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Periodontics > Etiology > Flashcards

Etiology Flashcards

1
Q

Periodontal Pathogenesis
Environment factors:
Microbial factors:
Host factors:

A

smoking
plaque/biofilm
susceptibility

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2
Q

Materia Alba
(4)

A

*White cheeselike
accumulation
*A soft accumulation of
salivary proteins,
bacteria, desquamated
epithelial cells, and food
debris
*No organized structure
*Easily displaced with a
water spray

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3
Q

Dental Plaque
(4)

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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4
Q

Calculus
(2)

A

*Mineralized dental
plaque forms the hard
deposit
*Generally covered by a
layer of unmineralized
dental plaque

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5
Q

What is
Dental Plaque?

A

The structurally and
functionally organized,
species-rich
microbial biofilms
that form on teeth

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6
Q

Main etiology for
Periodontal diseases

A

Dental caries

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7
Q

Dental Plaque
Composition (3)

A

Water 70%
Microorganisms 70% (dry weight)
Intracellular Matrix 30% (dry weight)

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8
Q

Dental Plaque
Intracellular Matrix
Organic component
(4)

A

Polysaccharides
Proteins
Glycoproteins
Lipids

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9
Q

Dental Plaque
Intracellular Matrix
Inorganic component
(4)

A

Calcium
Phosphorous
Other minerals
Sodium
Potassium
Fluoride

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10
Q

1 gram of plaque contains approximately
— bacteria
(And human body has approximately 1012 bacteria)

A

10^11

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11
Q

More than — distinct microbial species
can be identified with highly sensitive
molecular techniques

A

500

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12
Q

What is dental plaque?

A

B. It is the structurally and functionally organized, species‐rich
microbial biofilm that form on teeth.

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13
Q

Sites of Accumulation
(4)

A

Gingival thirds
Cracks, pits and fissures
Under overhanging restorations
Around malaligned teeth

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14
Q

Classification
based on the position on the
tooth surface toward the
gingival margin (3)

A

Supragingival plaque
Marginal plaque
Subgingival plaque

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15
Q

Subgingival plaque
(3)

A

*Tooth attached
plaque
*Unattached plaque
*Epithelial associated
plaque

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16
Q

Supragingival plaque

A

Gram+ cocci and short rods
Aerobic environment
Slight diversity

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17
Q

Subgingival plaque

A

Gram- rods and spirochete
Anaerobic environment
Great diversity

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18
Q

Supragingival plaque
result

A

Calculus formation and root caries

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19
Q

Marginal plaque
result

A

Direct contact with gingival margin
Initiation and development of gingivitis

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20
Q

Subgingival plaque
result

A

Tissue destruction

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21
Q

Supragingival plaque
Subgingival plaque
Disruption of both is critical during
periodontal treatment.
why?

A

No supragingival plaque control
following disruption of subgingival
microflora allows rapid repopulation of
microorganisms that could lead to
periodontitis.

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22
Q

Formation of Dental Plaque
(3)

A

Step 1:
Formation of the pellicle
Step 2:
Initial colonization of bacteria
Step 3:
Secondary colonization and plaque
maturation

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23
Q

Acquired pellicle:

A

Adsorption of a conditioning film
- An organic material layer coated on all surfaces in
the oral cavity, including hard and soft tissues.

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24
Q

Acquired pellicle
Components derived from

A

saliva and crevicular
fluid.

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25
Q

Acquired pellicle
bacteria

A

Gram+ facultative microorganisms are involved

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26
Q

Initial stage of the development of the plaque

A

acquired pellicle

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27
Q

Formation of the Pellicle

A

*Reversible adhesion between the microbial cell
surface (adhesins) and the conditioning film
(receptors)
- Alters the charge and the free energy of the
surface which increases efficiency of the bacterial
adhesion

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28
Q

Pellicle serves as a

A

protective barrier

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29
Q

Initial Colonization
*Adherence - Coadhesion
(3)

A
  • Primary colonizers - secondary colonizers
  • Bacterial mass continue to grow
  • Alteration in the oxygen gradient, anaerobic
    conditions emerge in the deeper layers of the deposits
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30
Q

SKIPPED
Primary colonizers
(5)

A

*Streptococcus spp.
*Hemophilus spp.
*Neisseria spp.
*Actinomyces spp.
*Veillonella spp.

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31
Q

SKIPPED
Secondary colonizers
(4)

A

*Prevotella intermidia.
*Capnocytophaga spp.
*Fusobacterium nucleatum
*Porphyromonas gingivalis

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32
Q

Colonization and Maturation
Coaggregation
(2)

A
  • Secondary colonizers adhere to the bacteria that
    are already in the plaque mass
  • A significant feature can be seen by naked eye
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33
Q

Maturation
(2)

A
  • Through further colonization and growth of
    additional species
  • Quorum sensing: cell-cell signaling
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34
Q
  • Quorum sensing: cell-cell signaling
    (2)
A
  • Environment modification
  • metabolic interaction
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35
Q

Structure of Dental Plaque
— running through plaque mass
Distinct — produced by matrix
Steep —
— results in bacterial resistance

A

Open fluid-filled channels
microenvironment
Chemical gradients (oxygen, pH)
Quorum sensing

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36
Q

Periodontal Microbiology
Corn-cob formation

A

Coccal‐shaped cells attach along the tip of gram negative filamentous organisms
An example of inter-bacterial adherence or coaggregation

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37
Q

Dental calculus is

A

calcified dental plaque,
composed primarily of calcium phosphate
mineral salts.

38
Q

Calculus
Location: Supragingival
Detection
Color/Texture
Source of
mineralization
Distribution

A

At or above the gingival margin
Visual
Creamy-whitish to dark yellow or even
brownish mass of moderate hardness
Saliva
Buccal Max. molars & Lingual Mand.
incisors

39
Q

Calculus
Location: Subgingival
Detection
Color/Texture
Source of
mineralization
Distribution

A

Below the gingival margin
Tactile or Radiographic
Brownish to black calcified hard
mass
GCF
varies

40
Q

Calculus
Composition
Organic component
(4)

A

Leukocytes
Microorganisms
Desquamated epithelial cells
Protein polysaccharide complexes

41
Q

Calculus
Composition
Inorganic component
70 - 90% comprising of
(3)

A

Calcium phosphate
Calcium carbonate
Magnesium phosphate

42
Q

Calculus
Mineralization
(2)

A
  • The mineralization starts in centers which
    arise intracellularly in bacterial colonies or
    extracellularly from matrix with
    crystallization nuclei
  • At least 2/3 of the inorganic component is
    crystalline in structure.
43
Q

Four main crystal forms:

A
  • Hydroxyapatite (HA) 58% [Ca10(PO4)6(OH)2]
  • Whitlockite (WHT) 21% [Ca10(HPO4)(PO4)6 ]
    may contain some Magnesium
  • Octacalcium phosphate (OCP) 12%
    [Ca8(PO4)4(HPO4)25HO]
  • Brushite 9% [CaHPO4-2H2O] only in early
    stage
44
Q

Supragingival calculus is deposited in layers;
Subgingival calculus is commonly deposited in

A

rings or ledges on root surfaces, but it may also
appear on veneers.

45
Q

vPlaque mineralization varies between and within
individuals and different region of oral cavity.
Calcification has been reported as early as

A

4- 8
hours.

46
Q

Some subjects may form supra- gingival calculus
in 2 weeks, at which time the deposit may already
contain approximately —% of the inorganic
material found in mature calculus.

A

80

47
Q

Nevertheless, the formation of dental calculus with
the mature crystalline composition of old calculus
may require

A

months to years.

48
Q

Evaluation of calculus by conventional radiography showed
- Low sensitivity:
- High positive predictive value -

A

radiographic deposits were detected on only
44% of surfaces that demonstrated calculus microscopically.

when you see radiographic
calculus, 92% of the surfaces do have calculus microscopically.

49
Q

Four modes of calculus attachment
(4)

A
  • Lock into areas of cementum resorption
  • Attach to irregularities of the cementum surface
  • By bacterial penetration into the cementum
  • By an organic pellicle
50
Q

Calculus is a contributing factor or —
etiologic factor

A

SECONDARY

51
Q

Calculus is a contributing factor or SECONDARY
etiologic factor
- It is always covered by

A

unmineralized viable
bacterial plaque. It extends the sphere of influence
of bacterial plaque (keeps it in close contact with
tissues)

52
Q

It hinders adequate — control

A

plaque

53
Q

1900s
1960s
1990s

A

Nonspecific Plaque Hypothesis
Specific Plaque Hypothesis
Ecologic plaque Hypothesis

54
Q

Nonspecific
Plaque
Hypothesis
(4)

A
  • Direct relationship between the
    total amount of plaque and the
    amplitude of the pathogenic effect
  • Concept inherited: Control of
    periodontal disease depends on
    control of plaque accumulation
  • Standard of care: oral
    hygiene measures, non-
    surgical/ surgical
    debridement
  • All plaque are not equally
    pathogenic
55
Q
  • All plaque are not equally
    pathogenic
    (2)
A
  • Not all Gingivitis develop into
    destructive periodontitis
  • Site specificity in the pattern
    of disease was demonstrated
    in some individuals with
    periodontitis
56
Q

Specific Plaque Hypothesis
The pathogenicity depends on
the presence of or increase in

A

specific microorganisms
- A. Actinomicetemcomitans
in localized aggresive
periodontitis

57
Q

Specific Plaque Hypothesis
- Targeted treatment strategies
aim to

A

control or eliminate the
particular pathogenic
organisms

58
Q

Specific Plaque Hypothesis
are pathogens present or absent in disease?

A

!!!Pathogens may be present at the absence of disease!!!

59
Q

microbes to know (3)

A

P. gingivalis
B. forsythus
T. denticola

60
Q

microbes present without disease

A

***B. forsythus
->T. forsythensis
->T. forthysia

61
Q

Ecologic
plaque
Hypothesis
Microbiologic Specificity
(3)

A
  • Both the total amount of dental
    plaque and the specific
    microbial composition of plaque
    may contribute
    -Environmental factors drives the
    selection and enrichment of
    specific bacteria
  • Microbial homeostasis: the state
    of the dynamic equilibrium
62
Q

Polymicrobial Synergy and Disbiosis

A

Combines the concepts of “disrupted
homeostasis” and “keystone
pathogen” but questions the primary
importance of the red complex

63
Q

Kochs Postulates
Criteria for Identification of Periodontopathogens
*Be routinely isolated from
*Be grown in
*Produce a similar disease
when
*Be recovered from lesions in a

A

diseased individuals
pure culture in lab
inoculated into susceptible lab animals
diseases lab animal

64
Q

Socransky’s Criteria
*Be — with disease
*Be — or decreased in
sites that demonstrate clinical
resolution
*Demonstrate a alteration in
*Be capable of causing disease
in
*Demonstrate

A

associated
eliminated
host cellular or immune response
experimental models
virulence factors

65
Q

A. Actinomycetemcomitans
Association

A

Increased in localized aggressive periodontitis
lesions. Some in chronic periodontitis
lesions.

66
Q

A. Actinomycetemcomitans
Elimination

A

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

67
Q

A. Actinomycetemcomitans
Host response

A

Increased serum and local antibody levels

68
Q

A. Actinomycetemcomitans
Animal studies

A

Capable of inducing disease in gnotobiotic
rats

69
Q

A. Actinomycetemcomitans
Virulence factors

A

Host tissue cell adherence and invasion,
leukotoxin, protease, collagenase,
epitheliotoxin, FIF, bone resorption inducing
factors

70
Q

P. Gingivalis
Association

A

Increased in periodontitis lesions, found
associated with the crevicular epithelium

71
Q

P. Gingivalis
Elimination

A

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

72
Q

P. Gingivalis
Host response

A

Increased systemic and local antibody levels

73
Q

P. Gingivalis
Animal studies

A

Important in experimental mixed infections

74
Q

P. Gingivalis
Virulence factors

A

Host tissue cell adherence and invasion,
trypsin-like enzyme, collagenase, fibrinolysis,
phospholipase A, endotoxin, gingipains,
factors that affect PMN function

75
Q

P. gingivalis is known as a
notorious periodontal
pathogen. Which complex
of color does it belong to?
A. Yellow complex
B. Green complex
C. Orange complex
D. Red complex

A

D. Red complex

76
Q

Toxins and enzymes

A
  • Bacterial products that promote tissue destruction:
    lipopolysaccharides(LPS), leukotoxin, gingipains,
    collagenase, protease
77
Q

Adhesins

A
  • Factors that promote
    colonization: fimbria,
    gingipains
78
Q

Evading mechanisms
* The production of an extracellular —
* Proteolytic degradation of host immunity components:
* Modulate host response:
* Invasion of gingival epithelial cells:

A

capsule
gingipains
bind serum components on bacterial cell surface
lipopolysaccharides(LPS)

79
Q

Bacteria of Gingivitis
(8)

A

Actinomyces spp.
Capnocytophaga spp.
Campylobacter spp.
Streptococcus spp.
Parvimonas micra
Fusobacterium nucleatum
Prevotella intermedia
Treponema spp.

80
Q

Bacteria of Periodontitis
Specific Bacteria in Disease
(8)

A

Aggregatibacter actinomycetemcomitans (Type b)
Porphyromonas gingivalis
Prevotella intermedia
Parvimonas micra
Fusobacterium nucleatum
Tannerella forsythia
Treponema denticola
Spirochetes

81
Q

Bacteria of Necrotizing Periodontal DIsease
(4)

A

Fusobacterium nucleatum
Prevotella intermedia
Treponema spp.
Spirochetes

82
Q

Bacteria Associated with Pregnancy and Puberty
(2)

A

Prevotella intermedia
Capnocytophaga spp.

83
Q

Bacteria in Abscess of the Periodontium
(5)

A

Fusobacterium nucleatum
Parvimonas micra
Prevotella intermedia
Porphyromonas gingivalis
Spirochetes

84
Q

Health
(5)

A

Gram +ve
Cocci
Nonmotile
Facultative anaerobes
Fermenting

85
Q

Disease
(5)

A

Gram -ve
Rod
Motile
Obligate anaerobes
Proteolytic

86
Q

Choose correct answer for the
specific bacteria observed in
correlated periodontal disease
A. In diseased sites, more gram positive, nonmotile cocci are
observed
B. In healthy sites, more orange and red complex bacteria are
observed
C. A. actinomycetemcomitans and P. gingivalis are highly related to periodontitis
D. Capnocytophaga spp. is usually found in periodontal abscess

A

C. A. actinomycetemcomitans and P. gingivalis are highly related to periodontitis

87
Q

Transmission of Periodontal Pathogens
Source: Saliva
Bacteria involved:
Donor-recipient:

A

A. actinomycetemcomitans & P. gingivalis
Parent to child & Spouse to spouse

88
Q

A —% chance of transmission between spouses

A

20-30

89
Q

Does not always result in periodontal disease in the recipient spouse.
Stronger bacterial transmission was found from

A

parent to child

90
Q

!!!Periodontal pathogens are — but not readily —!!!

A

communicable
transmissible

91
Q

Goals of
Plaque Control
(4)

A

Disrupt ecological
succession
Reduce degree of
organization
“Healthy” plaque (G+, aerobic, indigenous flora)
Shift in flora compatible
with health

92
Q

Future Advances
Modulating —
—
Target proteins that are essential for —
Limitation of the identifying the —

A

host response (i.e. Resolvins)
Antibiotics
the maintenance of Biofilm
microbial risk markers

Periodontics (13 decks)

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