OST Exam 1: Part 2 (Anna)

Question 1

Q5: MGJ

What does MGJ stand for. Where is it found?

Answer 1

MGJ stands for the mucogingival junction.

It is found at the base of the gingival mucosa and the top of the alveolar mucosa.

Question 2

Q5: MGJ

What type of epithelium makes up the gingival tissue and hard palate?

Answer 2

• Keratinized epithelium

Question 3

Q5: MGJ

What type of epithelium makes up the alveolar mucosa?

Answer 3

non-keratinized epithelium

Question 4

Q5: MGJ

Attached gingiva is is measured from where to where?

Answer 4

– Attached gingiva is measured from the gingival sulcus to the MGJ

(look at picture)

Question 5

Q6: Know about normal patterns of attached tissue

What’s the equation used to find out how much attached gingiva there is?

– Is it possible to have no attached gingiva?

Answer 5

Attached Gingiva= Kerantinized(KG)- Sulcus (PD)

i. KG=Gingival Margin (GM) to Marginal Gingival Junction (MGJ)
ii. Calculation Example: 9 mm of gingiva, 3 mm is the sulcus, then 6 mm is the attached gingiva
iii. It is possible to have no attached gingiva (apical to the MGJ)

Question 6

Q6: Gingival width

– Which teeth has more keratinized tissue. Incisors or premolars?

Answer 6

Incisors>Molars>Premolars

Alphabetical order :)

Question 7

Q6:

Palate is made of what kind of tissue
– Is there a MGJ present on the palate?

Answer 7

Palate is all keratinized. It doesn’t have an MGJ

Question 8

Q12: Epidemiology: risk, risk factors

What two factors are associated with Gingival Disease risk factors?

Answer 8

Gingival Disease Risk Factors:

i. Oral Hygiene Status
ii. Hormonal Changes (smoking)

Question 9

Q12: Epidemiology: 
Aggressive Periodontitis Risk Factors
i: What microbe is associated with it?
II: What kind of defection?
III: aggressive periodontitis risk factors is found predominantly in what race?

Answer 9

Aggressive Periodontitis Risk Factors

i. Aggregatibacter actinomycetemcomitans (A.A.)
ii. Defective neutrophil function
iii. African American

Question 10

Q12: Chronic Periodontitis

What kind of factors are associated with chronic periodontitis:

Answer 10

i. Microorganism
ii. Diabetes
iii. Osteoporosis
iv. Genetic Factors
v. Smoking
vi. Nutrition
vii. HIV/AIDS
viii. Stress

Question 11

Q13:

Drawing on the slide that she shows all the time (Drawing that she started lecture with):

Answer 11

Look at the review Shane sent out for pictures

Question 12

Q15: Biofilms

a. What is another term for biofilm?
b. -Define biofilm:
c. What type factors may be enhanced?
d. What kind of community do biofilms form and what does it lead to?
d(i): what are these microorganisms resistant to?
d(ii): Where do they spread?

Answer 12

Biofilms:

a. Dental plaque is biofilm
b. Bacterial populations adherent to each other or to surfaces and enclosed matrix
c. Pathogenicity and virulence may be enhanced
d. Form a cooperating community of microorganism that lead to colonies
i. Resistant to antibiotics, antimicrobials, and host response
ii. Spread apically along root surface

Question 13

Q16: Calculus information:

What is calculus?

Answer 13

Calcified plaque

Question 14

Q16: Calculus formation:

What are the four modes of attachment in calculus formation:

Answer 14

Four Modes of Attachment

i. Organic pellicle
ii. Penetration into cementum
iii. Mechanical locking with surface irregularities
iv. Close adaptation to undersurface depressions
* poor restorations, anatomical abnormalities, systemic disease, and oral habits can contribute to formation

Question 15

Q17: Cytokines

What are the cytokines associated with the following:
I. Bone resorption
II. Connective tissue breakdown
III. bone resorption with PGE2

Answer 15

Cytokines

i. IL-1B = bone resorption
ii. MMP(1&8)= connective tissue breakdown
iii. TNF alpha= bone resorption with PGE2

Question 16

Q18: Pathogenesis Stages
** Know the chart

For Initial stage:

• • Onset time after plaque formation:
• • Histopathological
• • Features:

Answer 16

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

Question 17

Q18: Pathogenesis Stages
** Know the chart

For Early stage:

• • Onset time after plaque formation:
• • Histopathological
• • Features:

Answer 17

• • Onset after plaque formation: 4-7 days
• • Histopathological: T-cell lesion
• • Features: Clinical signs of gingivitis: Redness, bleeding, edema

Question 18

Q18: Pathogenesis Stages
** Know the chart

For Established stage:

• • Onset time after plaque formation:
• • Histopathological
• • Features:

Answer 18

• • Onset after plaque formation: 2-3 wks
• • Histopathological: B-cell lession: plasma cells
• • Features: Clinical signs of gingivitis: Chronic gingivitis

Question 19

Q18: Pathogenesis Stages
** Know the chart

For Advanced stage:

• • Onset time after plaque formation:
• • Histopathological
• • Features:

Answer 19

• • Onset after plaque formation: Undetermined
• • Histopathological: alveolar bone loss, pocket formation, B-cell lesion. Irreversible
• • Features: Periodontitis

Question 20

Q19: Smoking

Why is there less bleeding with smokers?

• -Will there be any red, inflamed tissue?
• • Resistance in smoker?
• • (smokers or non-smokers)… will have less clinical inflammation than non-smokers with similar local factors

Answer 20

• • less bleeding due to tough fibrotic tissue.
• • You will never see the red, inflamed tissue.
• • With a smoker, you probably will come up against a lot of resistance and less bleeding, but you will still have periodontal disease.
• • Smokers have less clinical inflammation than non-smokers with similar local factors.

Question 21

Q19:

What happens to the pocket depths and attachment loss in smokers:

Answer 21

– increased pocket depths and increased attachment loss.

Question 22

Q20:

Current smokers who have smoked 100+ cigarettes are how many times more likely to have periodontal disease?

Answer 22

Four times

Question 23

Q20:

Former smokerrs who have smoked 100+ cigarettes and do not currently smoke are how many times more likely to have periodontal disease?

Answer 23

1.6 times

Question 24

Q20:

smoking effects:
– Is gingivitis associated with smoking reversible?

Answer 24

• • Reversible with cessation
• • Decrease effects as increase years of not smoking
• • Cessation programs are important

Question 25

Q20: Smoking

Effects – Microbiology

• • Effect on rate of plaque accumulation
• • Increase pathogen in what kind of pockets?
• • What kind of microorganisms present?

Answer 25

• No effect on rate of plaque accumulation
• Increase pathogens in shallow pockets
• Increase pathogens in deep pockets
• Mixed results on specific microorganisms

Question 26

Q20: Smoking

Effects – Immunology

• • Increase or decrease immune response to challange?
• • Increase or decrease in PMN, chemotaxis, and phagocytosis
• Increase or decrease TNFα, PGE2 and MMP8 (all cytokines increase)

Answer 26

• Decrease immune response to challenge
• Decrease PMN chemotaxis and phagocytosis
• Increase TNFα, PGE2 and MMP8 (all cytokines increase)

Question 27

Q20: Smoking

Effects – Maintenance

Answer 27

• Increase in pocket depths
• Decrease in attachment gain
• Trends toward recurrent disease

Question 28

Q20: Smoking

Effects – GTR Surgery (Guided tissue regeneration)

Answer 28

• Gain in clinical attachment
• Decreased recession
• Gain in bone
• Decreased membrane exposure
• ***** Smoker’s results will not be as good as nonsmoker’s response to procedures.

Question 29

Smoking effects:

Smokers vs. non- smokers 
Cal (clinical attachment loss) gain:
Recession:
Bone gain:
ME:

Answer 29

Smoking Effects - GTR Surgery
			Smokers	Non-smokers
CAL gain		1.2 mm		3.2 mm
Recession		2.8 mm		1.3 mm
Bone gain		0.5 mm		3.7 mm
ME			10/10	         15/28