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23 Cards in this Set
- Front
- Back
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1. What are the clinical features of aggressive periodontitis?
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1. Inflammation
2. Bone loss (occurs rapidly) **vertical bone loss b/c it occurs so rapidly |
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2. What is the age of onset for aggressive periodontitis?
What are three other criteria for dx of aggressive periodontitis? |
May develop between 11 and 30 yrs of age
**often starts during the circumpuberatal age (11-14) 1. Systemically healthy 2. Only permanent teeth are affected 3. Little or no involvement of deciduous teeth |
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3. What are the two classifications of aggressive periodontitis?
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1. Localized aggressive periodontitis
-localized juvenile periodontitis -localized early onset periodontitis 2. Generalized aggressive periodontitis -generalized juvenile -generalized early onset |
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4. What are the characteristics of localized aggressive periodontitis?
Three things... |
1. Localized mainly to first permanent molars and/or incisors
2. Only a few (<2) teeth other than 1st molars and incisors may be involved 3. Disease usually commences during circumpubertal age (11-14) |
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5. What are two characteristics of generalized aggressive periodontitis?
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1. Affects persons under 30 yrs of age
2. Affects the 1st permanent molars, incisors and 3 or more other teeth |
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6. What are the etiological and risk factors for aggressive periodontitis?
Six things... |
1. Pathogenic microorganisms
2. Host immune defects 3. Genetic predispositions 4. Race-ethnicity 5. Herpes virus infections 6. Other factors |
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7. What has a bigger role as an etiological and risk factor for aggressive periodontitis?
What about for chronic periodontitis? |
Genetics (aggressive)
Environmental (chronic) |
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8. What are the two main groups of pathogenic microorganisms in aggressive periodontitis?
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1. AA
(aggregatibacter actinomycetemcomitans) -JP2 strain 2. Porphyromonas gingivalis |
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9. What are the virulence factors of AA?
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1. Leukotoxic strain
(affects immune system) 2. Antibody reaction -elicits antibody rxn which can cause damage to host 3. Invasion of tissue (invade epithelial tissue) |
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10. What were the finding of the study "Progression of periodontal disease in relation to presence of AA JP2 strain"?
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1. JP2 clone of AA is important etiological factor for periodontal attachment loss in children and adolescents
2. Co-occurence of non-JP2 clones of AA reduces the risk of development of aggressive periodontitis |
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11. What are the three effects of AA leukotoxin?
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1. Help evade local host defenses
2. Cytotoxic to human neutrophils and monocytes 3. Lethal effect on human T lymphocytes |
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12. How does P. gingivalis colonize subgingival sites?
How are it's virulence factors? What cells does it affect? |
Colonized by adhering to available substrates
Potent virulence factors *antibody reaction Gingival epithelial cells |
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13. What are some host immune defects that can be a risk factor for developing aggressive periodontitis?
Five things... |
1. Leukocytes adhesion defects
2. Neutrophil chemotaxis defects 3. Phagocyte abnormalities 4. Antibody level 5. Hyper-responsive macrophage phenotype *more important in chronic periodontitis |
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14. How do serum IgG and IgA antibody levels to periodontal pathogens AA and P. gingivalis differ between localized and generalized aggressive periodontitis?
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Significantly elevated in generalized aggressive periodontitis
Not significantly elevated in localized aggressive periodontitis |
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15. What evidence is there for the role of genetic factors in aggressive periodontitis?
(two things) How is familial aggregation seen in aggressive periodontitis? What type of disease is it most likely? |
1. Familial aggregation
2. Association w/ known genetic markers Occurs more frequently w/in families Autosomal dominant disease w/ reduced penetrance |
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16. What is the risk of being diagnosed with aggressive periodontitis?
What association is seen with genetic markers? |
Parents, offspring and siblings have a 50% risk
**probably autosomal dominant Multiple genes may contribute to etiology with these genes probably having a relatively small effect |
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17. Which gene polymorphisms show a significant association w/ aggressive periodontitis?
(four) Which gene polymorphism shows inconsistent results? |
1. IL-6
2. IL-10 3. Vitamin D receptor gene 4. Neutrophil formylpeptide receptors IL-1 |
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18. What do results from the National Survey of US Children show about race-ethnicity in regards to aggressive periodontitis?
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1. African-American adolescents 14-17 yrs old are 15 times more likely to develop aggressive periodontitis than whites
2. Hispanic adolescents 14-17 yrs old are 4 times more likely to develop aggressive periodontitis than whites |
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19. What association is there between race and a specific bacterial strain in aggressive periodontitis?
How are genetic predispositions to aggressive periodontitis varied by race? |
Highly leukotoxic strain of AA is found more often in aggressive periodontitis patients of African descent
IL1 alpha and IL-1 beta gene polymorphisms 1. Highly frequent in African-American 2. Moderately frequent in Caucasians 3. Infrequent in Chinese-Americans |
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20. Which herpes viruses is a possible etiological factor involved in the initiation and progression of aggressive periodontitis?
What is the rational for this? (three things) |
Active human cytomegalovirus (HCV) infection
1. Immunosuppression 2. Establishment & growth of subgingival periodontal pathogens 3. Herpes virus reactivation |
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21. How is aggressive periodontitis a multifactorial disease?
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1. Demographic
2. Environmental 3. Biological |
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22. What are factors that affect aggressive periodontitis?
Eight things... |
1. Infection
2. Oral hygiene 3. Local factors 4. Race-ethnicity 5. Host immune factors 6. Smoking 7. Genetic predispositions 8. Socioeconomic |
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23. What is the treatment of aggressive periodontitis?
Four things... |
1. Elimination of local factors
2. Oral hygiene 3. Microbiological testing and antibiotic prescription 4. Periodontal surgery therapy |
