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AU 15 - Periodontology > Periodontal pathogens > Flashcards

Periodontal pathogens Flashcards

1
Q

What is the Non-Specific Plaque Hypothesis?

A

Plaque control is important in perio treatment
All plaque bacteria are considered bad
Any accumulation of micro-organisms at or below the gingival margin cause inflammation

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2
Q

What is the Specific Plaque Hypothesis?

A

Specific organisms in the dental plaque are the etiological agents and not all bacteria are bad
Microbial composition of disease sites are different from healthy sites
Local debridement and systemic antibiotics can control LAP (localized, aggressive periodontitis)

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3
Q

Which Plaque Hypothesis guides our clinical thinking today?

A

Specific Plaque Hypothesis

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4
Q

What are the major contributors to periodontal disease initiation and progression?

A

The virulent periodontal pathogen
The local environment
Host susceptibility

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5
Q

What about the pathogen is a prerequisite to perio disease initiation and progression?

A

The STRAIN, not the species is important (a strain of something can be healthy, and a different strain of the same species can cause disease)
The pathogen must express virulence factors
The pathogen must be in the right location (adjacent to the epithelium, apical part of the pocket)

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6
Q

Niche saturation

A

When primary colonizers come in, they take up every single thing and prevent foreign colonization
This is a sign of gingival health

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7
Q

What can increase host susceptibility to perio disease?

A

HIV
Diabetes
Smoking

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8
Q

Ecological Plaque Hypothesis

A

There are no ‘good’ or ‘bad’ bacteria, but only certain things the body can tolerate
If there is a shift in ecology (more acidic, less aerobic, etc), bad things can happen

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9
Q

Oral dysbiosis

A

Pathogens require primary colonizers for attachment, and possibly other things for nutrition
These pathogens are always present, but their numbers can spike when the environment changes and gives them a chance to grow

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10
Q

What three bacteria have the highest association with periodontal disease?

A

P. gingivalis
A. actinomycetemcomitans
T. forsythia

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11
Q

Actinobacillus Actinomycetemcomitans biology

A 
Non-motile
Gram-
Sacchrolytic (breaks down sugars)
Capnophilic (works well with lots of CO2)
Round end rods
Star-shaped colonies
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12
Q

What is the evidence for A. actinomycetemcomitans as a pathogen?

A

High numbers associated with periodontitis (seen at active and prospective sties)
Eliminating or supressing it results in successful therapy
Host responds to high levels of systemic and local antibody response
It has a bunch of virulence factors
It inhibits growth of S. sanguis
It induces disease in animal models

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13
Q

What is the evidence against A. actinomycetemcomitans as a pathogen?

A

It isn’t seen in all cases of aggressive periodontitis
It is seen periodontically healthy subjects
Some research shows in needs a base pair deletion to be disease-associated

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14
Q

How many serotypes are there of A. actinomycetemcomitans and what are they based on?

A

5

They are based on polysaccharides on the surface of the organism

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15
Q

What serotype of A. actinomycetemcomitans is associated with localized aggresive periodontitis in the USA?

A

Serotype B

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16
Q

What is interesting about Serotype A of A. actinomycetemcomitans?

A

It is health-associated in Finland, but disease-associated in Japan

17
Q

How do we treat periodontitis with A. actinomycetemcomitans?

A

Mechanical and chemotheraputic approach is vital
Amoxicillin + Metronidazole along with RPD is effective with A. actinomycetemcomitans
All patients w/ LAP require a surgical approach as well to eliminate tissue reservoirs

18
Q

What virulence factors are associated with A. actinomycetemcomitans?

A

Leukotoxin
Fibroblast inhibiting factor
Endotoxin
Collagenase

19
Q

P. gingivalis biology

A 
Gram-
Anaerobic
Non-motile
Asachrolytic rods
Black pigment bacteriodes
20
Q

What substances does P. gingivalis produce?

A 
Collagenase
Proteosomes
Hemolysins
Endotoxins
Fatty acids
NH2
H2S
Indole
21
Q

What role do cysteine proteinases serve?

A

They are important in protein degradation and in the maturation of P. gingivalis cell surface proteins

22
Q

What is the evidence for P. gingivalis as a pathogen?

A

Elevated in lesions of periodontitis, progressing lesions, and the presence indicates increased risk for attachment loss
Successful therapy leads to elimination and a lowered antibody level
The host responds with antibodies
It has several virulence factors and invades epithelial cells
It induces disease in animal studies

23
Q

What is the evidence against P. gingivalis as a pathogen?

A

It is seen in healthy mouths
Not always seen in diseased mouths
There is a high antibody response
It is not numerous in subgingival communities (even in disease)

24
Q

Tannerella forsythia biology

A

Gram-
Anaerobic
Spindle shaped
Highly pleomorphic rods
Requires N-acetylmuramic acid (NAM) for growth
Co-cultivates with F. nucleatum
Has a serrated S-layer on the cell surface

25
Q

What does the S-layer on T. forsythia do?

A

It mediates adhesion
Provides hemagglutination
It is its most well-known virulence factor

26
Q

What is the evidence for T. forsythia as a pathogen?

A

Elevated in lesions of periodontitis and progressing lesions, and the presence indicates an increased risk for attachment loss
Elimination results in successful therapy
Hosts respond with elevated levels of antibodies
It has several virulence factors
It induces disease in animal tests

27
Q

Treponoma denticola biology

A

Gram-
Anaerobic
Helical-shaped
Highly motile
1st identified in Acute necrotizing ulcerative gingivitis (ANUG)
There are several different species that are hard to distinguish

28
Q

Prevotella intermedia/nigrescens biology

A 
Gram-
Short, round-ended rod
Anaerobic
Black pigmented bacteriodes
Luxuriant growth in naphthoquinone
Associated with puberty/pregnancy gingivitis
Elevated in NUG
29
Q

What is the evidence for P. intermedia/nigrescens as a pathogen?

A 
Seen in progressing sites
Demonstrated in intercellular spaces
Induces alveolar bone loss in rats
Sites with these show persistent BOP
Amoxicillin and Metro decreases BOP and Pi/Pn levels
Releases MMP-8 and 9 in pockets
30
Q

Fusobacterium nucleatum biology

A

Gram -
Anaerobic
Spindle-shaped rod
Early colonizer in plaque - bridge organism
Most common isolate cultured from subgingival mucosa in health and disease
Can induce cell death in leaukocytes

31
Q

What does F. nucleatum release?

A

Cytokines
Elastase
Oxygen radical from leukocytes

32
Q

T/F - we only remove bad plaque

A

False - even though only certain types of plaque, we are unable to selectively kill them.
So, we do wholesale plaque removal

33
Q

T/F - If a patient has any periodontal disease, you should NOT place an implant

A

True

34
Q

What targets can we use to disrupt biofilm?

A

Exopolysaccharide degraders
Early colonizers
Anti-adhesins
Interrupt cell-to-cell communication

35
Q

Why can’t vaccines be used to prevent periodontitis?

A

There are too many different organisms that can cause it

AU 15 - Periodontology (8 decks)

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