of Secondary colonizers in Oral dysbiosis

A

act as community actovists to bring together bacteria

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9
Q

what is needed for disease initiation and progession

A

A virulent perio pathogen
a specific local environment
Host susceptibility

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10
Q

do all bacterial pathogens of a species cause disease

A

No, P. gingibalis with type I and V FimA genotypes are healthy
- II and IV cause disease

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11
Q

what must a pthogen have to be a virulent periodontal pathogen

A

Must express virulence factors in the right location site

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12
Q

how can the local envirnoment prevent pathogens

A

Colonization by beneficial species can dilute the level of pathogens, and even inhibit them vis ROS

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13
Q

what does the presence of Iron lead to

A

leads to lots of pathogens

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14
Q

where does Iron come from for pathogens to feed on

A

From bleeding

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15
Q

Iron effect on P. gingivalis

A

Increases outer membrane protein expression

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16
Q

Roll of S. Cristatus in pathogens

A

can inhibit A. a pthogens and inhibit FimA expression by P.gingivalis leading to less disease

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17
Q

what host factors can increase host susceptibility

A

HIV
Diabetes
Smoking

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18
Q

Steps of PAthogenic mechanisms

A

Colonization

  • adhersion
  • Coaggregation
  • Nutrient Utilization
  • Competitive inhibition
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19
Q

what allows bacteria to bind to host receptors

A 
Adhesins 
 - type I or IV collagen
 - Sialic acid
 - galactosyl residues
Fimbriae
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20
Q

what does Veillonella use to eat

A

Lactaet made by streptococci

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21
Q

what does Campylobacter use to eat

A

Formate made by selenomonas

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22
Q

what does Porphyromonas use to eat

A

Hemin from blood in sulcus

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23
Q

how does A pathogen competiviely inhibit other organisms

A

BActeriocins

Hydrogen peroxide production

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24
Q

how does A pthogen overcome host defenses

A
  • Desquamation of the epithelium
  • prevent binding of antibodies
  • kill/evade phagocytic cells
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25
Q

what does a pathogen do when doing desquamation of the epithelium

A

Invade epithelium

bind to underlying cells

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26
Q

how does a pathogen prevent antibodies from bindnig

A

IgG and IgA proteases

mimicing host antigens

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27
Q

how doe a pathogen avoid.kill phagocytic cells

A

LEukotoxin

Non-lethal suppression of immune cells

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28
Q

what are the big 3 periodontal pathogens

A

P. gingivalis
A Actinomycetemcomitans
T. Forsythia

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29
Q

what colors are the primary/healthy colonizers of the subgingival microbial complex

A

Yellow
Green
Blue
purple

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30
Q

what color are the tertiary colonizers of the subgingival microbial complex

A

Red

orange

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31
Q

Red Subgingival microbial complexes repressent what

A

Always with disease, and goes away once you begin to cure complex bacteria
- associated with periodontities

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32
Q

what color of the subgingval microbial complex is recgonized secondary colonizers

A

orange

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33
Q

do the orange subgingival microbial complexes causes disease

A

May or may not cause disease

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34
Q

can Aggregatibacter actinomycetemcomitans move

A

No, non-motile

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35
Q

is Aggregatibacter actinomycetemcomitans gram positive

A

No, gram negative

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36
Q

Aggregatibacter actinomycetemcomitans source of energy

A

saccharolytics

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37
Q

what envirnoment does Aggregatibacter actinomycetemcomitans prefer

A

High CO2

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38
Q

shape of Aggregatibacter actinomycetemcomitans

A

Round-ended rod with star shaped colonies

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39
Q

how common is AA in periodontitis

A

High numbers, found in active sites

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40
Q

what happens when you remove/suppress AA in periodontitis

A

Successful therapy

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41
Q

where does AA tend to find itself

A

In Recurrent lesions

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42
Q

how does a Host respond to AA

A

Systemic and local antibody response

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43
Q

what are the VIrulence factors for AA

A 
Tissue Invasion into epithelial and endothelial cells
Leukotoxin
Fibroblast inhibiting factor
Endotoxin
Collagenase
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44
Q

AA affect on other organisms

A

INhibits growth of commensals such as Streptococcus sanguis

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45
Q

what happens when we give animals AA

A

Induced disease

46
Q

what is leukotoxin

A

Kills neutrophils

47
Q

do we always find AA in periotdontisis

A

No, not always

48
Q

Does AA always cause disease

A

no, can be found in healthy subjects

49
Q

what clusters of the leukotoxin gene causes idesase

A

Cluster II is severe disease

CLuster XII and XIV assocaited to healthy

50
Q

when does AA more likely to cause disease

A

with a 530 bp deletion (23x more likely to be disease associated than full length promote

51
Q

how many AA serotypes are there

A

5

52
Q

what determines the serotype of AA

A

polysaccharides on the surface of an organism

53
Q

what are the dominant antigens for a serotype

A

Serotype specific surface antigens

54
Q

how many serotypes infect a patient

A

Only one at a type

55
Q

what AA serotype is most commonly associated with localized aggressive perio in the USA

A

b

56
Q

what AA serotype is associated with health in finland, but disease in Japan

A

a

57
Q

importantce of serotype on immunity

A

has a role in resistance to phagocytosis and killing PMNs

58
Q

what are the VIrulence factors of AA

A 
Leukotoxin
Cytolethal distending toxin (CDT)
Chaperonin 60
LPS
OMP, vesicles
Fimbriae
Actinobacillin
Collagenase
Immunosuppresiive factor
59
Q

action of Leukotoxin

A

Induces apoptosis

60
Q

action of LPS

A

apoptosis, bone resorption etc

61
Q

what promotes AA colonization and persistence in the oral cavity

A

adhesins
bacteriocins
invasins
antibiotic resistance

62
Q

where can AA adhere in the oral cavity

A

tooth surface
Oral bacteria
epithelial cells
ECM

63
Q

is porphyromonas gingivalis gram neg or pos

A

Gram negative

64
Q

how does Porphymonas gingivalis feel about O2

A

Anaerobic

65
Q

can porphyromonas gingivalis move

A

No, non-motile

66
Q

what is the shape of porphyromonas gingivalis

A

asacharolytic rods

67
Q

what color is porphyromonas gingivalis

A

Black pigmented bacteriodes

68
Q

what does porphyromonas gingivalis produce

A 
collagenase
proteases
hemolysins
endotoxin
fatty acids
NH3
H2S
indole
69
Q

what is the importance of cystein proteinases in porphyromonas gingivalis

A

Protein degredation

maturation of cell surface proteins (fimA fimbrillin)

70
Q

what shows the Pg is a pathogen

A

More in lessions, and persense leads to increased risk of atachment loss
elimination leads to successful therapy (lower Antibody level)
Higher antibody is subjects with periodontis
Virulence factors, plus epithelial cell invasion
induces decesase in aminals

71
Q

what shows that Pg may not be a pathogen

A

Seen in health
not always in disease
High antibody response
not a lot in the subgingival community

72
Q

what Pg virulence factors are involved in colonization and attachment

A

Fimrbiae
hemagglutinins
OMPs
vesicles

73
Q

how does P. gingivalis evade (modulate) host respsonse

A

Ig and complement proteases
LPS
capsule
Other antiphagocytic products

74
Q

what aids in multiplying in P. gingivalis

A

Proteinases

Hemolysins

75
Q

what is involved in damaging host tissues for P. gingivalis

A 
Proteinases (Arg-, lysgingipains)
collagenase
Trypsin-like activity
fibronlytic
keratinolytic
other hydrolytic activities
76
Q

how do we treat P. gingivalis

A

mechanical and chemotherapeutic

  • aoxicillin 500mg and metronidaszole 250mg effective for reducing bacteria
  • surgical approach to eliminate tissue reservoirs
77
Q

how does Knowledge of bactireia change how we treat periodontitis

A

palque removal and control rational
targeted antimicrobial therapy
control of disease before all other treatment due to cross-infection

78
Q

what are the targets to disrupt biofilm

A

Exopolysaccharide degraders
Target early colonizers
anti-adhesions
interrupt cell-cell communication

79
Q

can we use vaccines to prevent perio

A

Not a good idea

80
Q

what are the microbio tests we do

A

Microbial sensitivity

Chairside (BANA test-pg, Td, Fn)

81
Q

other names for Tannerella forsythia

A

Bacteroides forsythus

Tannerella forsythensis

82
Q

is tanneralla forsythia gram pos or neg

A

Gram negative

83
Q

how does Tannerella forsythia fell about air

A

Anaerobic

84
Q

shape of tannerella forsythia

A

Spindle-shaped as a highly pleomorphic rod

85
Q

what does Tannerela forsythia need to survive

A

N-acetylmuramic acid (NAM)

86
Q

what does Tannerella forsythia co-cultivate with

A

F nucleatum

87
Q

what does the serrated S-layer on the cell surface of tannerella forsythia

A

Mediates Adhesion

Hemaglutionation

88
Q

what shows that Tf is a pathogen

A 
Found in perio lesions
low in healthy people
Elimination gives successful therapy, and recurrent lessions harbor organisms
reduced in successfully treatment 
elevant antibody
virulence factors
invades epithelial cells
induced disease in rats
89
Q

is treponema denticola gram negative or positive

A

Gram negative

90
Q

how does Treponema denticola feel about O2

A

anaerobic

91
Q

what is the shape of treponema denticola

A

Helical-shaped

92
Q

can treponema denticola

A

high motile microorganisms

93
Q

where was treponema denticola 1st identified

A

ANUG

94
Q

is prevotella intermedia/ nigrescens gram negative or possitive

A

Gram negative

95
Q

Shape of prevotella intermedia/nigrescens

A

Short, round-ended rod

96
Q

how does Prevotella intermedia/ nigrescens feel about O2

A

Anaerobic

97
Q

What color is Prevotella intermedia/ nigrescens

A

Black pigmented Bacteriodes

98
Q

what does Prevotella intermedia/nigrescens grow well in

A

Luxuriant growth in naphthoquinone

99
Q

when in Prevotella intermedia/nigrescens appear during life

A

Puberty/pregnancy gingivitis

100
Q

where is prevotella intermedia/nigrescenes elevated

A

NUG

101
Q

evidence for Prevotella intermedia and treponema denticola as pthogens

A

Seen in progressing sites
demonstrated in intercellular spaces
induce alveolar bone loss
sites with it have BOP

102
Q

is Fusobacterium nucleatum gram neg or pos

A

Gram negative

103
Q

how does Fusobacterium nucleatum feel about area

A

Anaerobic

104
Q

shape of fusobacterium nucleatum

A

Spindle shaped rod

105
Q

when does Fusobacterium nucleatum colonized

A

Early colonizer in plaque

106
Q

roll of Fusobacterium nucleatum in plaque

A

Bridging organisms

107
Q

where is fusobacterium nucleatum most commonly isolated

A

From subgingival microbiotia in health and disease

108
Q

what does Fusobacterium nucleatum do to leukocytes

A

Induce cell death in leukocytes

- release of cytokines, elastase, oxygen radicals

109
Q

how many oral species are there

A

700

110
Q

how many gram positive species associated with disase

A

Several

111
Q

how many gram negative species assocaited with healtyh

A

Several

112
Q

what are the red pathogens

A

P. gingibalis
B. FOrsythus
T. Denticola

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