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Oral Soft tissues > Exam 1 part 2 > Flashcards

Exam 1 part 2 Flashcards

(56 cards)

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1
Q

What type of category does pregnancy and gingivitis fall into for gingivitis

A

Pregnancy associated gingivitis –> Plaque induced gingivitis

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2
Q

What are the medications involved in gingival overgrowth

A

Anti-convulsants/Anti-seizure - Dilantin
Ca channel blockers - Nifedipine
Immunosuppresants - Cyclosporin
(as well as oral contraceptives)

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3
Q

What is the difference between risk and risk factor

A

Risk: the likelihood a person will get a disease in a specified time period
Risk factor: Before manifestation, a factor that puts them at a greater risk for developing the disease

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4
Q

Identify the microorganisms involved in Chronic PD

A

Porphyromonas gingivalis (Proteases)
Tannerella forsythia
Treponema denticola
Aggregatibacter actinomycetemcomitans (leukotoxin)

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5
Q

Identify the microorganisms involved in Aggressive PD

A 
Aggregatibacter actinomycetemcomitans
Porphyromonas gingivalis (some patients)
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6
Q

Identify the microorganisms involved in Necrotizing PD

A

Prevotella intermedia ( also seen in preg. ass. gingivitis)
Spirochetes (invade CT)
Fusiform bacilli

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7
Q

What is the portal of entry for microorganisms involved in PD

A

Sulcular epithelium ulcerations and direct penetration of host epithelial or CT cells

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8
Q

Define biofilm

A

Cooperating community of microorganisms arranged in microcolonies surrounded by protective matrix
- Dental plaque is a biofilm

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9
Q

T or F, Plaque spreads horizontally across buccal surface of tooth

A

False, Spreads apically along rot surface

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10
Q

What is calculus?

A

Calcified dental plaque

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11
Q

T or F, Calculus is a secondary contributing factor to PD

A

True

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12
Q

Calculus’s role in disease

A

Harbors bacteria –> induces damage

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13
Q

What immune cells first come to the pocket

A

PMN –> first repsonder

  • phagocytize material in sulcus.
  • Migrate into sulcus/pocket from leaky ulcerative gingival epithelium
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14
Q

What do mast cells do

A

Release amines

Increases vascular permeability

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15
Q

What do macrophages do

A

Present antigen to T cells

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16
Q

T-lymphocytes

A

lymphokines and delayed hypersensitivity

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17
Q

B-lymphocytes

A

may differentiate into plasma cells

- Active in antibody formation

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18
Q

Describe the 5 points of tooth associated subgingival plaque

A
  1. Densely, adherent, biofilm
  2. G+ rods, cocci, filaments
  3. Facultative aerobes/anaerobes
  4. Remove by SRP (mechanical removal)
  5. Less virulent
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19
Q

Describe tissue associated subgingival plaque (5)

A
  1. Loosely adherent
  2. G- motile anaerobes
  3. Spriochetes
  4. Remove surgically
  5. More virulent
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20
Q

Describe unattached subgingival plaque

A
  1. Free swimming in pocket
  2. G- motile anaerobes
  3. Spirochetes
  4. Remove by flushing
  5. More virulent
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21
Q

Describe microbial shift, healthy –> gingivitis –> periodontitis

A

From G+ to G-
from Cocci to rods (later spirochetes)
From non-motile to motile
From facultative to obligate anaerobes

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22
Q

Describe the color of supragingival and subgingival calculus

A

supragingival: whitish, yellow
Subgingival: dark brown, hard and dense

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23
Q

T or F, Roughness of calculus increases surface area

Study These Flashcards
A

true

But it is not a mechanical irritant

24
Q

T or F, Calculus increases density in which plaque can accumulate but decreases bacteria concentration

Study These Flashcards
A

First statement true

Second statement false, it increases bacteria concentration

25
4 factors that can cause calculus
1. Anatomical abnormalities (enamel pearl, fluted root) 2. Physical irritants: amalgam overhang, rest. contours 3. Habits: mouth breathing, factitious injuries 4. Systemic disease: DM
26
4 calculus attachments
1. Pellicle 2. Penetrate cementum 3. Lock into surface irregularities (CEJ, crown margin) 4. Into depression/concavities in roots (ex: premolar roots > canine roots, multirooted teeth more prone to perio disease)
27
Describe the Initial stage of pathogenesis - Onset after plaque formation - Histopathological - Features
- 2-4 days - Acute inflammation: vasculitis, PMNs, Macrophages - subclinical, no gingivitis, increased flow of gingival crevicular flow
28
Describe the Early stage of pathogenesis - Onset after plaque formation - Histopathological - Features
- 4-7 days - T-cell lesion - Clinical signs of gingivitis, redness, bleeding, edema
29
Describe the Established stage of pathogenesis - Onset after plaque formation - Histopathological - Features
- 2-3 weeks - B-cell lesion: plasma cells - Chronic gingivitis
30
Describe the Advanced stage of pathogenesis - Onset after plaque formation - Histopathological - Features
- Undetermined time (not sure if periodontitis will occur) - Alveolar bone loss, pocket formation, B-cell lesion - Periodontitis
31
Which cytokines cause bone resorption
IL-1 B | TNFalpha
32
What is the genetic influence of Interleukin-1 on periodontal disease?
It has been shown that polymorphisms associated with the activity of IL-1 are resonsible for 2-4 times increase in macrophage IL-1 production. This profile has shown to have individuals with more severe periodontal disease. -The polymorphism does not cause disease, it makes the individual response more severe.
33
T or F, MMP(1&8) is a cytokine and is involved in bone resorption
False, it is a proteinase, not a cytokine, but is found with cytokines. It breaks down connective tissue
34
What cells are involved in advanced lesion of paige and schroder
B cell lesion
35
T or F, Smoking decreases the clinical expression of inflammation and therefore less clinical inflammation than non-smokers
True,
36
Does smoking contribute to PD? What if one stops smoking?
Yes, Current smokers have 4 times as much periodontal disease and Former smokers have only 1.6 times as much periodontal disease
37
T or F, smokeless tobacco has a systemic effect on PD
False, only a localized effect on attachment loss, no effects on periodontitis
38
T or F, Smoking effects are irreversible.
False, they are reversible with cessation of smoking
39
T or F, Smoking has increases the rate of plaque accumulation
False, No effect
40
Does smoking allow for an increased number of pathogens?
Yes, increased in both shallow and deep pockets
41
How does smoking effect the immune response to challenge
It decreases the immune response, decreases PMN chemotaxis and pagocytosis and Increases TNF-alpha, PGE2, MMP-8 expression
42
Do smokers have an increased response or decreased response to nonsurgical therapy & surgical therapy
``` Decreased response to: S&RP Less pocket depth reduction Less gain in attachment Increase likelihood for failed implants ```
43
T or f, Smokers have trends toward recurrent disease after tx
true
44
What is the difference between recurrent and refractory
Recurrent: relapse Refractory: non-responsive to tx modalities
45
T or f, smokers have less overall tooth loss
False, more
46
What causes a significant portion of the damage seen in periodontal disease?
Normal host response
47
Host response is mediated by what:
MMPs such as collagenase (collagen breakdown) Prostaglandins (bone resorption) Osteoclasts (bone resorption)
48
What is the main goal of host modulation?
Change host response to bacteria - Regulating the tissue damaging host response, typically using drugs - target MMPs, Prostaglandins, Osteoclasts
49
What is the major drug for host modulation
Periostat, which is a small does of the antibiotic doxycycline
50
When we collect data, what is most important in all the data we collect when diagnosing PD?
Clinical attachment loss | CAL and probing depths increasing can tell if disease is getting worse
51
What does healthy gingiva look like?
Scalloped gingival margin Papillas between teeth are knife-like Pink (salmon) indicative of health
52
What does diseased gingiva look like?
Blunted/bulbous/rounded interproximally Red (inflammation) Increased bleeding on probing Loss of clinical attachment levels/recession
53
T or F, Only increasing probing depths and clinical attachment loss are associated with disease progression
True
54
What are the percentages of different occurrences at the cemento-enamel junction
Overlap (60-65%) Butt (30%) Exposed dentin (5-10%)
55
Dimensions of cementum
16-60 u Coronal | 150+ u apical
56
T or F, Apical, Furcal and Distal surfaces increases with age
True

Oral Soft tissues (5 decks)

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