OST Exam 1: Part 2 (Anna) Flashcards
Q5: MGJ
What does MGJ stand for. Where is it found?
MGJ stands for the mucogingival junction.
It is found at the base of the gingival mucosa and the top of the alveolar mucosa.
Q5: MGJ
What type of epithelium makes up the gingival tissue and hard palate?
- Keratinized epithelium
Q5: MGJ
What type of epithelium makes up the alveolar mucosa?
non-keratinized epithelium
Q5: MGJ
Attached gingiva is is measured from where to where?
– Attached gingiva is measured from the gingival sulcus to the MGJ
(look at picture)
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?
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)
Q6: Gingival width
– Which teeth has more keratinized tissue. Incisors or premolars?
Incisors>Molars>Premolars
Alphabetical order :)
Q6:
Palate is made of what kind of tissue
– Is there a MGJ present on the palate?
Palate is all keratinized. It doesn’t have an MGJ
Q12: Epidemiology: risk, risk factors
What two factors are associated with Gingival Disease risk factors?
Gingival Disease Risk Factors:
i. Oral Hygiene Status
ii. Hormonal Changes (smoking)
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?
Aggressive Periodontitis Risk Factors
i. Aggregatibacter actinomycetemcomitans (A.A.)
ii. Defective neutrophil function
iii. African American
Q12: Chronic Periodontitis
What kind of factors are associated with chronic periodontitis:
i. Microorganism
ii. Diabetes
iii. Osteoporosis
iv. Genetic Factors
v. Smoking
vi. Nutrition
vii. HIV/AIDS
viii. Stress
Q13:
Drawing on the slide that she shows all the time (Drawing that she started lecture with):
Look at the review Shane sent out for pictures
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?
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
Q16: Calculus information:
What is calculus?
Calcified plaque
Q16: Calculus formation:
What are the four modes of attachment in calculus formation:
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
Q17: Cytokines
What are the cytokines associated with the following:
I. Bone resorption
II. Connective tissue breakdown
III. bone resorption with PGE2
Cytokines
i. IL-1B = bone resorption
ii. MMP(1&8)= connective tissue breakdown
iii. TNF alpha= bone resorption with PGE2
Q18: Pathogenesis Stages
** Know the chart
For Initial stage:
- Onset time after plaque formation:
- Histopathological
- Features:
- -Onset after plaque formation: 2-4 days
- Histopathological: Acute inflammation: vasculitis, PMNs, Macrophages
- Features: Subclinical, no gingivitis, increased flow of gingival crevicular flow
Q18: Pathogenesis Stages
** Know the chart
For Early stage:
- Onset time after plaque formation:
- Histopathological
- Features:
- Onset after plaque formation: 4-7 days
- Histopathological: T-cell lesion
- Features: Clinical signs of gingivitis: Redness, bleeding, edema
Q18: Pathogenesis Stages
** Know the chart
For Established stage:
- Onset time after plaque formation:
- Histopathological
- Features:
- Onset after plaque formation: 2-3 wks
- Histopathological: B-cell lession: plasma cells
- Features: Clinical signs of gingivitis: Chronic gingivitis
Q18: Pathogenesis Stages
** Know the chart
For Advanced stage:
- Onset time after plaque formation:
- Histopathological
- Features:
- Onset after plaque formation: Undetermined
- Histopathological: alveolar bone loss, pocket formation, B-cell lesion. Irreversible
- Features: Periodontitis
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
- 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.
Q19:
What happens to the pocket depths and attachment loss in smokers:
– increased pocket depths and increased attachment loss.
Q20:
Current smokers who have smoked 100+ cigarettes are how many times more likely to have periodontal disease?
Four times
Q20:
Former smokerrs who have smoked 100+ cigarettes and do not currently smoke are how many times more likely to have periodontal disease?
1.6 times
Q20:
smoking effects:
– Is gingivitis associated with smoking reversible?
- Reversible with cessation
- Decrease effects as increase years of not smoking
- Cessation programs are important
Q20: Smoking
Effects – Microbiology
- Effect on rate of plaque accumulation
- Increase pathogen in what kind of pockets?
- What kind of microorganisms present?
- No effect on rate of plaque accumulation
- Increase pathogens in shallow pockets
- Increase pathogens in deep pockets
- Mixed results on specific microorganisms
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)
- Decrease immune response to challenge
- Decrease PMN chemotaxis and phagocytosis
- Increase TNFα, PGE2 and MMP8 (all cytokines increase)
Q20: Smoking
Effects – Maintenance
- Increase in pocket depths
- Decrease in attachment gain
- Trends toward recurrent disease
Q20: Smoking
Effects – GTR Surgery (Guided tissue regeneration)
- 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.
Smoking effects:
Smokers vs. non- smokers Cal (clinical attachment loss) gain: Recession: Bone gain: ME:
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
