Perio Ii

Front 1

1. In periodontal health what constitutes most of the subgingival microbiota?

What makes up the rest?

Back 1

Facultative and then Gram + rods

Anaeorbic and others

**75% facultative, gram-positive rods and cocci

Front 2

2. What are some of the facultative and gram-positive rods and cocci in periodontal health subgingival microbiota?

Back 2

1. Actinomyces species
2. Rothi dentocariosa
3. Cpanocytophaga species
4. S. sanguis
5. S. mitis
6. S. oralis

Front 3

3. What dominates in gingivitis subgingival microbiota?

What about in periodontitis?

Back 3

Increase from 15% to 50% in gram-negative anaerobes

75% are gram-negative anaerobes

Front 4

4. What are some risk factors for periodontitis?

8 things...

Back 4

1. Poor oral hygiene
2. Smoking
3. Genetic predisposition
4. Older age
5. Obesity
6. Psychosocial stress
7. Poorly controlled diabetes
8. Subgingival infection w/ specific pathogenic bacteria

Front 5

5. What did Miller say about dental plaque in the etiology of periodontal disease in the early 1900's?

Back 5

Periodontal disease is the result of an infectious process caused by bacteria

**no specific species found

Front 6

6. What is the non-plaque etiology of periodontitis postulated between 1920-1960?

Back 6

Periodontal health causes periodontitis

Causes include....
-traumatic occlusion
-systemic diseases
-genetic status
-atrophy or degeneration
-mechanical irritation by local factors
-infection (rarely considered)

Front 7

7. What did the study by Paul Keyes and Likins in 1946 demonstrate?

Back 7

First longitudinal documentation of a direct relationship between microbial dental plaque growth and subsequent periodontitis development

**One of the 1st to sue "dental plaque" as possible etiologic factor in periodontitis

Front 8

8. What did Keyes study utilize?

What did the study ultimately show?

Back 8

First reliable animal model to study the etiology and approaches to prevent dental caries and periodontal disease

Heavy dental plaque growth in periodontally healthy hamsters led to periodontal tissue destruction

Periodontal health maintained w/ absence of heavy dental plaque

Front 9

9. What is the non-specific plaque hypothesis?

Back 9

All dental plaque microorganisms thought to be equally capable of causing periodontal pathology if present in high enough numbers

**dominated until late 1960's

Front 10

10. What is the specific plaque hypothesis?

Back 10

Certain dental plaque microorganisms are specifically capable of causing periodontal pathology

Periodontal disease related more to quality of plaque composition rather than merely plaque quantity

Front 11

11. What did Jordand and Keyes study in 1964 demonstrated?

Back 11

First documentation of microbial specificity in the pathogenesis of periodontitis and infectious spread of periodontopathic bacteria

**Actinomyces viscosus assoc. w/ experimental periodontitis and root caries in hamsters

Front 12

12. What did Listgarten say about microbial specificity in periodontitis in 1976?

What did Slots say about microbial specificity in aggressive periodontitis and chronic (adult) periodontitis?

What did Tanner and Sacrnasky/Haffajee say about microbial specificity in periodontitis?

Back 12

More gram-negative and spirochete in periodontitis

Aggressive - AA
Chronic - porphyromonas gingivalis

Specific microbial species associated w/ progressive attachment loss

Front 13

13. Is there an increased risk for periodontal breakdown if a person has a high subgingival % of health-associated organisms?

What are the odds of the site being disease active if total "pathogens" compromise >30% of subgingival microbiota?

Back 13

No increased risk

Odds are > 15 to 1

Front 14

14. What organisms are associated with the initiation of chronic periodontitis?

Back 14

Red Complex

1. Porphyromonas gingivalis
2. Tannerella forsythia
3. Treponema denticola

**Organisms are present before breakdown

Front 15

15. What are some plaque microorganisms associated w/ progression of periodontitis?

Back 15

1. Gram-positive
-enterococcus faecalis
-S. aureus

2. Gram-negative
-enteric rods
-pseudomonads (intestinal bacteria)

3. Yeasts
-candida albicans

**contribute once lesion begins

Front 16

16. What is a periodontal superinfection?

Back 16

Emergence or overgrowth of microbial species in subgingival microbiota secondary to antimicrobial therapy which perpetuates periodontitis disease activity

Front 17

17. What is Socransky's criteria for periodontal pathogens?

Back 17

1. Organism must be assoc w/ disease

2. Organism must be eliminated or reduced at successfully treated site

3. Organism must produce a host response

Front 18

18. What is Socransky's criteria for periodontal pathogens?

Back 18

4. Organism must be capable of causing disease in experimental animal models

5. Organism must possess virulence factors which may account for tissue destruction

Front 19

19. What constitutes the Red Complex?

Back 19

1. Porphyromonas gingivalis

2. Tanneralla forsynthia

3. Treponema denticola

Front 20

20. What type of organisms is p. gingivalis?

What are the potential virulence factors of p. gingivalis?
(seven things)

Back 20

Gram-negative, non-motile anaerobic rod

1. Tissue invasive (epithelial cells)
*where it hides from host immune system

2. Collagenase enzyme production
3. Trypsin-like proteolytic enzyme
4. Fibrinolysin
5. Endotoxin
6. Hydrogen sulfide (cytotoxic bacteria)
7. Keratinase

Front 21

21. What type of organism is Teneralla forsythia?

What does is produce?

What does it have a high affinity for?

Back 21

Gram-negative, non-motile anaerobic rod

**originally identified as "fusiform bacteroides"

Trypsin-like proteolytic enzyme

Crevicular epithelium

**invades epithelial cell invasion

Front 22

22. What are the odds of detection T. forsythia in periodontitis patients vs age-matched controls?

How is it in obese persons?

Back 22

10.4 higher odds

Higher in obese persons w/ periodontal health/gingivitis

**may be reason in part that obese persons have 5.3 greater odds of exhibiting periodontitis

Front 23

23. What type of organism is Treponema denticola?

What type of enzyme activity does it have?

What does it have a strong associate with?

Back 23

Gram-negative anaerobic, spirochete (motile)

Trypsin-like proteolytic enzyme activity

Advance adult periodontitis and recurrent periodontitis

**tissue-invasion in necrotizing

Front 24

24. What are the microbial species associated w/ initiation of localized aggressive periodontitis (occurs in younger patients)?

Where is breakdown first seen?

What can detection of AA in periodontally healthy children serve as a risk marker for?

Back 24

AA
(aggregatibacter actinomycetemocmitans)

First molars and incisors

Initiation of localized aggressive periodontitis (LAP)

Front 25

25. What are the virulence factors of AA?

(A. actinomycetemcomitans)

Five things...

Back 25

1. Gingival tissue invasion

2. Cytolethal distending toxin
(upgrades apoptosis)

3. Collagenase enzyme

4. Endotoxin potent in bone resorption

5. Leukotoxin (JP2 clone)
*kills monocytes & neutrophils

Front 26

26. What is oral carriage of the AA JP2 clone in adolescens of west-African or north-African descend associated with?

What does the elimination of JP2 clone result in?

What are novel phylotypes?

Back 26

18x greater risk of periodontal attachment loss and LAP onset

Markedly reduced gingival inflammation

Organisms that we can't grow but know are there

Front 27

27. Using species-specific 16S rRNA and PCR amplification what species are more prevalent in periodontitis (prevalence ratio)?

Back 27

1. Treponema denticola (3.7)

2. Porphyromonas gingivalis (3.4)

3. Tanneralla forsythia (2.1)

Front 28

28. What does the Human Oral Microbe Identification Microarray (HOMIM) allow?

Back 28

Simultaneous detection of about 300 of the most prevalent oral bacterial species, including a number that cannot yet be grown in vitro

Sensitivity is about 0.1%

Limit of detection is about 10^4 cells

Front 29

29. What classic periodontal organisms are significantly more prevalent in "refractory" periodontitis?

Back 29

1. Red complex

2. Selenomonas noxia

3. Eubacterium nodatum

4. Prevotella species

5. Campylobacter species

**many classical periodontal pathogens and some "unusual" species were found post-treatment

Front 30

30. What is an important determinant in the clinical development of periodontitis "refractory" or "resistant" to various forms of periodontal therapy?

Back 30

Persistence of classical periodontal pathogens and "unusual" bacterial pathogens in the post-treatment subgingival microbiota

Front 31

31. What is more common in spouses of periodontitis subjects?
(two things)

Back 31

1. AA and P. gingivalis
2. Deeper probing depths

**followed 23 married couples for 7 yrs

**10 yrs of co-inhabitation did not influence periodontal condition of spouses

Front 32

32. What is type II filmA gene important for?

Back 32

Important factor in P. gingivalis spousal transmission

Front 33

33. How is poor supragingival plaque control associated w/ colonization by putative periodontal pathogenic bacteria?

Back 33

46.4 odds of P. gingivalis at site w/ plaque index score of 2-3

9.6 odds for AA

21.4 odds for P. intermedia

Front 34

34. How is deep probing depths associated w/ colonization by putative periodontal pathogenic bacteria?

Back 34

15.3 odds of P. gingavlis in > 5mm periodontal site vs. < 3mm site

Front 35

35. What microorganisms are more common in smokers?
(four)

What are the odds of P. micros and F. nucleatum in treated chronic periodontitis smokers?

Back 35

1. T. forsythia
2. P. micros
3. Fusobacterium nucleatum
4. Campylobacter rectus

13.8 odds

Front 36

36. What is more commonly found in smoking periodontitis patients post-treatment?
(four)

What does smoking do?
(two things)

Back 36

1. AA
2. P. intermedia
3. P. micros
4. F. nucleatm

1. Changes environment
2. Immunosuppressant

Front 37

37. What complex species are more common in smokers?

How is colonization of shallow sites in smokers?

Back 37

Red and orange complex species

Greater colonization of shallow sites (shallow site = < 4mm)

**shallower sites usually aren't conducive for colonization

Front 38

38. How is race associated w/ colonization by putative periodontal pathogenic bacteria?

Back 38

P. gingivalis is more common in chronic periodontitis in black (African-American) patients

**could be due to genetics

Front 39

39. How is geographic location associated w/ colonization by putative periodontal pathogenic bacteria?

Back 39

Mean proportions of P. gingivalis shows marked difference between USA, Sweden, Brazil and Chile

*even with adjusting for age, mean PD, gender, and smoking

**sanitization (water)

Front 40

40. What is the ecological plaque hypothesis?

Back 40

Certain dental plaque microorganisms are preferentially selected and increase as a result of changes in local oral environment which adversely alters normal protective microbial homeostatic mechanisms

Front 41

41. What viruses are associated with periodontitis?

Back 41

1. CMV (cytomegalovirus)
2. EBV - 1
3. Herpes simplex virus

**P. gingivalis and Dialister pneumosintes

Front 42

42. How do herpes viruses affect the immune system?

What the herpes virus do in regards to P. gingivalis and D. pneumosintes?

How is the interaction between EBV and P. gingivalis?

What does this mean?

Back 42

Immunosuppressive

May set stage for overgrowth

Bidirectional

1. EBV reactivation suppresses host defenses permiting overgrowth

2. P. gingavlis has potential to induce EBV reactivation

Front 43

43. How does P. gingivalis infection affect the protective anti-viral host response?

What are three periodontopathic properties of Herpes viruses that lead to destructive periodontal disease?

Back 43

It downgrades it or suppresses it

1. Cytokines/chemokines
-inflammation
-bone resorption
-collagen degradation

2. Immunosuppression
-overgrowth

3. Cytotoxicity
-tissue necrosis

Front 44

44. What is Slots "formula" for severe periodontitis?

Four things...

Back 44

1. Specific periodontal bacteria

2. Inadequate protective anti-bacterial antibody response

3. Activation of herpes virus in periodontium

4. Inadequate protective anti-viral T-cell response

**sufficiently long period of time to produce tissue destruction

Front 45

45. What is dental calculus?

Does it directly contact gingival tissue?

What type of factor is dental calculus?

What type of etiologic factor for periodontitis is dental calculus?

Back 45

Represents mineralized bacterial plaque covered by unmineralized viable bacterial plaque organisms

No

Prominent plaque-retentive factors

Secondary etiologic factor

Front 46

46. How does supragingival calculus affect dental plaque growth?

How does this occur?

What color is supragingival calculus?

What are the two most common locations?

Back 46

Enhances dental plaque growth

Organisms live on rough retentive outer surface and seed onto tooth surfaces

White color

1. Lingual of mandibular incisors
2. Buccal of maxillary molars

Front 47

47. What color is subgingival calculus?

How is it detected?

Where is it found?

Back 47

Usually dark in color

Must us tactile method of finding it (#11-12 explorer)
*cannot be visually detected

Found throughout dentition where plaque control is poor and gingival inflammation is present

Front 48

48. How is calculus detected using a #11 or #12 explorer?

Back 48

1. Use side of explores to explore interproximal surfaces for subgingival calculus

2. Wrap curve of instrument around tooth surface and hold handle parallel to long axis of tooth

3. Move explorer in up-down motion w/ light touch

Front 49

49. If it is a smooth surface what does that indicate?

If it is a rough surface what does that indicate?

Back 49

Smooth - no detectable calculus

Rough surface, ledge or catch - subgingival calculus

Front 50

50. Why doe dental calculus adhere tenaciously to tooth surface?

What do calculus crystals penetrate?

Back 50

Due to calcification of pellicle beneath dental plaque

**makes removal of subgingival calculus difficult

Tooth surface irregularities where small pits and irregularities occur at sites previously inserted by lost Sharpey's fibers

Front 51

51. How is dental calculus attachment to titanium dental implants?

What does this permit?

Back 51

Less intimate than to tooth root surfaces

Permits calculus to be chipped off of dental implants w/o adverse effects to the dental implant surface

Front 52

52. What are the four different crystals of calcium phosphate that dental calculus consists of?

Back 52

1. Brushite

2. Octa Ca phosphate

3. Hydroxyapatitie

4. Whitlockite
*prominent in subgingival calculus