Perio

Front 1

1. What acute infections could be of bacterial origin?

Back 1

1. Periodontal abscess

2. Perocornitis

3. Acute necrotizing ulcerative gingivits (ANUG)

Front 2

2. What does a periodontal abscess develop from?

What is it filled with?

What can be done?

Back 2

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

Front 3

3. What happens if there is inadequate drainage?

How do periodontal abscesses appear?

Back 3

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

Front 4

4. Where is a periodontal abscess located?

How can you detect it?

Back 4

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

Front 5

5. What are there characteristics of a periodontal abscess?

Back 5

1. No periapical radiolucency

2. Usually no history of heat or cold sensitivity

3. Swelling usually coronally

Front 6

6. What are the characteristics of pulpitis?

Back 6

1. Apical swelling

2. Cannot detect pocket communication

3. Have periapical radiolucency

4. History of heat sensitivity

Front 7

7. What is a combined perio/endo abscess?

Back 7

Have a combination of signs and symptoms characterized by a fistulous tract communicating w/ a sulcus or periodontal pocket

Front 8

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?

Back 8

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

Front 9

9. What are some treatment considerations?

Back 9

1. Change the ecosystem

2. Antibiotic use

Front 10

10. How can the ecosystem be changed?

Back 10

Even if only some of the microorganisms in an ecosystem are destroyed or inhibited, the environment of the entire ecosystem will be changed

Front 11

11. How can antibiotic use destroy the ecosystem even if the specific pathogen is not susceptible to the antibiotic themselves?

Back 11

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

Front 12

12. What is the ideal antibiotic use?

Back 12

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

Front 13

13. What is done for unresponsive infections?

Are topical antibiotics effective?

Back 13

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

Front 14

14. What is pericornitis?

Where does this occur?

Back 14

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

Front 15

15. What are some symptoms of pericornitis?

Back 15

1. Pain

2. Erythema

3. Lymphadenopathy

Front 16

16. What is lymphadenopathy

Why is pericornitis dangerous?

Back 16

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)

Front 17

17. What is the treatment for perocornitis?

Back 17

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

Front 18

18. What is ANUG?

How is the host defenses?

How does it spread?

Back 18

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

Front 19

19. What are the clinical features of ANUG?

Back 19

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

Front 20

20. What are clinical features of ANUG?

Back 20

5. Linear erythema under pseudomembrane

6. Spreads to adjacent tissues if not controlled

7. Foul breath

Front 21

21. What is the clinical appearance of ANUG?

Back 21

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

Front 22

22. What are some extra-oral signs of ANUG?

Back 22

1. May be lymphadenopathy

2. May present w/ elevated temperature

3. Uncontrolled local spread (NOMA) or systemic spread in severely debilitated usually starving people

Front 23

23. What microorganisms are involved in ANUG?

Back 23

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

Front 24

24. What is the etiology of the microorganisms of ANUG?

What factors influence the host's defenses?

Back 24

The microorganisms are opportunistic pathogens requiring a compromised host defense

1. Nutritional deficiencies
2. Psychological stress
3. Debilitating diseases

Front 25

25. What are the four histological zones of ANUG?

1 and 2

Back 25

**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

Front 26

26. What are the four histological zones of ANUG?

3 and 4

Back 26

Zone 3 - necrotic zone
-disintegrated tissue components and large spirochetes

Zone 4 - zone of spirochete infiltration
-intact tissues invaded by spirochetes

Front 27

27. What is the treatment for ANUG?

Back 27

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

Front 28

28. What are the residual lesions of ANUG like?

Back 28

1. Interdental craters remain

2. Irregular gingival contours may be notable

**tissue damage doesn't come bakc

Front 29

29. What are some acute gingival infections that are of viral origin?

Back 29

1. Acute herpetic gingivostomatitis

2. Herpangina

3. Acute recurrent gingivities

Front 30

30. What virus causes acute herpetic gingivostomatitis?

What are the two types of it?

How is primary acute herpetic gingivostomatitis?

Back 30

Herpes virus type 1

1. Primary
**first exposure to HSV 1
2. Secondary

Usually in children and subclinical (asymptomatic)

Front 31

31. How is primary acute herpetic gingivostomatitis when there is clinical disease?

What does it affect?

Where does the virus become latent?

Back 31

Presents as rupturing small vesicles that can become confluent w/ other vesicles

Can affect any intraoral tissues

Becomes latent in neuronal ganglia

Front 32

32. When does secondary acute herpetic gingivostomatitis occur?

How is it different from primary?

Back 32

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

Front 33

33. What does secondary acute herpetic gingivostomatitis affect?

What do lip lesions cause a predisposition to?

Back 33

Attached gingiva (marginal gingiva, palate) and lip

Lip lesions predispose to squamous cell carcinoma when chronic sun exposure is superimposed

Front 34

34. What is the treatment and prevention for acute herpetic gingivostomatitis?

Back 34

1. Antiviral ointment (zovirax) for minor lip lesions

2. Antiviral capsules

3. Sunscreen for lower lip (preventive)

**primary and secondary are contagious

Front 35

35. What are the characteristics of acute recurrent gingivitis?

Back 35

1. Sudden onset of pain

2. Affects marginal gingiva

3. Gingival swelling

4. No necrosis

5. Spreads to adjacent gingiva

Front 36

36. What is the etiology of acute recurrent gingivitis?

Back 36

Unknown microbial component but it responds to antibiotics

May be secondary herpes w/o noticeable ulceration

**probably a variant of secondary herpes

Front 37

37. Who is herpangina common in?

Back 37

Young patients usually presenting w/ URI (upper respiratory infection)

Front 38

38. How does candid albicans infection appear?

Back 38

As typical pseudomembrane formation or painful erythematous mucosa on tongue or other oral tissues

"Burning tongue" may be candida infection

Front 39

39. How can candida albicans infections be treated?

Back 39

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