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Perio - Exam 1 > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

What are 6 infections in the oral cavity?

A

Caries

Periapical lesions

Fungal

Viral

Abscesses

Periodontal

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2
Q

Difference b/t gingivitis and periodontitis?

A

Periodontitis has attachment loss and bone loss

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3
Q

Those with periodontitis may experience how much attachment loss?

A

0.1 mm/year loss of attachment

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4
Q

If periodontitis is present, what else is happening?

A

Gingivitis

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5
Q

T/F - Patients can go flux back and forth from periodontal health to periodontal disease.

A

TRUE

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6
Q

What are the 3 triangles that confluence into the disease triangle?

A

Microbial plaque

Genetics/Host factors

Acquired/Environmental factors

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7
Q

What is the most elementary distinction to be made during periodontal diagnosis?

A

Differentiation b/t health, gingivitis, and periodontitis

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8
Q

T/F - SRP is done with periodontitis, but not necessarily with gingivitis.

A

TRUE

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9
Q

What is Koch’s Postulates?

A

Take a pathogen from diseased tissue, grow it, and re-isolated it to show the causative agent of an infectious disease

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10
Q

What is the route PMNs take to get to site of infection?

A

Blood vessels -> CT -> Junctional epithelium -> Site of infection

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11
Q

1965 study on dental plaque.

A

Students underwent a rigorous program to have periodontal health.

One half the class did not brush teeth

Other half the class did brush teeth

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12
Q

What were the major findings of Loe, 1965?

A

Time necessary for clinical gingivitis to occur varied from 10-21 days

Re-institution of oral hygiene resulted in resolution of gingival inflammation in about 1 week

Appearance of gram (-) flora preceded the onset of clinically detectable gingivitis by 3-10 days.

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13
Q

What 2 results were drawn from the Loe study?

A

Showed gingivitis could be experimentally produced in humans by allowing plaque to accumulate

Reversal of gingivitis can be accomplished by plaque removal

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14
Q

T/F - If you’ve had gingivitis, then you are at the greatest risk for gingivitis and periodontitis.

A

TRUE

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15
Q

Clinical health means what?

A

What we see clinically

Does not mean that that site is physiologically healthy

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16
Q

What is the nonspecific plaque hypothesis?

A

Increased plaque mass directly related to increased severity of disease

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17
Q

What is the 1970’s model of periodontal disease?

A

Poor oral hygiene

Bacterial plaque formation

Calculus formation

Periodontal pockets

Alveolar bone loss

Tooth loss

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18
Q

3 things believed in the 70s about periodontal disease?

A

All bacteria on tooth surface are harmful

Host response important and protective against bacteria from invading

Gingivitis progresses to periodontitis with bone and tooth loss

  • Untreated periodontitis progresses slowly and steadily
  • all individuals and all teeth are susceptible
  • Hygiene and age are major risk factors for disease
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19
Q

Does gingivitis always lead to periodontitis.

A

No. Not always

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20
Q

What is the specific plaque hypothesis from the 70s and 80s?

A

Single or limited number of periodontopathic organisms are responsible for disease and severity of disease

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21
Q

T/F - Both the specific and nonspecific hypotheses are very dependent on the potential direct pathologic effects of dental plaque.

A

TRUE

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22
Q

Name some enzymes that cause tissue destruction.

A

Collagenase

Hyaluronidase

Chondroitin sulfatase

Proteases

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23
Q

What other things do bacteria release that cause cell death?

A

Exotoxin

Endotoxin (gram negative)

Mucopeptides (gram positive)

Ammonia

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24
Q

T/F - Loe also found that not all individuals get periodontitis.

A

TRUE

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25
Q

What did Goodson find?

A

Recurrent acute episodes followed by remission independent site activity

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26
Q

What is the modern plaque hypothesis?

A

Periodontopathic flora are necessary, and not sufficient, for disease

Periodontal diseases are specific mixed infections which cause periodontal destruction in the appropriately susceptible host

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27
Q

Microbial plaque comes from what 5 things?

A

Bacteria

Fungus

Protozoans

Viruses

Mycoplasm

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28
Q

Define periodontal disease.

A

Infectious disease process that involves inflammation

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29
Q

What does periodontal disease involve?

A

The structures of the periodontium resulting in loss of tissue attachment and destruction of the alveolar bone

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30
Q

Periodontal disease is any disease of the periodontium with what two basic forms?

A

Gingivitis

Periodontitis

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31
Q

Define clinical periodontal health.

A

The tissues are free from clinical inflammation

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32
Q

Define gingivitis.

A

Inflammatory process confined to the gingival tissues

  • Caused by nonspecific accumulation of plaque
  • Usually is reversible
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33
Q

Define periodontitis.

A

Inflammation not confined to the gingiva, but involves the attachment apparatus: cementum, PDL, alveolar bone, and soft tissues

THIS STARTS AS GINGIVITIS, BUT PROGRESSES TO DESTROY THE BONE AND SOFT TISSUES THAT SUPPORT THE TOOTH

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34
Q

Characteristics of health teeth and gingiva.

A

Pink gingiva

No bleeding with flossing and brushing

Fresh breath

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35
Q

What does gingivitis look like?

A

Red, swollen gingiva

Bleeding gingiva w/ flossing and brushing

Possible bad breath or taste

No bone loss

No tooth mobility

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36
Q

What does early periodontitis look like?

A

Red, swollen gingiva

Bleeding gingiva on flossing and brushing

Persistent bad breath or taste

Slight bone loss

Possible tooth mobility

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37
Q

Moderate periodontitis looks like what?

A

Red, swollen gingiva

Bleeding gums on flossing and brushing

Persistent bad breath or taste

Moderate bone loss

Tooth mobility and root exposure

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38
Q

What does advanced periodontitis look like?

A

Red, swollen gingiva

Bleeding gingiva on flossing and brushing

Persistent bad breath or taste

Severe bone loss

Severe tooth mobility and root exposure

Possible tooth loss

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39
Q

In the 1970s, what was the hypothesis for periodontal disease?

A

Increased plaque mass directly related to increased severity of disease

All bacteria on teeth are harmful

ALL INDIVIDUALS AND ALL TEETH W/IN AN INDIVIDUAL ARE SUSCEPTIBLE

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40
Q

WHAT CAUSES PERIODONTAL DISEASE? 2 THINGS

A

DENTAL/MICROBIAL PLAQUE

ENDOTOXINS

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41
Q

What is the modern plaque hypothesis (90s)?

A

Periodontopathic flora necessary, but not sufficient, for disease.

Diseases are specific mixed infections which causes periodontal destruction in the appropriately susceptible host

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42
Q

What are some acquired and environmental risk factors for periodontal disease?

A 
Poor hygiene
Age
Meds
Tobacco
Stress
Immune defects
Nutritional deficiencies
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43
Q

What are some INNATE risk factors for periodontal disease?

A 
Race
Sex
Genetics
Congenital immunodeficiencies
Phagocytosis dysfunction
Down’s Syndrome
Papillon-Lefevre/Ehlers-Dantos syndrome
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44
Q

What is the etiologic factor that causes periodontal disease?

A

DENTAL PLAQUE

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45
Q

What is calculus?

A

Mineralized biofilm (dead bacteria)

Inert, but the biofilm adhered to it is the issue causing disease

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46
Q

What does calculus do?

A

Provides a surface for the plaque to attach

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47
Q

What are two types calculus?

A

Supragingival calculus

Subgingival calculus

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48
Q

What are some properties of biofilms?

A

Cooperating community of microorganisms
-Arranged in microcolonies with channels b/t the microcolonies
-Microcolonies are surrounded by protective matrix
-Differing environments w/in the microcolonies in the biofilm
-Primitive communication system
-QUORUM SENSING
—Microbial gene expression differs when microorganisms are in a biofilm
-RESISTANT TO ANTIBIOTICS, ANTIMICROBIALS, AND HOST RESPONSE

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49
Q

What are the Koch’s Postulates for Periodontics?

A

Putative pathogens must be found in large numbers in diseased sites

Absence of pathogens in health

Must be able to demonstrate immune response to putative pathogens

Virulence factors can often be demonstrated

Animal models should simulate human disease

Elimination should result in clinical improvement

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50
Q

How long does it take to re-establish pathogenicity?

A

6 weeks

*After SRP, it takes 3 weeks to accumulate and then 3 more weeks to go bad

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51
Q

WHAT 3 ORGANISMS ARE IN THE RED COMPLEX?

A

Porphyromonas gingivalis

Tannerella forsythensis (Bacteroides forsythus)

Treponema denticola

Red: TF/BF PG TD!

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52
Q

What are the other complexes and how are they organized?

A

EARLY COLONIZERS

  • Blue
  • Purple
  • Green
  • Yellow

LATE COLONIZERS

  • Orange
  • Red
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53
Q

Bacteria bind to what?

A

NOT THE TOOTH SURFACE!

ATTACHED TO GLYCOPROTEINS ON THE SURFACE (PELLICLE)

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54
Q

What do the early colonizers bind to?

A

The pellicle (glycoproteins from the saliva)

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55
Q

What do the late colonizers bind to?

A

The early colonizers

*It takes about 42 days (6 wks) to get to a pathogenic biofilm

So it goes: tooth structure->biofilm pellicle->early colonizers->late colonizers (orange and red complexes)

56
Q

What happens to the early colonizers after the late colonizers bind?

A

They die due to lack of nutrients and O2

This creates calculus

57
Q

What are the steps of plaque formation? 6 steps

A

Association - Pellicle forms

Adhesion - W/in hrs, bacteria loosely bind to pellicle (planktonic bacteria)

Proliferation - Bacteria spreads throughout mouth and multiplies

Microcolonies - Steptococci secrete protective layer*

Biofilm formation - Microcolonies form complex groups with metabolic advantages

Growth/Maturation - Biofilm develops a primitive circulatory system

58
Q

How does fluid flow thru a biofilm?

A

Thru fluid channels “under” the biofilm b/t the biofilm and pellicle

59
Q

Quorum sensing in G- organisms involves 2 regulatory components: the ____________ __________ protein (R protein) and the ______ ____________ produced by the autoinducer synthase.

A

Transcriptional activator

AI molecule

60
Q

Tell me the layers of biofilm.

A

Tooth surface

Pellicle

Dead bacteria in an anaerobic environment

Live, aerobic bacteria

Oxygen

Substrate

61
Q

In the anaerobic layer, what is the REDOX potential?

A

LOW REDOX POTENTIAL

62
Q

What are 4 mechanisms of antibiotic resistance w/in biofilms?

A

1 - Antibiotic poorly/slowly penetrates

2 - A conc gradient of a metabolic substrate leads to zones of slow or non-growing bacteria

3 - Adaptive stress response is expressed by some of the cells

4 - Small fraction of cells differentiate into a highly protected persistent state

63
Q

T/F - Bioflims provide a source of antibiotic resistance.

T/F - Antibiotics don’t do anything to dead bacteria.

A

TRUE

TRUE

64
Q

Give me a summary of biofilm.

A

Advanced ecosystem that is the etiology of periodontal disease

Fluid gradient helps move nutrients around and allows for bacterial communication

Keeps the inhabitants safe by making host defense mechanisms difficult to penetrate the environment and resist the effects of antimicrobials

65
Q

T/F - Biofilm needs to be disrupted, even if we can’t completely remove it.

A

TRUE

66
Q

T/F - SRP only disrupts about 13% of the biofilm.

A

TRUE

*If done correctly, the biofilm can grow w/o needing to be disrupted for up to 48 hours w/o problems

67
Q

What is periodontitis caused by? (Interaction-wise)

A

Interaction of plaque and the susceptible host defense immune system

68
Q

Periodontal disease:

Etiology?

Initiation?

Progression?

A

Etiology: Microbial plaque

Initiation: Non-specific plaque accumulation

Progression: G- bacteria and susceptible host

69
Q

Sub-gingival plaque samples were analyzed from the distal, mid-buccal, and lingual aspects of canines, pre-molars, and molars after 96 hours of plaque accumulation. Tell me which site had greater plaque accumulation in the following list?

Distal - Mid-buccal

Mid-buccal - Lingual

Posterior - Anterior

A

Distal > Mid-buccal

Mid-buccal > Lingual

Posterior > Anterior

70
Q

The majority of dental and periodontal diseases originate where on the tooth?

A

The interproximal area

*Any tooth brush, regardless of brushing method, does not completely remove interdental plaque - it is unkeratinized!

71
Q

In general, there is a strong relation b/t poor oral _________ and __________.

A

Hygiene

Gingivitis

72
Q

T/F - The relation b/t poor oral hygiene and the risk for developing periodontitis is not as strong as the relation b/t poor oral hygiene and gingivitis.

A

TRUE

73
Q

Not all _________ progresses to __________, BUT all _____________ is preceded by _____________.

A

Gingivitis

Periodontitis

Periodontitis

Gingivitis

74
Q

What are virulence factors?

A

Properties that enable the bacteria to cause disease

75
Q

The virulence factors of fimbrea, pili, and fibrillae, what are their mechanisms of action?

A

Bacterial attachment, prevention of phagocytosis

76
Q

What is the mechanism of action for the capsule virulence factor?

A

Protection, attachment, prevent phagocytosis

77
Q

What is the mechanism of action for the endotoxin virulence factor?

A

Activation of inflammatory response, cytokine production, bone resorption

78
Q

Exotoxins are released by what?

A

From viable organisms into environment

-Very susceptible to denaturation

79
Q

Endotoxins are made by what?

A

LPS - Lipopolysaccharides

-Resistant to heat and chemical denaturation

80
Q

By attaching to the pellicle, the bacteria avoid displacement by the ______ flow.

A

GCF

This is another bacterial virulence factor - the ability to adhere

81
Q

Bacteria may enter the host by _________ in the epi or by direct ________ into the host tissues (less common).

A

Ulcerations

Penetration

82
Q

Most bacteria enter the CT via what?

A

PASSIVE INVASION

-Swallowing creates a force and can drive bacteria into the CT

83
Q

More than ___% of all Americans suffer from gingivitis.

A

90%

84
Q

About ___% of all American adults suffer from periodontitis.

A

50%

85
Q

How does the body respond to bacteria entering the tissue?

A

Inflammation, immune response, damage to soft tissue, and cell signals to start bone resorption

86
Q

What is the formula for periodontal disease?

A

Pathogenic flora + lack of beneficial bacteria + susceptible host = Periodontal disease

87
Q

Aggregatibacter actinomycetemcomitans was formerly known as?

A

Actinobacillus actinomycetemcomitans

*This bug is associated with aggressive periodontitis

88
Q

Healthy bacteria tend to be what?

A

Aerobic G+ cocci,

89
Q

Bad bacteria tend to be what?

A

Anaerobic, G- bacteria

90
Q

What are some other bad bacteria present in periodontitis?

A

Porphyromonas gingivalis

Prevotella intermedia

Tannerella forsythia

Fusobacterium nucleatum

Peptostreptococcus micros

Campylobacter rectus - THIS ONE IS MOTILE**

91
Q

What are 5 beneficial bacteria?

A

Actinomyces sp.

Strep mitis

Strep sanguis

Capnocytophaga sp

V parvula

92
Q

Pellicle is made up of what?

A

Glycoproteins

-Proteins with carbohydrate moieties

**A thin, BACTERIA-FREE layer of salivary proteins that attach to the tooth surface w/in minutes of a professional cleaning

93
Q

What are some factors that INCREASE a host’s susceptibility?

A

Impaired neutrophils

Inadequate immune response

LPS responsiveness

AIDS

Diabetes

Smoking

Drugs

Other

94
Q

W/in hours of the pellicle forming, what happens?

A

Bacteria begin to attach to the outer surface of the pellicle (via fimbriae on bacteria)

95
Q

Supragingival plaque is found where?

A

Coronal plaque

Marginal plaque

96
Q

Subgingival plaque is found where?

A

Attached plaque*

  • Tooth
  • Epithelium
  • Connective tissue

Unattached plaque (Planktonic - this can be the worst)

97
Q

Attached sub-gingival plaque is what?

A

Zone of subgingival plaque directly attached to the surface of the tooth (coated in biofilm) of calculus in the sulcus and pocket

98
Q

Unattached subgingival plaque is what?

A

Zone of sub-g plaque not directly attached to the tooth surface

Mostly G-, motile bacteria and resides b/t the outer position of the attached plaque and sulcular epithelium

In direct contact with both the junctional and sulcular epithelium

99
Q

____________ plaque influences (increases the ability to grow) subgingival plaque, however, once ___________ plaque is established, the ___________ plaque, in essence, no longer affects it.

A

Supragingival

Subgingival

Supragingival

100
Q

Which plaque is being disrupted through tooth brushing and/or SRP?

A

Supragingival plaque

101
Q

Tell me the process of how subgingival plaque is created.

A

Biofilm -> supragingival plaque (which creates an anaerobic environment) -> Subgingival plaque (now unaffected by supragingival plaque)

102
Q

The water in the ultrasonic does what?

A

Helps to flush away debris and endotoxins

103
Q

How is calculus attached to the tooth? 2 ways

A

Mechanical retention on tooth, still covered by biofilm, in nooks and crannies

Direct on the pellicle

104
Q

T/F - Unattached plaque is typically the most pathogenic.

A

TRUE

105
Q

What is the critically important zone in a pocket?

A

The partially lysed CT fibers.

*Causes JE to move apically and can be the beginning of bone resorption

106
Q

Young, supragingivial plaque is made of what?

A

Mostly G+ cocci and rods, with some G- cocci and rods

107
Q

Aged supragingival plaque has an increase in what type of bacteria?

A

G- anaerobic

*This can get down into the sulcus and cause pocketing

108
Q

How can young and aged supragingival plaque be distinguished?

A

Disclosing tablet

109
Q

Differences b/t Supra and sub gingival plaque?

Matrix
Flora
Motile bacteria
Oxygen req’s
Metabolism
A

Supra

  • Matrix - 50% matrix
  • Flora - Mostly G+
  • Motility - Few
  • Oxygen req’s - Aerobic, unless thick
  • Metabolism - Predominately carbs

Sub

  • Matrix - Little or no matrix
  • Flora - Mostly G-
  • Motility - Common
  • Oxygen req’s - High anaerobic areas
  • Metabolism - Predominately proteins (usually from body tissues [breakdown of collagen in the pocket])
110
Q

Planktonic bacteria is typically what? G+/G-?

A

G-

111
Q

Subgingival plaque can be tooth-associated or epithelium-associated. Tell me the differences b/t the two.

A

Tooth-Associated

  • Mostly G+, but turns into G-
  • Does NOT extend to JE
  • May penetrate cementum
  • Associated with calculus formation and root caries

Epi-Associated

  • G+ and G-
  • DOES extend to JE
  • May penetrate epi and CT
  • Associated with gingivitis and periodontitis
112
Q

What is the litmus test of how good SRP was?

A

Tissue state a few weeks (~6) later

113
Q

Which bacteria have a very strong association with periodontal diseases?

A

RED Complex

  • Porphyromonas gingivalis
  • Tannerella forsythensis (Bacteroides forsythensis)
  • Treponema denticola
  • *Also:
  • Aggregatibacter actinomycetemcomitans**
114
Q

What 5 bacteria are associated with abscesses of the periodontium?

A

Fusobactrium nucleatum

Prevotella intermedia

Peptostreptococcus micros

Bacteroides forsythus

Porphyromonas gingivalis

115
Q

Less than 5% of the population has what?

A

Refractory disease

  • T. Forsythia
  • P. Gingivalis
  • P. Intermedia
  • C. Recta
116
Q

What bacteria are associated with chronic periodontitis?

A 
P. Gingivalis
P. Intermedia
F. Nucleatum
A.a
C. Recta
T. Forsythia
117
Q

What is associated with localized, aggressive periodontitis (LAP)?

A

A.a

P. Intermedia

P. Gingivalis

118
Q

What is ANUG?

A

Necrotizing, ulcerated gingivitis

-P. Intermedia - can burrow into epi cells

119
Q

HIV-associated gingivitis is mostly due to what?

A

CANDIDA ALBICANS

120
Q

Tell me about Aggregatibacter actinomycetemcomitans.

A

Small, non-motile

G-

Fac ana

Saccharolytic - Digest sugars

Coccobacillus

Small convex colonies with a star-shaped center

121
Q

What is the most pathogenic serotype of Aggregatibacter actinomycetemcomitans?

A

B

122
Q

Aggregatibacter actinomycetemcomitans has the ability to __________ host epi cells.

A

INVADE

*Like spirochetes

123
Q

What is an exotoxin?

A

Extracellular substance produced by bacteria which are toxic to certain cells or tissues of the body
-Botulinum, tetanus

*Actively released from living cells

For some reason, know that LEUKOTOXIN is and EXOTOXIN

124
Q

What is an endotoxin?

A

Released when cells die

LPS

125
Q

What do leukotoxins do?

A

Produced by Aggregatibacter actinomycetemcomitans and is thought to KILL PMNs and MONOCYTES from blood and PMNs from the pocket

126
Q

When LPS is released what 3 things can happen?

A

Cytotoxic effects

Complement activation

Bone resorption (Direct or indirect)

127
Q

Tell me about Porphyromonas gingivalis.

A

G-, nonmotile, rod

Ana

Asaccharolytic

Invades epi cells

Able to grow at elevated pH

Thick capsule - Resist phagocytosis

Forms dark brown-black colonies

“Black pigmented bacteroides”

128
Q

What other virulence factors does Porphyromonas gingivalis have, besides a capsule?

A

LPS - Stims cytokine secretion in monocytes and macrophages

Fimbriae - Binds bacterium to host tissues, produce and deliver of toxins and colonization antigens

Proteinases - Including collagenase

Toxic products

129
Q

Tell me about Tannerella forsythia.

A

G-

Ana

Spindle-shape

Pleopmorphic

Invades epi cells

-Formerly know as bacteroides forsythus

130
Q

Tell me about Prevotella intermedia.

A

G-

Ana

Short, round rod

Elevated in ANUG

“Black pigmented bacteroides”
—Uses heme as a primary foodstuff

131
Q

Tell me about fusobacterium nucleatum.

A

G-

Ana

Spindle

MOST COMMON ISOLATE FROM SUBGINGIVAL SAMPLES

132
Q

Tell me about campylobacter rectus.

A

G-

Ana

Short, motile vibrio

Produces a leukotoxin

Forms convex, spreading, or corroding colonies on blood agar plates

133
Q

Tell me about peptostreptococcus micros.

A

G+ - THIS IS THE ONLY PERIO PATHOGEN THAT IS GRAM +*

Ana

Small coccus

Asaccharolytic

134
Q

Tell me about spirochetes.

A

G-

Ana - Very anaerobic, they stink

Helical shaped

Related to NUG

Their intermediates are bad

135
Q

Tell me the layers of a tooth with stuff on it.

A

Enamel
Pellicle
Biofilm/plaque
Calculus

Perio - Exam 1 (3 decks)

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