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Oral Soft tissues > Exam 1 part 2 > Flashcards

Exam 1 part 2 Flashcards

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

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

A

First statement true

Second statement false, it increases bacteria concentration

25
Q

4 factors that can cause calculus

A
  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
Q

4 calculus attachments

A
  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
Q

Describe the Initial stage of pathogenesis

  • Onset after plaque formation
  • Histopathological
  • Features
A
  • 2-4 days
  • Acute inflammation: vasculitis, PMNs, Macrophages
  • subclinical, no gingivitis, increased flow of gingival crevicular flow
28
Q

Describe the Early stage of pathogenesis

  • Onset after plaque formation
  • Histopathological
  • Features
A
  • 4-7 days
  • T-cell lesion
  • Clinical signs of gingivitis, redness, bleeding, edema
29
Q

Describe the Established stage of pathogenesis

  • Onset after plaque formation
  • Histopathological
  • Features
A
  • 2-3 weeks
  • B-cell lesion: plasma cells
  • Chronic gingivitis
30
Q

Describe the Advanced stage of pathogenesis

  • Onset after plaque formation
  • Histopathological
  • Features
A
  • Undetermined time (not sure if periodontitis will occur)
  • Alveolar bone loss, pocket formation, B-cell lesion
  • Periodontitis
31
Q

Which cytokines cause bone resorption

A

IL-1 B

TNFalpha

32
Q

What is the genetic influence of Interleukin-1 on periodontal disease?

A

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
Q

T or F, MMP(1&8) is a cytokine and is involved in bone resorption

A

False, it is a proteinase, not a cytokine, but is found with cytokines. It breaks down connective tissue

34
Q

What cells are involved in advanced lesion of paige and schroder

A

B cell lesion

35
Q

T or F, Smoking decreases the clinical expression of inflammation and therefore less clinical inflammation than non-smokers

A

True,

36
Q

Does smoking contribute to PD? What if one stops smoking?

A

Yes, Current smokers have 4 times as much periodontal disease and Former smokers have only 1.6 times as much periodontal disease

37
Q

T or F, smokeless tobacco has a systemic effect on PD

A

False, only a localized effect on attachment loss, no effects on periodontitis

38
Q

T or F, Smoking effects are irreversible.

A

False, they are reversible with cessation of smoking

39
Q

T or F, Smoking has increases the rate of plaque accumulation

A

False, No effect

40
Q

Does smoking allow for an increased number of pathogens?

A

Yes, increased in both shallow and deep pockets

41
Q

How does smoking effect the immune response to challenge

A

It decreases the immune response, decreases PMN chemotaxis and pagocytosis and Increases TNF-alpha, PGE2, MMP-8 expression

42
Q

Do smokers have an increased response or decreased response to nonsurgical therapy & surgical therapy

A 
Decreased response to:
S&RP
Less pocket depth reduction
Less gain in attachment
Increase likelihood for failed implants
43
Q

T or f, Smokers have trends toward recurrent disease after tx

A

true

44
Q

What is the difference between recurrent and refractory

A

Recurrent: relapse
Refractory: non-responsive to tx modalities

45
Q

T or f, smokers have less overall tooth loss

A

False, more

46
Q

What causes a significant portion of the damage seen in periodontal disease?

A

Normal host response

47
Q

Host response is mediated by what:

A

MMPs such as collagenase (collagen breakdown)
Prostaglandins (bone resorption)
Osteoclasts (bone resorption)

48
Q

What is the main goal of host modulation?

A

Change host response to bacteria

  • Regulating the tissue damaging host response, typically using drugs
  • target MMPs, Prostaglandins, Osteoclasts
49
Q

What is the major drug for host modulation

A

Periostat, which is a small does of the antibiotic doxycycline

50
Q

When we collect data, what is most important in all the data we collect when diagnosing PD?

A

Clinical attachment loss

CAL and probing depths increasing can tell if disease is getting worse

51
Q

What does healthy gingiva look like?

A

Scalloped gingival margin
Papillas between teeth are knife-like
Pink (salmon) indicative of health

52
Q

What does diseased gingiva look like?

A

Blunted/bulbous/rounded interproximally
Red (inflammation)
Increased bleeding on probing
Loss of clinical attachment levels/recession

53
Q

T or F, Only increasing probing depths and clinical attachment loss are associated with disease progression

A

True

54
Q

What are the percentages of different occurrences at the cemento-enamel junction

A

Overlap (60-65%)
Butt (30%)
Exposed dentin (5-10%)

55
Q

Dimensions of cementum

A

16-60 u Coronal

150+ u apical

56
Q

T or F, Apical, Furcal and Distal surfaces increases with age

A

True

Oral Soft tissues (5 decks)

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