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Perio Final > Exam #1 Review > Flashcards

Exam #1 Review Flashcards

(78 cards)

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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
What does a segregation analysis tell us?
Tells us the pattern of diseases segregating in families - can determine if occurence in family is constant with the genetic model
26
Which genetic model passes periodontitis?
Almost all of them
27
What did a linkage analysis tell us about the chromosomal location of aggressive periodontitis?
There are multiple forms and many locations where it can be found
28
How do you measure CAL?
CAL = PD + recession
29
What is biologic width measurement
2mm
30
KEratinized gingiva
The marginal gingiva and the attached gingiva
31
Free gingival groove
Junction between the attached gingiva and the marginal gingiva Corresponds with the CEJ Only observable in 30-40% of adults
32
Free gingival margin
Coronal end of the gingiva | Located 1.5-2.0mm coronal to the CEJ
33
Mucogingival junction
Border between the keratinized gingiva and the alveolar mucosa
34
What does the 'width' of the gingiva mean?
Height occluso-cervically
35
What does the 'thickness' of the gingiva mean?
Thickness B-L
36
T/F - The mucogingival junction moves as the tooth erupts
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
What is the purpose of gingival fibers?
Reinforce the gingiva Provide resilience and tone Maintain architechtural form and integrity
38
What are the different types of gingival fibers?
Circular Dentogingival Dentoperiosteal Transseptal
39
Circular fibers
Encircle the tooth like a cuff
40
Dentogingival fibers
Fan out from the supra-crestal cementum into the free gingiva
41
Dentoperiosteal fibers
Run from supra-crestal cementum into attached fibers
42
Transseptal fibers
Run from tooth to tooth and embed into the cementum
43
What are the different theories about plaque as an etiological agent?
Non-specific plaque hypothesis Specific plaque hypothesis Ecological Plaque hypothesis Oral dysbiosis
44
Non-specific plaque hypothesis
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
Specific plaque hypothesis
Specific organisms in the dental plaque are etiological agents Not all bacteria are bad This guides our clinical thinking today
46
Ecological plaque hypothesis
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
Oral dysbiosis
Pathogens require 1' colonizer for attachment, and possibly other things Pathogens are always present, but their numbers spike when the environment changes
48
1' Colonizers
Gram+ and Gram- | Streptococci that bind pellicle proteins
49
2' Colonizers
Bridge species - F. nucleatum
50
3' Colonizers
P. gingivalis
51
Quorum sensing
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
What does quorum sensing depend on?
Cell density
53
Auto-inducer 1 or 2
Turns on in response to cell density
54
Pathogenic bacteria produce what in high levels?
AI-2
55
AI-2 may determine what?
The switch from comensal to pathogenic community
56
What is more resistant, planktonic or biofilm bacteria?
Biofilm bacteria are 1000-1500x more resistance than planktonic
57
What are biofilms more resistant?
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
Exo-polymers
Retard diffusion - ion-exchange mechanism prevents highly charged molecules from reaching deeper zones - Extra-cellular enzymes inactivate antibiotics (B-lactamases, formaldehyde dehyrogenase)
59
Neutrophil chemotaxis
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
T-cell structure
2 glycoprotein chains (a and B) with variable segments
61
What do variable segments of T-cells determine?
The type of immune response
62
TCR in periodontitis
Differ before and after surgery | Differ between chronic and aggressive periodontitis
63
What are the two T-cell types and what do they differ in?
Th1 and Th2 | They differ in cytokine profile
64
What cytokines coincide with Th1?
IL-2 IFN-y TNF-a
65
What cytokines coincide with Th2?
``` IL-4 IL-5 IL-6 IL-10 IL-13 ```
66
B-cell response
Humoral immunity triggered in response to soluble antigens
67
Ag-Ab complex
Activates complement | Facilitates opsonization
68
What T cells activate B-cell response?
Th2
69
What are the two types of B-cells?
Conventional (B2) | Autoreactive (B1)
70
Conventional B cells (B2)
Produce antibodies against bacteria | Levels decrease in healthy and treated sites
71
Autoreacttive B cells (B1)
Produce auto-antibodies | Levels do not decrease after treatment
72
IL-10
Con contribute to both Th1 and Th2 | Normally knocks down cell-mediated response and increases humoral response
73
What is lots of IL-10 an indicator of?
Stabalized perio lesion
74
What is little IL-10 an indicator of?
Lesion is progressing
75
Initial lesion
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
Early lesion
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
Established lesion
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
Advanced lesion
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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