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Periodontics I > Etiology > Flashcards

Etiology Flashcards

1
Q

what are the factors involved in periodontal pathogenesis

A
  • environment factors
  • microbial factors
  • host factors
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2
Q

what bacteria lead to gingival inflammation

A

gram positive

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3
Q

gingival inflammation alters:

A

subgingival environment

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4
Q

what causes gingivitis

A

host immune and inflammatory reactions together with genetic predisposition and environmental influences able to contain infection

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5
Q

what causes periodontitis

A

host immune and inflammatory reactions together with genetic predisposition and environmental influences unable to contain infection

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6
Q

what is dental plaque

A

the structurally and functionally organized species rich microbial biofilms that form on teeth

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7
Q

dental plaque is the main etiologic agent for:

A
  • periodontal diseases
  • dental caries
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8
Q

describe materia alba and what is it made of

A
  • white cheeselike accumulation
  • a soft accumulation of salivary proteins, bacteria, desquamated epithelial cells and food debris
  • no organized structure
  • easily displaced with water spray
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9
Q

describe dental plaque

A
  • resilient clear to yellow-grayish substance
  • primarily composed of bacteria in a matrix of salivary glycoproteins and bacterial products
  • considered to be a biofilm
  • impossible to remove by rinsing or spraying
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10
Q

describe calculus

A
  • mineralized dental plaque forms the hard deposit
  • generally covered by a layer of unmineralized dental plaque
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11
Q

what is dental plaque composed of

A
  • 70% water
  • 70% microorganisms
  • 30% intracellular matrix
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12
Q

what are the organic components of the intracellular matrix of dental plaque

A
  • polysaccharides
  • proteins
  • glycoproteins
  • lipids
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13
Q

what are the inorganic components in the intracellular matrix of dental plaque

A
  • calcium
  • phosphorus
  • other minerals such as sodium, potassium, fluoride
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14
Q

1 gram of plaque contains approximately:

A

10^11 bacteria

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15
Q

more than ______ microbial species can be identified with highly sensitive molecular techniques

A

500

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16
Q

what are the sites of accumulation of dental plaque

A
  • gingival thirds
  • cracks, pits and fissures
  • under overhanging restorations
  • around malaligned teeth
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17
Q

what is the classification of dental plaque based on

A

the position on the tooth surface toward the gingival margin

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18
Q

what are the classifications of dental plaque

A
  • supragingival plaque
  • marginal plaque
  • subgingival plaque
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19
Q

what are the types of subgingival plaque

A
  • tooth attached plaque
  • unattached plaque
  • epithelial associated plaque
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20
Q

what type of bacteria are in supragingival plaque

A

gram positive cocci and short rods

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21
Q

what is the environment of supragingival plaque

A
  • aerobic environment
  • slight diversity
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22
Q

what is the environment and type of bacteria in subgingival plaque

A
  • gram negative rods and spirochete
  • anaerobic environment
  • great diversity
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23
Q

what does supragingival plaque lead to

A

calculus formation and root caries

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24
Q

what does marginal plaque lead to

A

direct contact with gingival margin
- initiation and development of gingivitis

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25
Q

what does subgingival plaque lead to

A

tissue destruction

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26
Q

what are the steps for formation of dental plaque

A

step 1: formation of the pellicle
-step 2: initial colonization of bacteria
- step 3: secondary colonization and plaque maturation

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27
Q

what is the acquired pellicle formed by

A

adsorption of a conditioning film

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28
Q

what is the acquired pellicle

A

an organic material layer coated on all surfaces in the oral cavity including hard and soft tissues

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29
Q

acquired pellicle components are derived from:

A

saliva and crevicular fluid

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30
Q

what microbes are involved in the acquired pellicle

A

gram positive facultative microorganisms

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31
Q

how long does it take for the pellicle to form

A

1 minute

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32
Q

how is the pellicle formed

A

reversible adhesion between microbial cell surface (adhesins) and the conditioning film (receptors)

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33
Q

what does the reversible adhesion between microbial cell surface (adhesins) and the conditioning film (receptors) alter

A

the charge and the free energy of the surface which increases efficiency of the bacterial adhesion

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34
Q

how long does the reversible adhesion between microbial cell surface (adhesins) and the conditioning film (receptors) take

A

2 hours

35
Q

what happens in initial colonization

A

adherence and coadhesion

36
Q

what happens in initial colonization

A
  • bacterial mass continue to grow
  • alteration in the oxygen gradient, anaerobic conditions emerge in the deeper layers of the deposits
  • there are primary colonizers to secondary colonizers
37
Q

how long does initial colonization stage take

A

4-8 hours

38
Q

what are the primary colonizers

A
  • streptococcus spp.
  • hemophilus spp.
  • neisseria spp.
  • actinomyces spp.
  • veilonella spp.
39
Q

what are the secondary colonizers

A
  • prevotella intermedia.
  • capnocytophaga spp.
  • fusobacterium nucleatum
  • porphyromonas gingivalis
40
Q

what happens in colonization and maturation

A
  • coaggregation
  • maturation
41
Q

how long does coaggregation

A

4-8 hours

42
Q

what happens in coaggregation in plaque

A
  • secondary colonizers adhere to the bacteria that are already in the plaque mass
  • a significant feature can be seen by naked eye
43
Q

what happens in maturation of plaque

A
  • through further colonization and growth of additional species
  • quorum sensing: cell-cell signaling
44
Q

what does quorum sensing do

A
  • environment modificatino
  • metabolic interaction
45
Q

how long does maturation of plaque take

A

12 hours

46
Q

what is the structure of dental plaque

A
  • open fluid filled channels running through plaque mass
  • distinct microenvironment produced by matrix
  • step chemical gradients for oxygen and pH
  • quorum sensing results in bacterial resistance
47
Q

what is corn cob formation

A
  • coccal shaped cells attach along the tip of gram negative filamentous organisms
  • an example of inter-bacterial adherence or coaggregation
48
Q

what is the nonspecific plaque hypothesis

A
  • direct relationship between the total amount of plaque and the amplitude of the pathogenic effect
  • control of periodontal disease depends on control of plaque accumulation
  • all plaque are not equally pathogenic
49
Q

what is the standard of care in the nonspecific plaque hypothesis

A

oral hygiene measure, non- surgical/surgical debridement

50
Q

what is meant by “all plaque are not equally pathogenic” in the nonspecific plaque hypothesis

A
  • not all gingivitis develop into destructive periodontitis
  • site specificity in the pattern of disease was demonstrated in some individuals with periodontitis
51
Q

what is the specific plaque hypothesis

A
  • the pathogenicity depends on the presence of or increase in specific microorganisms
  • targeted treatment strategies aim to control or eliminate the particular pathogenic organisms
52
Q

what specific organisms increases pathogenicity in the specific plaque hypothesis

A

A. actinomicetemcomitans

53
Q

what is the ecologic plaque hypothesis

A
  • both the total amount of dental plaque and the specific microbial composition of plaque may contribute
  • microbial homeostasis: the stae of the dynamic equilibrium
54
Q

what are Kochs postulates

A
  • be routinely isolated from diseased individuals
  • be grown in pure culture in lab
  • produce similar disease when inoculated into susceptible animals
  • be recovered from lesions in a diseased lab animal
55
Q

what are the criteria for identification of periodontopathogens

A
  • Kochs postulates
  • Socransky’s criteria
56
Q

what are Socransky’s criteria

A
  • be associated with disease
  • be eliminated or decreased in sites that demonstrate clinical resolution
  • demonstrate an alteration in host cellular or immune response
  • be capable of causing disease in experimental models
  • demonstrate virulence factors
57
Q

what is the association of A. actinomycetemcomitans

A

increased in localized aggressive periodontitis lesions, some in chronic periodontitis lesions

58
Q

what is the elimination of A. actinomycetemcomitans

A

suppressed or eliminated in successful therapy, can be found in recurrent lesions

59
Q

what is the host response to A. actinomycetemcomitans

A

increased serum and local antibody levels

60
Q

what did the animal studies on A. actinomycetemcomitans show

A

capable of inducing disease in gnotobiotic

61
Q

what are the virulence factors for A. actinomycetemcomitans

A

host tissue cell adherence and invasion and leukotoxin! - main ones
-protease, collagenase, epitheliotoxin, FIF, bone resorption inducing factors

62
Q

what is the association for p. gingivalis

A

increased in periodontitis lesions, found associated with the crevicular epithelium

63
Q

how is p. gingivalis eliminated

A

suppressed or eliminated in successful therapy, can be found in recurrent lesions

64
Q

what is the host response to p. gingivalis

A

increased systemic and local antibody levels

65
Q

what did the animal studies in p. gingivalis show

A

important in experimental mixed infections

66
Q

what are the virulence factors of p. gingivalis

A
  • host tissue cell adherence and invasion, endotoxin, gingipains- main ones!
  • trypsin-like enzyme, collagenase, fibrinolysis, phospholipase A, factors that affect PMN function
67
Q

what are the toxins and enzyme bacterial products that promote tissue destruction

A
  • LPS
  • leukotoxin
  • gingipains
  • collagenase
  • protease
68
Q

what are the adhesins and what do they do

A
  • promote colonization
  • fimbria
  • gingipains
69
Q

what are the evading mechanisms bacteria use as virulence factors

A
  • the production of an extracellular capsule
  • proteolytic degradation of host immunity components: gingipains
  • modulate host response: bind serum components on bacterial cell surface
  • invasion of gingival epithelial cells: LPS
70
Q

what are the bacteria of gingivitis

A
  • actinomyces spp.
  • capnocytophaga spp.
  • campylobacter spp.
  • streptococcus spp.
  • parvimonas micra
  • fusobacterium nucleatum
  • prevotella intermedia
  • treponema spp.
71
Q

what are the bacteria of periodontitis

A
  • aggregatibacter actinomycetemcomitans (type B)
  • porphyromonas gingivalis
  • parvimonas micra
  • fusobacteria nucleatum
  • tannerella forsynthis
  • treponema denticola
  • spirochetes
72
Q

what are the bacteria of necrotizing periodontal disease

A
  • fusobacterium nucleatum
  • prevotella intermedia
  • treponema spp.
  • spirochetes
73
Q

what are the bacteria associated with pregnancy and puberty

A
  • prevotella intermediia
  • capnocytophaga spp.
74
Q

what are the bacteria in abscess of the periodontium

A
  • fusobacterium nucleatum
  • parvimonas micra
  • prevotella intermedia
  • porphyromonas gingivalis
  • spirochetes
75
Q

what are the bacteria of peri-implantitis

A

comparable microbiota to that of periodontitis

76
Q

what are the healthy bacteria

A
  • gram positive
  • cocci
    -nonmotile
  • facultative anaerobes
  • fermenting
77
Q

what are the types of bacteria in disease

A
  • gram negative
  • rod
  • motile
  • obligate anaerobces
  • proteolytic
78
Q

what is the source of transmission of periodontal pathogens

A

saliva

79
Q

what are the bacteria involed in the transmission of periodontal pathogens

A
  • A-. actinomycetemcomitans
  • p. gingivalis
80
Q

what is the donor-recipient in the transmission of periodontal pathogens

A
  • parent to child
  • spouse to spouse
81
Q

what percentage of transmission of periodontal pathogens between spouses

A

20-30%

82
Q

is periodontal disease always the result in the transmission of periodontal pathogens from spouse to spouse

A

no

83
Q

is there stronger bacterial transmission from spouse to spouse or parent to child

A

parent to child

84
Q
A

Periodontics I (13 decks)

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