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PERIO I > Etiology > Flashcards

Etiology Flashcards

1
Q

Periodontal Pathogenesis Factors

A
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2
Q

Periodontal Pathogenesis flow chart

A
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3
Q

Materia Alba

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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4
Q

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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5
Q

Calculus

A

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

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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

plaque is main etiology for?

A

Main etiology for
Periodontal diseases
Dental caries

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8
Q

Dental Plaque
Composition

A

Water: 70% total
Microorganisms: 70% dry weight
Intracellular Matrix: 30% dry weight

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9
Q

Dental Plaque Intracellular Matrix organic components

A

Polysaccharides
Proteins
Glycoproteins
Lipids

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10
Q

dental plaque intracell matrix inorganic components

A

Calcium- Phosphorous
Other minerals
Sodium
Potassium
Fluoride

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11
Q
  • 1 gram of plaque contains approximately
    ____ bacteria
A

10^11

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12
Q
  • More than ____ distinct microbial species
    can be identified with highly sensitive
    molecular techniques in plaque
A

500

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13
Q

Sites of Plaque Accumulation

A

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

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14
Q

dental plaque location classification

A

Classification based on the position on the
tooth surface toward the gingival margin
Supragingival plaque
marginal plaque
Subgingival plaque

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15
Q

Subgingival plaque types

A

*Tooth attached plaque
*Unattached plaque
*Epithelial associated plaque

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16
Q

Supragingival plaque spp/morph? why? diversity?

A

Gram+ cocci and short rods
Aerobic environment
Slight diversity

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17
Q

Subgingival plaque spp/morph? why? diversity?

A

Gram- rods and spirochete
Anaerobic environment
Great diversity

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18
Q

Supragingival plaque can lead to:

A

Calculus formation and root caries

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19
Q

Marginal plaque leads to:

A

Direct contact with gingival margin
Initiation and development of gingivitis

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20
Q

subg plaque leads to:

A

Tissue destruction

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21
Q

suprag and subg plaque with perio tx

A

Disruption of both is critical during periodontal treatment.
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 steps

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

Formation of the pellicle

A
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24
Q

Initial colonization of bacteria

A
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25
Q

Secondary colonization and plaque maturation

A
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26
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.
- Components derived from saliva and crevicular fluid.
- Gram+ facultative microorganisms are involved
Initial stage of the development of the plaque
occurs at enamel within 1 min

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27
Q

Formation of the Pellicle: binding of 1 colonizers
interactions? effects of this? timeframe?

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
occurs at enamel within 2 hrs

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28
Q

Initial Colonization

A

*Adherence - Coadhesion
- Primary colonizers - secondary colonizers
- Bacterial mass continue to grow
- Alteration in the oxygen gradient, anaerobic
conditions emerge in the deeper layers of the deposits
occurs at enamel with 4-8hrs

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29
Q

*Primary colonizers of plaque

A

mainly gram +
*Streptococcus spp.
*Hemophilus spp.
*Neisseria spp.
*Actinomyces spp.
*Veillonella spp.
She Has Nice Ass Viens

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30
Q

Secondary colonizers of plaque

A

Mainly gram -
*P. intermidia.
*Capnocytophaga spp.
*F. nucleatum
*P. gingivalis
penelope cant find purpose

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31
Q

Colonization and Maturation of plaque: coaggregation
seen?
where/when?

A

*Coaggregation
- Secondary colonizers adhere to the bacteria that are already in the plaque mass
- A significant feature can be seen by naked eye
- at enamel within 4-8hrs

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32
Q

plaque maturation
how?
quorum sensing?
when?

A
  • Through further colonization and growth of additional species
  • Quorum sensing: cell-cell signaling: Environment modification and metabolic interaction
  • within 12hrs
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33
Q

bacterial detatchment from plaque

A

can detatch and colonize elsewhere

34
Q

cell-cell comms in plaque

A

can comm to establish favorable environment (metabolics)

35
Q

fluid channels in plaque

A

Open fluid-filled channels running through plaque mass, movement of nutrients

36
Q

microenvironment of plaque

A

Distinct microenvironment produced by matrix
Steep chemical gradients (oxygen, pH)

37
Q

Quorum sensing results in:

A

Quorum sensing results in bacterial resistance

38
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

39
Q

Dental calculus is:

A

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

40
Q

locations of calc

A

supra and sub g

41
Q

supra vs subg calc
location?
detection?
color/texture?
source of mineral?
distribution?

A
42
Q

Calculus Composition organic component

A

Leukocytes
Microorganisms
Desquamated epithelial cells
Protein polysaccharide complexes

43
Q

Calculus Composition inorganic component

A

70 - 90% comprising of Calcium phosphate,
Calcium carbonate, Magnesium phosphate

44
Q

Calculus Mineralization

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.
45
Q

main crystal forms of calculus

A
  • Hydroxyapatite (HA) 58%
  • Whitlockite (WHT) 21% may contain some Magnesium
  • Octacalcium phosphate (OCP) 12%
  • Brushite 9% only in early stage
46
Q

supra vs subg calc deposition

A
  • Supragingival calculus is deposited in layers;
    Subgingival calculus is commonly deposited in
    rings or ledges on root surfaces, but it may also
    appear on veneers.
47
Q

Plaque mineralization variabilty
reported as early as?

A
  • Plaque mineralization varies between and within individuals and different region of oral cavity. Calcification has been reported as early as 4- 8 hours.
48
Q
  • Some subjects may form supra- gingival calculus in ___ weeks, at which time the deposit may already contain approximately ___% of the inorganic material found in mature calculus.
A
  • Some subjects may form supra- gingival calculus in 2 weeks, at which time the deposit may already contain approximately 80% of the inorganic material found in mature calculus.
49
Q

the formation of dental calculus with
the mature crystalline composition of old calculus may require how much time?

A

the formation of dental calculus with
the mature crystalline composition of old calculus may require months to years.

50
Q

calculus on radiographs

A
  • Low sensitivity: radiographic deposits were detected on only 44% of surfaces that demonstrated calculus microscopically.
  • High positive predictive value - when you see radiographic calculus, 92% of the surfaces do have calculus microscopically.
51
Q

Calculus Attachment Modes

A
  1. Lock into areas of cementum resorption
  2. Attach to irregularities of the cementum surface
  3. By bacterial penetration into the cementum
  4. By an organic pellicle
52
Q

Calculus
Clinical Implications
- etiologic factor?
- It is always covered by? sphere influence?
tissues)
- It hinders?

A
  • Calculus is a contributing factor or SECONDARY etiologic factor
  • It is always covered by unmineralized viable
    bacterial plaque. It extends the sphere of influence of bacterial plaque (keeps it in close contact with tissues)
  • It hinders adequate plaque control
53
Q

Microbiologic Specificity thru time

A
54
Q

Nonspecific Plaque Hypothesis
- Direct relationship between?
- Concept inherited?
- Standard of care?

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
55
Q

Nonspecific Plaque Hypothesis contraindictions
- equally pathogenic?
- Gingivitis develop into destructive periodontitis?
- Site specificity?

A
  • All plaque are not equally pathogenic
  • 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?
- A. Actinomicetemcomitans?
- Targeted treatment?

A
  • The pathogenicity depends on the presence of or increase in specific microorganisms
  • A. Actinomicetemcomitans in localized aggresive periodontitis
  • Targeted treatment strategies aim to control or eliminate the particular pathogenic organisms
57
Q

Specific Plaque Hypothesis contraindication

A

Pathogens may be present at the absence of disease

58
Q

Ecologic plaque Hypothesis

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
59
Q

Polymicrobial Synergy and Disbiosis

A

Combines the concepts of “disrupted
homeostasis” and “keystone pathogen” but questions the primary importance of the red complex
current concept we use today

60
Q

three bacteria to know

A

P gingivalis
P denticola
T forsynthia

61
Q

Kochs Postulates

A

*Be routinely isolated from diseased individuals
*Be grown in pure culture in lab
*Produce a similar disease when inoculated into susceptible lab animals
*Be recovered from lesions in a diseases lab animal

62
Q

Socransky’s Criteria
*Be associated with?
*Be eliminated or decreased?
*Demonstrate a alteration in?
*Be capable of causing disease in?
*Demonstrate?

A

*Be associated with disease
*Be eliminated or decreased in sites that demonstrate clinical resolution
*Demonstrate a alteration in host cellular or immune response
*Be capable of causing disease in experimental models
*Demonstrate virulence factors

63
Q

criteria for Identification of Periodontopathogens

A

Kochs Postulates and Socransky’s Criteria

64
Q

A. Actinomycetemcomitans
Association:
Elimination:
Host response:
animal studies:
VF:

A

Association: Increased in localized aggressive periodontitis lesions. Some in chronic periodontitis lesions.
Elimination: Suppressed or eliminated in successful therapy, can be found in recurrent lesions
Host response: Increased serum and local antibody levels
Animal studies: Capable of inducing disease in gnotobiotic rats
Virulence factors: Host tissue cell adherence and invasion, leukotoxin, protease, collagenase, epitheliotoxin, FIF, bone resorption inducing factors

65
Q

P. Gingivalis
Association
Elimination
Host response
Animal studies
Virulence factors

A

Association: Increased in periodontitis lesions, found associated with the crevicular epithelium
Elimination: Suppressed or eliminated in successful therapy, can be found in recurrent lesions
Host response: Increased systemic and local antibody levels
Animal studies: Important in experimental mixed infections
Virulence factors:Host tissue cell adherence and invasion, trypsin-like enzyme, collagenase, fibrinolysis, phospholipase A, endotoxin, gingipains, factors that affect PMN function

66
Q

Toxins and enzymes of bacteria

A
  • Bacterial products that promote tissue destruction:
    lipopolysaccharides(LPS), leukotoxin, gingipains,
    collagenase, protease
67
Q

Adhesins of bacteria

A
  • Factors that promote colonization: fimbria, gingipains
68
Q

Evading mechanisms of bacteria

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: lipopolysaccharides(LPS)
69
Q

Virulence
Factors of bac

A

Toxins and enzymes
Adhesins
Evading mechanisms

70
Q

Bacteria of Gingivitis

A

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

71
Q

Bacteria of Periodontitis

A

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

72
Q

Bacteria of Necrotizing Periodontal DIsease

A

F. nucleatum
P. intermedia
Treponema spp.
Spirochetes
for penelope this sucks

73
Q

Bacteria Associated with Pregnancy and Puberty

A

Prevotella intermedia
Capnocytophaga spp.
Gingival inflammation results from an increased secretion of sex steroid hormones during puberty/pregnancy

74
Q

Bacteria in Abscess of the Periodontium

A

Fusobacterium nucleatum
Parvimonas micra
Prevotella intermedia
Porphyromonas gingivalis
Spirochetes

75
Q

Bacteria of peri-implantitis

A

Comparable microbiota to that of periodontitis

76
Q

Healthy Versus Diseased Sites environments
gram? shape? motility?
aerobic? metabolism?

A
77
Q

Transmission of Periodontal Pathogens
source? pathogens? routes?

A

Periodontal pathogens are communicable but not readily transmissible

78
Q

Goals of Plaque Control

A

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

79
Q

future individualization of tx

A

Modulating host response (i.e. Resolvins)
Antibiotics
Target proteins that are essential for the maintenance of Biofilm
Limitation of the identifying the microbial risk markers

80
Q

future individualization of tx

A

Modulating host response (i.e. Resolvins)
Antibiotics
Target proteins that are essential for the maintenance of Biofilm
Limitation of the identifying the microbial risk markers

PERIO I (13 decks)

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