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AU14 - Periodontology Exam 1 > 09/05 - Periodontal Pathogens > Flashcards

09/05 - Periodontal Pathogens Flashcards

1
Q

What is the non-specific plaque hypothesis?

A
  • plaque control important in periodontal treatment
  • all plaque bacteria considered bad
  • any accumulation of micro-organisms at or below the gingival margin causes inflammation
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2
Q

What is the specific plaque hypothesis?

A
  • specific organisms in dental plaque are the etiological agents
  • microbial composition of disease sites different from healthy sites
  • local debridement and systemic antibioitcs could control LAP
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3
Q

What are the prerequisites for disease initiation and progression?

A
  • VIRULENT PERIODONTAL PATHOGEN: P. gingivalis with type II and IV fimA genotypes; virulence factors; right location in the site (adjacent to epithelium, apical part of the pocket)
  • LOCAL ENVIRONMENT: colonization by beneficial species dilutes and inhibits pathogens; effect of local “regulon”/subgingival environment (iron increases outer membrane protein expression in P. gingivalis and S. cristatus can inhibit fimA expression)
  • HOST SUSCEPTIBILITY: HIV infection; diabetes; smoking
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4
Q

What are the 4 different ways through which pathogens colonize?

A
  • ADHESINS ON BACTERIA BIND HOST RECEPTORS: type I or IV collagen, sialic acid, galactosyl residues; bacteria have fimbriae or outer membrane proteins
  • COAGGREGATION
  • NUTRIENT UTILIZATION: Veillonella uses lactate made by streptococci; Campylobacter uses formate made by Selenomonas; Porphyromonas uses hermin from blood in sulcus
  • COMPETITIVE INHIBITION: bacteriocins; hydrogen perioxide production
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5
Q

What are the 3 ways through which pathogens overcome host defenses?

A
  • DESQUAMATION OF EPITHELIUM: invade epithelium and bind to underlying cells
  • PREVENT ANTIBODY-BINDING: IgG and IgA proteases; mimic host antigens
  • PREVENT PHAGOCYTIC CELLS: leukotoxin; non-lethal suppression of immune cells
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6
Q

The World Workshop in 1996 designated 3 pathogens. What are they?

A
  • P. gingivalis
  • A. actinomycetemcomitans
  • T. forsythia
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7
Q

Is Actinobacillus actinomycetemcomitans (AA) motile? Gram positive or negative? How does it get its energy? Aerobic or anaerobic? Shape of bacteria and colonies?

A
  • non-motile
  • gram-negative
  • saccharolytic (breaks down carbs for energy)
  • capnophlic (thrive in high CO2)
  • round-ended rod; star-shaped colonies
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8
Q

What is the evidence of AA as a pathogen based on association?

A
  • high numbers associated with agressive periodontisis
  • detected in active sites
  • detected in prospective studies
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9
Q

What is the evidence of AA as a pathogen based on elimination?

A
  • elimination or suppression resulted in successful therapy

- recurrent lesions harbor the species

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10
Q

What is the evidence of AA as a pathogen based on host response? It also inhibits ___ and induces ___.

A
  • high levels of systemic and local antibody response
  • inhibits growth of commensals (S. sanguis)
  • induces disease in animal models
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11
Q

What is the evidence of AA as a pathogen based on virulence factors?

A
  • tissue invasive (epithelial and endothelial cells)
  • leukotoxin
  • fibroblast inhibiting factor
  • endotoxin
  • collagenase
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12
Q

What is the evidence AGAINST AA being a pathogen?

A
  • not seen in all cases of aggressive periodontitis
  • seen in periodontally healthy subjects
  • genetic analysis of the leukotoxin gene (13 clusters identified; II seen in severe disease; XII and XIV associated with health)
  • AA with 530 bp deletion is 23x more likely to be disease-associated than AA with full length promoter region
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13
Q

There are ___ serotypes of AA which are based on ___. ___ are the dominant antigens.

A
  • 5
  • polysaccharides on the surface of an organism
  • serotype-specific surface antigens (SPA)
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14
Q

Serotype ___ of AA is most commonly associated with localized aggressive periodontitis in the USA. It has a role in resistance to ___.

A
  • b

- resistance to phagocytosis and killing by PMNs

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15
Q

Serotype ___ of AA is health-associated in Finland and disease-associated in Japan.

A

a

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16
Q

For an AA infection, ___ and ___ approach is vital to treatment. ___ and ___ are effective in reducing bacterial load. ___ approach is required to eliminate tissue reservoirs.

A
  • mechanical
  • chemotherapeutic
  • amoxicillin 500 mg
  • metronidazole 250 mg
  • surgical
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17
Q

Which of the following is not a virulence factor produced by A. actinomycetemcomitans?

a. leukotoxin
b. collagenase
c. lipoteichoic acid
d. lipopolysaccharide

A

c. lipoteichoic acid

18
Q

Is Porphyromonas gingivalis gram positive or negative? Aerobic or anaerobic? Motile? What is the shape of the bacteria and the color of the colonies?

A
  • gram-negative
  • anaerobic
  • non-motile
  • asacharolytic rods; black pigmented Bacteriodes
19
Q

What is produced by PG?

A
  • collagenase
  • proteases
  • hemolysins
  • endotoxin
  • fatty acids
  • NH3
  • H2S
  • indole
20
Q

For PG, what are cysteine proteases important for?

A
  • protein degradation

- the maturation of cell surface proteins such as fimA fimbrillin

21
Q

What is the evidence (4) of PG as a pathogen based on association?

A
  • elevated in lesions of periodontitis
  • lower in healthy sites and subjects
  • elevated in progressing lesions
  • presence indicates increased risk for attachment loss
22
Q

What is the evidence (3) of PG as a pathogen based on elimination?

A
  • elimination results in successful therapy
  • recurrent lesion harbor organisms
  • successful therapy lowered antibody level
23
Q

What is the evidence of PG as a pathogen based on host response?

A

elevated antibody in serum/saliva of subjects with periodontisis

24
Q

What is the evidence of PG as a pathogen based on virulence factors?

A
  • several factors

- invades epithelial cells in vitro

25
Q

What is the evidence of PG as a pathogen based on animal studies?

A
  • induces disease in gnotobiotic rats

- immunization decreased disease in animals

26
Q

What is the evidence AGAINST PG as a pathogen?

A
  • seen in health
  • not always seen in disease
  • high antibody response
  • not numerous in the subgingival community
27
Q

Is Tannerella forsynthia gram positive or negative? Aerobic or anaerobic? What is the shape of the bacteria?

A
  • gram-negative
  • anaerobic
  • spindle shaped; highly pleomorphic rod
28
Q

What does TF require? With what bacteria does it co-cultivate? What is on its cell surface and what does that do?

A
  • requires N-acetylmuramic acid (NAM)
  • co-cultivates with F. nucleatum
  • serrated S-layer on cell surface (mediates adhesion and hemagglutination)
29
Q

What is the evidence of TF as a pathogen based on association?

A
  • elevated in lesions of periodontitis
  • lower in healthy sites and subjects
  • elevated in progressing lesions
  • presence indicates increased risk of attachment loss
30
Q

What is the evidence of TF as a pathogen based on elimination?

A
  • elimination results in successful therapy
  • recurrent lesion harbor organism
  • reduced in successfully treated peri-implants
31
Q

What is the evidence of TF as a pathogen based on host response?

A

elevated antibody in serum/saliva of subjects with refractory periodontitis

32
Q

What is the evidence of TF as a pathogen based on virulence factors?

A
  • several factors

- invades epithelial cells in vitro

33
Q

What is the evidence of TF as a pathogen based on animal studies?

A

induces disease in gnotobiotic rats

34
Q

Is Spirochetes gram negative or positive? Aerobic or anaerobic? What shape is the bacteria? Are they motile?

A
  • gram-negative
  • anaerobic
  • helical-shaped
  • highly motile organisms
35
Q

Is Prevotella intermedia/nigrescens gram positive or negative? What is the shape of the bacteria and the appearance of the colonies? Aerobic or anaerobic?

A
  • gram-negative
  • short, round-ended rod; black pigmented Bacteriodes
  • anaerobic
36
Q

Prevotella intermedia/nigrescens has luxuriant growth in ___. It is associated with what types of gingivitis? It is elevated in ___.

A
  • naphthoquinone
  • puberty/pregnancy gingivitis
  • NUG
37
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 Pi/Pn show persistent BOP
  • amox + metro decreases BOP and Pi/Pn levels
  • releases MMP-8 and -9 in pockets
38
Q

Fusobacterium nucleatum is gram positive or negative? Aerobic or anaerobic? What shape is the bacteria? What is this bacteria’s role?

A
  • gram-negative
  • anaerobic
  • spindle-shaped rod
  • early colonizer in plaque; bridging organism
39
Q

Is FN found supra or subgingival? It can induce ___. What does it release?

A
  • subgingival microbiota in health and disease
  • induce cell death in leukocytes
  • releases cytokines, elastase and oxygen radicals from leukocytes
40
Q

The organism that is found MOST often in both remission and progression of adult periodontitis is:

a. Eubacterium timidum
b. Tannerella forsythia
c. Prevotella intermedia
d. Fusobacterium nucleatum

A

d. Fusobacterium nucleatum

41
Q

How many oral species are present? What % are uncultivated?

A
  • 700 oral species

- 60-80%

AU14 - Periodontology Exam 1 (11 decks)

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