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39 Cards in this Set
- Front
- Back
1. What acute infections could be of bacterial origin?
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1. Periodontal abscess
2. Perocornitis 3. Acute necrotizing ulcerative gingivits (ANUG) |
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2. What does a periodontal abscess develop from?
What is it filled with? What can be done? |
Develops from a periodontal pocket usually appearing as a superficial gingival swelling
Filled w/ pus Can break it open and drain it **until draining patient is in pain Once open can also scale and root plane |
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3. What happens if there is inadequate drainage?
How do periodontal abscesses appear? |
At high risk for subgingival infection
As gingival swellings which must be differentiated from puplitis **this is a periapcial abscess so becomes an endo problem |
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4. Where is a periodontal abscess located?
How can you detect it? |
Up high (superifical near gingival margin)
Can probe down into an abscess (greater than 2 or 3 mm pocket) **can detect a periodontal pocket leading to the abscess |
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5. What are there characteristics of a periodontal abscess?
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1. No periapical radiolucency
2. Usually no history of heat or cold sensitivity 3. Swelling usually coronally |
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6. What are the characteristics of pulpitis?
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1. Apical swelling
2. Cannot detect pocket communication 3. Have periapical radiolucency 4. History of heat sensitivity |
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7. What is a combined perio/endo abscess?
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Have a combination of signs and symptoms characterized by a fistulous tract communicating w/ a sulcus or periodontal pocket
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8. What types of bacteria are likely to cause a periodontal abscess?
What are mixed bacterial infections? How long does it take for a new ecosystem to develop? |
Same bacteria that causes or is involved in periodontitis
Late ecosystem pathogenic organisms inhabit the periodontal pocket (same organisms that cause periodontitis) 45 minutes after cleaning health related bacteria form an ecosystem |
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9. What are some treatment considerations?
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1. Change the ecosystem
2. Antibiotic use |
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10. How can the ecosystem be changed?
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Even if only some of the microorganisms in an ecosystem are destroyed or inhibited, the environment of the entire ecosystem will be changed
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11. How can antibiotic use destroy the ecosystem even if the specific pathogen is not susceptible to the antibiotic themselves?
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If the ecosystem environment changes the specific pathogen(s) may be denied growth requirements
**this is why sometimes even if an antibiotic is used which the pathogens are resistant, by chance the infection is controlled |
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12. What is the ideal antibiotic use?
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Broad spectrum approach such as metronidazole plus augmentin along w/ root planing and drainage
**augmentin is a penicillian derivative used for bacteria that is resistant to penicilian |
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13. What is done for unresponsive infections?
Are topical antibiotics effective? |
An anaerobic culture is submitted and a presumptive change in antibiotic therapy is instituted
Superficially effective in isolated sites but they are not suitable for periodontal disease or abscess control |
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14. What is pericornitis?
Where does this occur? |
Inflammation of excessive gingiva covering incompletely erupted teeth, most often lower third molars
Covering flap of tissue allows accumulation of food and microbial mass **have stagnate exudate so get bacterial growth Distal portion of 3rd molar |
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15. What are some symptoms of pericornitis?
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1. Pain
2. Erythema 3. Lymphadenopathy |
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16. What is lymphadenopathy
Why is pericornitis dangerous? |
Local lymph nodes are swollen
**hurt, puffy and movable The infection can spread b/c it will drain in direction of least resistance (can go into maxillary sinus and cranium) |
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17. What is the treatment for perocornitis?
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1. Local anesthesia and debridement w/ ultrasonics and antiseptics
2. Systemic antibiotics as needed 3. Possible extraction of 3rd molar 4. Possible reduction of tissue flap if tooth is to be retained |
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18. What is ANUG?
How is the host defenses? How does it spread? |
Rapid local tissue destruction due to inadequate control of periodontal flora
**usually don't get tissue destruction w/o periodontitis but this is the exception Lowered host defense Spreads if not controlled by host defense or treatment intervention |
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19. What are the clinical features of ANUG?
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1. Sudden onset of pain
2. Usually follows stressful times or debilitating disease 3. Pseudomembrane may appear on surface 4. May present crater-like lesions of interdental papilla |
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20. What are clinical features of ANUG?
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5. Linear erythema under pseudomembrane
6. Spreads to adjacent tissues if not controlled 7. Foul breath |
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21. What is the clinical appearance of ANUG?
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1. Pseudomembrane may not be apparent
2. Notable erythema 3. Bleeding 4. Necrosis 5. ANUG may be localized as well as generalized in tissue affected |
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22. What are some extra-oral signs of ANUG?
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1. May be lymphadenopathy
2. May present w/ elevated temperature 3. Uncontrolled local spread (NOMA) or systemic spread in severely debilitated usually starving people |
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23. What microorganisms are involved in ANUG?
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1. Spirochetes
**severe periodontal pathogen 2. Fusobacterium species **treatable w/ antibiotics but can only ID by microscope 3. Bacteroides melaninogenicus 4. Actinomyces odontolyticus 5. Selenomonas species |
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24. What is the etiology of the microorganisms of ANUG?
What factors influence the host's defenses? |
The microorganisms are opportunistic pathogens requiring a compromised host defense
1. Nutritional deficiencies 2. Psychological stress 3. Debilitating diseases |
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25. What are the four histological zones of ANUG?
1 and 2 |
**start superficial and move deep
Zone 1 - bacterial zone -most superficial zone consisting of a mixture of bacteria and fibrin Zone 2 - neutrophil rich zone -subjacent consisting of neutrophils and bacteria |
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26. What are the four histological zones of ANUG?
3 and 4 |
Zone 3 - necrotic zone
-disintegrated tissue components and large spirochetes Zone 4 - zone of spirochete infiltration -intact tissues invaded by spirochetes |
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27. What is the treatment for ANUG?
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Responds well to metronidazole and penicillins as well as other antibiotics
Although usually self-limiting, to be certain of preventing additional damage systemic antibiotics are neded |
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28. What are the residual lesions of ANUG like?
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1. Interdental craters remain
2. Irregular gingival contours may be notable **tissue damage doesn't come bakc |
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29. What are some acute gingival infections that are of viral origin?
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1. Acute herpetic gingivostomatitis
2. Herpangina 3. Acute recurrent gingivities |
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30. What virus causes acute herpetic gingivostomatitis?
What are the two types of it? How is primary acute herpetic gingivostomatitis? |
Herpes virus type 1
1. Primary **first exposure to HSV 1 2. Secondary Usually in children and subclinical (asymptomatic) |
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31. How is primary acute herpetic gingivostomatitis when there is clinical disease?
What does it affect? Where does the virus become latent? |
Presents as rupturing small vesicles that can become confluent w/ other vesicles
Can affect any intraoral tissues Becomes latent in neuronal ganglia |
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32. When does secondary acute herpetic gingivostomatitis occur?
How is it different from primary? |
Occurs after stress or trauma such as sun exposure to lower lip
Host response differs and it can have multiple occurrences often in the same sites |
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33. What does secondary acute herpetic gingivostomatitis affect?
What do lip lesions cause a predisposition to? |
Attached gingiva (marginal gingiva, palate) and lip
Lip lesions predispose to squamous cell carcinoma when chronic sun exposure is superimposed |
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34. What is the treatment and prevention for acute herpetic gingivostomatitis?
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1. Antiviral ointment (zovirax) for minor lip lesions
2. Antiviral capsules 3. Sunscreen for lower lip (preventive) **primary and secondary are contagious |
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35. What are the characteristics of acute recurrent gingivitis?
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1. Sudden onset of pain
2. Affects marginal gingiva 3. Gingival swelling 4. No necrosis 5. Spreads to adjacent gingiva |
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36. What is the etiology of acute recurrent gingivitis?
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Unknown microbial component but it responds to antibiotics
May be secondary herpes w/o noticeable ulceration **probably a variant of secondary herpes |
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37. Who is herpangina common in?
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Young patients usually presenting w/ URI (upper respiratory infection)
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38. How does candid albicans infection appear?
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As typical pseudomembrane formation or painful erythematous mucosa on tongue or other oral tissues
"Burning tongue" may be candida infection |
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39. How can candida albicans infections be treated?
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Will not respond to antibiotics
Only anti-fungal agents such as systemic diflucan and topical nystatin will work **topical application often is only partially effective |