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Perio Final > Exam #1 Review > Flashcards

Exam #1 Review Flashcards

1
Q

Gingivitis

A

Signs and symptoms that are confined to the gingiva
Presence of plaque that causes the issue
No CAL
Reversibility of the disease by removing the etiology

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2
Q

Periodontitis

A

Attachment loss

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3
Q

Chronic periodontiis

A

Slow to moderate progression
Seen in adults
Can be modified by systemic factors

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4
Q

Extent of chronic periodontitis

A

Localized = 30%

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5
Q

Severity of periodontitis

A 
Slight = 1-2mm CAL
Moderate = 3-4mm CAL
Severe = 5+mm CAL
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6
Q

Aggressive Periodontitis

A

Systemically healthy

Familial aggregation

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7
Q

Localized Aggressive Periodontitis

A

Young patients

1st molars and incisors plus =2 other teeth

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8
Q

Generalized Aggressive Periodontitis

A

1st molars and incisors plus >2 other teet

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9
Q

Mendelian trait

A

If you have the gene, you have the trait

If you don’t have the gene, you don’t have the trait

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10
Q

Polygenic traits

A

Requires a bunch of different genes develop one phenotype

Represented on a bell curve (most people in the middle, but some on the extremes)

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11
Q

Periodontitis Association with Mendelian genetics

A

There are only certain periodontic conditions associated with single gene mutations

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12
Q

Ehlers Danlos Syndrome mutation

A

Collagen defects

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13
Q

Neutropenias mutation

A

Neutrophil anomalies

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14
Q

Leukocyte Adhesion deficiency mutation

A

B-subunit leukocyte adhesion molecule

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15
Q

Hypophosphetasia mutation

A

B-alkaline phosphatase

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16
Q

Papillon Lefevre syndrome mutation

A

Cathepsin C defect

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17
Q

Haim Munk Syndrom mutation

A

Cathepsin C defect

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18
Q

Prepubertal Periodontitis mutation

A

Cathepsin C defect

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19
Q

Affresive periodontitis mutation

A

Cathepsin C defect

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20
Q

Monozygotic twins

A

Have identical genes

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21
Q

Diazygotic twins

A

Share half of genes

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22
Q

Disease cause wholly or partially by genetic factors has a higher rate in what type of twins?

A

Monozygotic

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23
Q

If monozygotic twids are not fully concordinant, what does this tell us about a disease?

A

Environmental factors must be etiologic

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24
Q

What do twin studies tell us about periodontitis?

A

Monozygotic twins were twice as likely to develop chronic periodontitis than diazygotics
This suggests that genetics make an important contribution

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25
Q

What does a segregation analysis tell us?

A

Tells us the pattern of diseases segregating in families - can determine if occurence in family is constant with the genetic model

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26
Q

Which genetic model passes periodontitis?

A

Almost all of them

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27
Q

What did a linkage analysis tell us about the chromosomal location of aggressive periodontitis?

A

There are multiple forms and many locations where it can be found

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28
Q

How do you measure CAL?

A

CAL = PD + recession

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29
Q

What is biologic width measurement

A

2mm

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30
Q

KEratinized gingiva

A

The marginal gingiva and the attached gingiva

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31
Q

Free gingival groove

A

Junction between the attached gingiva and the marginal gingiva
Corresponds with the CEJ
Only observable in 30-40% of adults

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32
Q

Free gingival margin

A

Coronal end of the gingiva

Located 1.5-2.0mm coronal to the CEJ

33
Q

Mucogingival junction

A

Border between the keratinized gingiva and the alveolar mucosa

34
Q

What does the ‘width’ of the gingiva mean?

A

Height occluso-cervically

35
Q

What does the ‘thickness’ of the gingiva mean?

A

Thickness B-L

36
Q

T/F - The mucogingival junction moves as the tooth erupts

A

False - so when the tooth erupts, the entire gingiva moves with it. Since marginal or free gingiva is also fixed in dimensions, the width of the attached gingiva increases

37
Q

What is the purpose of gingival fibers?

A

Reinforce the gingiva
Provide resilience and tone
Maintain architechtural form and integrity

38
Q

What are the different types of gingival fibers?

A

Circular
Dentogingival
Dentoperiosteal
Transseptal

39
Q

Circular fibers

A

Encircle the tooth like a cuff

40
Q

Dentogingival fibers

A

Fan out from the supra-crestal cementum into the free gingiva

41
Q

Dentoperiosteal fibers

A

Run from supra-crestal cementum into attached fibers

42
Q

Transseptal fibers

A

Run from tooth to tooth and embed into the cementum

43
Q

What are the different theories about plaque as an etiological agent?

A

Non-specific plaque hypothesis
Specific plaque hypothesis
Ecological Plaque hypothesis
Oral dysbiosis

44
Q

Non-specific plaque hypothesis

A

Plaque control is important in perio treatment
All plaque is considered bad
Any accumulation of micro-organisms at or below the gingival margin causes inflammation

45
Q

Specific plaque hypothesis

A

Specific organisms in the dental plaque are etiological agents
Not all bacteria are bad
This guides our clinical thinking today

46
Q

Ecological plaque hypothesis

A

There are no ‘good’ or ‘bad’ bacteria, but only certain things the body can tolerate
If there is a shift in ecology, bad things can happen

47
Q

Oral dysbiosis

A

Pathogens require 1’ colonizer for attachment, and possibly other things
Pathogens are always present, but their numbers spike when the environment changes

48
Q

1’ Colonizers

A

Gram+ and Gram-

Streptococci that bind pellicle proteins

49
Q

2’ Colonizers

A

Bridge species - F. nucleatum

50
Q

3’ Colonizers

A

P. gingivalis

51
Q

Quorum sensing

A

What does Regulation of expression of specific genes through accumulation of signaling compounds that mediate intracellular communication
Provides antibiotic resistance in dense biofilms
Encourages growth of beneficial species

52
Q

What does quorum sensing depend on?

A

Cell density

53
Q

Auto-inducer 1 or 2

A

Turns on in response to cell density

54
Q

Pathogenic bacteria produce what in high levels?

A

AI-2

55
Q

AI-2 may determine what?

A

The switch from comensal to pathogenic community

56
Q

What is more resistant, planktonic or biofilm bacteria?

A

Biofilm bacteria are 1000-1500x more resistance than planktonic

57
Q

What are biofilms more resistant?

A

They grow more slowly
-Antibiotics depend on cell turnover for efficacy
-Slow growers express ‘non-specific defense mechanisms’
Exopolymers retard diffusion
Biofilm bacteria express different genes

58
Q

Exo-polymers

A

Retard diffusion

  • ion-exchange mechanism prevents highly charged molecules from reaching deeper zones
  • Extra-cellular enzymes inactivate antibiotics (B-lactamases, formaldehyde dehyrogenase)
59
Q

Neutrophil chemotaxis

A

Neutrophils start in circulation
Presence of plaque can be communicated to the CT by proteases, LPS, F-Met-Leu-Phe
Those things talk to macrophages, which release cytokines (TNF, IL-1)
This increases adhesion molecule expression, and these can bind to neutrophils, which then go to the site

60
Q

T-cell structure

A

2 glycoprotein chains (a and B) with variable segments

61
Q

What do variable segments of T-cells determine?

A

The type of immune response

62
Q

TCR in periodontitis

A

Differ before and after surgery

Differ between chronic and aggressive periodontitis

63
Q

What are the two T-cell types and what do they differ in?

A

Th1 and Th2

They differ in cytokine profile

64
Q

What cytokines coincide with Th1?

A

IL-2
IFN-y
TNF-a

65
Q

What cytokines coincide with Th2?

A 
IL-4
IL-5
IL-6
IL-10
IL-13
66
Q

B-cell response

A

Humoral immunity triggered in response to soluble antigens

67
Q

Ag-Ab complex

A

Activates complement

Facilitates opsonization

68
Q

What T cells activate B-cell response?

A

Th2

69
Q

What are the two types of B-cells?

A

Conventional (B2)

Autoreactive (B1)

70
Q

Conventional B cells (B2)

A

Produce antibodies against bacteria

Levels decrease in healthy and treated sites

71
Q

Autoreacttive B cells (B1)

A

Produce auto-antibodies

Levels do not decrease after treatment

72
Q

IL-10

A

Con contribute to both Th1 and Th2

Normally knocks down cell-mediated response and increases humoral response

73
Q

What is lots of IL-10 an indicator of?

A

Stabalized perio lesion

74
Q

What is little IL-10 an indicator of?

A

Lesion is progressing

75
Q

Initial lesion

A

Vasculitis subadjacent to JE
Exudaiton of fluid into tissue and gingival sulcus
Increased migration of leukocytes into JE and sulcus
Serum proteins present extravascularly
Alteration of the most coronal portion of JE
Loss of perivascular collagen

76
Q

Early lesion

A

Accentuation of features of the initial lesion
Accumulation of lymphoid cells immediately subadjacent to JE
Cytopathic alteration in resident fibroblasts
Further loss of collagen network
Early proliferation of basal cells of JE
Inflammation changes are clinically evident

77
Q

Established lesion

A

Persistence of features of acute inflammation
Increased proportion of plasma cells
Presence of extravascular immunoglobulins in CT, JE, and sulcus
Continuing loss of collagen and matrix
Proliferation and lateral extension of JE
Early pocket formation may be evident
No apical migration of JE or bone loss yet

78
Q

Advanced lesion

A

Persistence of established lesion deatures
Increased proportion of plasma cells (~50%)
Extension of lesion into alveolar bone and PDL with significant bone loss
Continued loss of collagen fibers and matrix subadjacent to PE
Formation of pockets
Apical migration of JE

Perio Final (7 decks)

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