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periodontal pathogens Flashcards

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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
what does a pathogen do when doing desquamation of the epithelium
Invade epithelium | bind to underlying cells
26
how does a pathogen prevent antibodies from bindnig
IgG and IgA proteases | mimicing host antigens
27
how doe a pathogen avoid.kill phagocytic cells
LEukotoxin | Non-lethal suppression of immune cells
28
what are the big 3 periodontal pathogens
P. gingivalis A Actinomycetemcomitans T. Forsythia
29
what colors are the primary/healthy colonizers of the subgingival microbial complex
Yellow Green Blue purple
30
what color are the tertiary colonizers of the subgingival microbial complex
Red | orange
31
Red Subgingival microbial complexes repressent what
Always with disease, and goes away once you begin to cure complex bacteria - associated with periodontities
32
what color of the subgingval microbial complex is recgonized secondary colonizers
orange
33
do the orange subgingival microbial complexes causes disease
May or may not cause disease
34
can Aggregatibacter actinomycetemcomitans move
No, non-motile
35
is Aggregatibacter actinomycetemcomitans gram positive
No, gram negative
36
Aggregatibacter actinomycetemcomitans source of energy
saccharolytics
37
what envirnoment does Aggregatibacter actinomycetemcomitans prefer
High CO2
38
shape of Aggregatibacter actinomycetemcomitans
Round-ended rod with star shaped colonies
39
how common is AA in periodontitis
High numbers, found in active sites
40
what happens when you remove/suppress AA in periodontitis
Successful therapy
41
where does AA tend to find itself
In Recurrent lesions
42
how does a Host respond to AA
Systemic and local antibody response
43
what are the VIrulence factors for AA
``` Tissue Invasion into epithelial and endothelial cells Leukotoxin Fibroblast inhibiting factor Endotoxin Collagenase ```
44
AA affect on other organisms
INhibits growth of commensals such as Streptococcus sanguis
45
what happens when we give animals AA
Induced disease
46
what is leukotoxin
Kills neutrophils
47
do we always find AA in periotdontisis
No, not always
48
Does AA always cause disease
no, can be found in healthy subjects
49
what clusters of the leukotoxin gene causes idesase
Cluster II is severe disease | CLuster XII and XIV assocaited to healthy
50
when does AA more likely to cause disease
with a 530 bp deletion (23x more likely to be disease associated than full length promote
51
how many AA serotypes are there
5
52
what determines the serotype of AA
polysaccharides on the surface of an organism
53
what are the dominant antigens for a serotype
Serotype specific surface antigens
54
how many serotypes infect a patient
Only one at a type
55
what AA serotype is most commonly associated with localized aggressive perio in the USA
b
56
what AA serotype is associated with health in finland, but disease in Japan
a
57
importantce of serotype on immunity
has a role in resistance to phagocytosis and killing PMNs
58
what are the VIrulence factors of AA
``` Leukotoxin Cytolethal distending toxin (CDT) Chaperonin 60 LPS OMP, vesicles Fimbriae Actinobacillin Collagenase Immunosuppresiive factor ```
59
action of Leukotoxin
Induces apoptosis
60
action of LPS
apoptosis, bone resorption etc
61
what promotes AA colonization and persistence in the oral cavity
adhesins bacteriocins invasins antibiotic resistance
62
where can AA adhere in the oral cavity
tooth surface Oral bacteria epithelial cells ECM
63
is porphyromonas gingivalis gram neg or pos
Gram negative
64
how does Porphymonas gingivalis feel about O2
Anaerobic
65
can porphyromonas gingivalis move
No, non-motile
66
what is the shape of porphyromonas gingivalis
asacharolytic rods
67
what color is porphyromonas gingivalis
Black pigmented bacteriodes
68
what does porphyromonas gingivalis produce
``` collagenase proteases hemolysins endotoxin fatty acids NH3 H2S indole ```
69
what is the importance of cystein proteinases in porphyromonas gingivalis
Protein degredation | maturation of cell surface proteins (fimA fimbrillin)
70
what shows the Pg is a pathogen
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
what shows that Pg may not be a pathogen
Seen in health not always in disease High antibody response not a lot in the subgingival community
72
what Pg virulence factors are involved in colonization and attachment
Fimrbiae hemagglutinins OMPs vesicles
73
how does P. gingivalis evade (modulate) host respsonse
Ig and complement proteases LPS capsule Other antiphagocytic products
74
what aids in multiplying in P. gingivalis
Proteinases | Hemolysins
75
what is involved in damaging host tissues for P. gingivalis
``` Proteinases (Arg-, lysgingipains) collagenase Trypsin-like activity fibronlytic keratinolytic other hydrolytic activities ```
76
how do we treat P. gingivalis
mechanical and chemotherapeutic - aoxicillin 500mg and metronidaszole 250mg effective for reducing bacteria - surgical approach to eliminate tissue reservoirs
77
how does Knowledge of bactireia change how we treat periodontitis
palque removal and control rational targeted antimicrobial therapy control of disease before all other treatment due to cross-infection
78
what are the targets to disrupt biofilm
Exopolysaccharide degraders Target early colonizers anti-adhesions interrupt cell-cell communication
79
can we use vaccines to prevent perio
Not a good idea
80
what are the microbio tests we do
Microbial sensitivity | Chairside (BANA test-pg, Td, Fn)
81
other names for Tannerella forsythia
Bacteroides forsythus | Tannerella forsythensis
82
is tanneralla forsythia gram pos or neg
Gram negative
83
how does Tannerella forsythia fell about air
Anaerobic
84
shape of tannerella forsythia
Spindle-shaped as a highly pleomorphic rod
85
what does Tannerela forsythia need to survive
N-acetylmuramic acid (NAM)
86
what does Tannerella forsythia co-cultivate with
F nucleatum
87
what does the serrated S-layer on the cell surface of tannerella forsythia
Mediates Adhesion | Hemaglutionation
88
what shows that Tf is a pathogen
``` 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
is treponema denticola gram negative or positive
Gram negative
90
how does Treponema denticola feel about O2
anaerobic
91
what is the shape of treponema denticola
Helical-shaped
92
can treponema denticola
high motile microorganisms
93
where was treponema denticola 1st identified
ANUG
94
is prevotella intermedia/ nigrescens gram negative or possitive
Gram negative
95
Shape of prevotella intermedia/nigrescens
Short, round-ended rod
96
how does Prevotella intermedia/ nigrescens feel about O2
Anaerobic
97
What color is Prevotella intermedia/ nigrescens
Black pigmented Bacteriodes
98
what does Prevotella intermedia/nigrescens grow well in
Luxuriant growth in naphthoquinone
99
when in Prevotella intermedia/nigrescens appear during life
Puberty/pregnancy gingivitis
100
where is prevotella intermedia/nigrescenes elevated
NUG
101
evidence for Prevotella intermedia and treponema denticola as pthogens
Seen in progressing sites demonstrated in intercellular spaces induce alveolar bone loss sites with it have BOP
102
is Fusobacterium nucleatum gram neg or pos
Gram negative
103
how does Fusobacterium nucleatum feel about area
Anaerobic
104
shape of fusobacterium nucleatum
Spindle shaped rod
105
when does Fusobacterium nucleatum colonized
Early colonizer in plaque
106
roll of Fusobacterium nucleatum in plaque
Bridging organisms
107
where is fusobacterium nucleatum most commonly isolated
From subgingival microbiotia in health and disease
108
what does Fusobacterium nucleatum do to leukocytes
Induce cell death in leukocytes | - release of cytokines, elastase, oxygen radicals
109
how many oral species are there
700
110
how many gram positive species associated with disase
Several
111
how many gram negative species assocaited with healtyh
Several
112
what are the red pathogens
P. gingibalis B. FOrsythus T. Denticola

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