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Periodontics I > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

What does the modern plaque hypothesis say about periodontopathic flora?

A

That it is necessary, but not sufficient for the disease. The periodontopathic flora is the etiology, but not the pathogenesis.

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2
Q

What are the five aspects of microbial plaque that are considered the etiology of periodontal disease?

A 
Bacteria
Fungus
Protozoa
Virus
Mycoplasm
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3
Q

Do high socioeconomic status people have higher or lower periodontal disease?

A

They have higher, they drink water through water bottles instead of fluoridated tap water.

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4
Q

How is dental calculus and dental plaque involved with periodontal disease?

A

Dental plaque is the etiologic factor, while dental calculus is like the coral reef and provides an environment for the bacteria to grow or for the biofilm to grow on it. There is both supragingival and subgingival calculus.

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5
Q

What are some of the basic biofilm properties?

A

Microorganisms are arranged in microcolonies with channels between the microcolonies
Microcolonies are surrounded by protective matrix (which affects antibiotics effectiveness)
Microbial gene expression differs when microorganisms are in a biofilm (Quorum sensing)
Microorganisms in biofilm are resistant to antibiotics,
antimicrobials, and host response

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6
Q

What is microbial co-aggregation?

A

This is when the bacteria releases enzymes that cleave off terminal carbohydrate ends and allow them to attach to bacterial receptors as early colonizers on the plaque, and then they can add on and attach to each other, as late colonizers. And remember, the deeper the organisms are and the closer they are to the tooth, the more anaerobic they will be.

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7
Q

Who modified Koch’s postulates for periodontics and came up with the chart?

A

Socranksy

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8
Q

Which two colors from the chart are associated with organisms involved in disease sites?

A

Orange and Red

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9
Q

What are the three organisms in the red group?

A
  1. Porphyromonas Gingivalis (- and nonmotile)
  2. Bacteroides Forsythus (- and nonmotile)
  3. Treponema Denticola (motile)
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10
Q

What are the four hypothesized biofilm resistance mechanisms?

A
  1. The antibiotic penetrates slowly or incompletely
  2. A concentration gradient of a metabolic substrate or product leads to zones of slow or non-growing bacteria.
  3. An adaptive stress response is expressed by some of the cells
  4. A small fraction of the cells differentiate into a highly protected persister state
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11
Q

What does the fluid gradient do in plaque biofilm?

A

It helps move nutrients around, including into and out of the environment, and helps allow for bacterial communication.

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12
Q

Why is the green group so important?

A

They are mostly Gram negative and they are highly involved with the disease progression.

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13
Q

For periodontal disease, what are the main things involved with the etiology, initiation, and progression?

A

Etiology: Microbial plaque
Initiation: Non-specific plaque accumulation
Progression: Gram negative bacteria and susceptible host

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14
Q

In terms of plaque distribution, where around the tooth is most of the subgingival plaque found?

A

Distal, then mid-buccal, then lingual. Posterior teeth are worse off than anterior. Any tooth brush , regardless of the brushing method, does not completely remove interdental plaque. Even for patients with wide-open dental embrasures.

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15
Q

There is a strong relationship between oral hygiene and gingivitis. True or False?

A

True

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16
Q

There is a strong relationship between oral hygiene and the risk for developing periodontitis. True or False?

A

False

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17
Q

All gingivitis progresses to periodontitis and all periodontitis is preceded by gingivitis. True or False for both?

A

False, True

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18
Q

What is the definition of a virulence factor?

A

It is a property that enables the bacterium to cause disease. It can be something that allows for attachment, creates inflammatory responses, protection, etc.

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19
Q

Fimbrea is a virulence factor, what is its MOA?

A

Bacterial attachment, prevention of phagocytosis

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20
Q

Capsule is a virulence factor, what is its MOA?

A

Protection, attachment, prevention of phagocytosis

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21
Q

Endotoxin is a virulence factor, what is its MOA?

A

Activation of inflammatory response, cytokine production, bone resorption

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22
Q

What does bacteria avoid by attaching to surfaces like enamel, cementum, plaque, connective tissue?

A

It avoids displacement by the gingival crevicular fluid flow. This ability to adhere is a virulence factor.

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23
Q

How does bacteria usually penetrate the host?

A

They enter the host tissues through ulcerations in the epithelium, the breakdown of the sulcular epithelium which is non-keratinized.

24
Q

What is the mathematical formula for periodontal disease?

A

Pathogenic flora + lack of beneficial bacteria + susceptible host = Periodontal disease

25
Q

What are some characteristics of someone who is a susceptible host?

A 
Impaired neutrophils
Inadequate immune response
LPS responsiveness
AIDS
Diabetes
Smoking
Drugs
26
Q

What is the virulence factor that bacteria uses to attach to the outer surface of a pellicle?

A

They attach via fimbriae on bacteria

27
Q

What is the pellicle and how long does it take to form after a cleaning?

A

It is a thin bacteria-free layer of salivary proteins that attach to the surface of a tooth within minutes of a cleaning.

28
Q

What are the two types of subgingival plaque and the two types of supragingival plaque?

A 
Subgingival
1. Coronal plaque
2. Marginal plaque
Supragingival
1. Attached plaque (Tooth, epithelium, CT)
2. Unattached plaque
29
Q

What are the five main steps of plaque formation?

A
  1. Pellicle formation
  2. Attachment of bacteria (via fimbriae)
  3. Young supra-gingival plaque: mainly gram+ cocci and rods, some gram- cocci and rods
  4. Aged supra-gingival plaque: an increase in gram- anaerobic bacteria
  5. Sub-gingival plaque formation: Tooth-attached plaque and unattached epithelial plaque.
30
Q

What are the characteristics of unattached sub-gingival plaque?

A

The zone of sub-g plaque not directly attached to the tooth surface. Mostly consists of gram-negative, motile bacteria and resides between the outer position of the attached plaque and sulcular epithelium. In direct contact with both the junctional and sulcular epithelium.

31
Q

What are the main 5 differences between supra and subgingival plaque?

A
  1. Matrix - Supra is 50% matrix and Sub has little or no matrix
  2. Flora - Supra is mostly gram+ and Sub is mostly gram-
  3. Motile bacteria- Supra has few and Sub has many
  4. Anaerobic/aerobic - Supra is aerobic unless thick and Sub has high anaerobic areas
  5. Metabolism - Supra is mainly carbs and Sub is mainly proteins
32
Q

With attached subgingival plaque, what are the main characteristics between tooth associated and epithelium associated?

A
  1. Tooth-associated is mainly Gram+, does not extend to junctional epithelium, it may penetrate cementum, and is associated with calculus formation and root caries.
  2. Epithelium-associated is both gram+ and gram-, extends to junctional epithelium, it may penetrate epithelium and connective tissue, and is associated with gingivitis and periodontitis.
33
Q

What are the three bacteria that have a very strong association with periodontal disease?

A
  1. A.a., or Actinobacilus Actinomyce…
  2. P. gingivalis, or Porphyromonas Gingivalis
  3. T. forsythia, or Tanneralis Forsythia
34
Q

In chronic gingivitis, are there more Gram+ or Gram- bacteria found?

A

Gram+, 56% versus 44% Gram-

35
Q

Bacteria associated with pregnancy-associated gingivitis:

A

P. Intermedia

36
Q

Bacteria associated with adult necrotizing ulcerative gingivitis:

A

Spirochetes

P. Intermedia

37
Q

Bacteria associated with adult periodontitis: (these main ones are associated with any type of periodontitis really)

A 
P. Gingivalis
T. Forsythia
P. Intermedia
C. Rectus
A. Actinomyces
P. Micros
38
Q

Bacteria associated with localized juvenile periodontitis:

A

E. corrodens
E. bracy
Captocynophega
Herpes Virus

39
Q

Bacteria associated with generalized juvenile periodontitis:

A

E. corrodens
Captocynophega
Neisseria

40
Q

Bacteria associated with refractory periodontitis:

A

Wolinella recta

41
Q

Bacteria associated with abcesses of the periodontium:

A

P. Micros

F. Nucleatum

42
Q

Bacteria associated with HIV-associated gingivitis:

A 
Canida albicans
P. gingivalis
P. intermedia
F. nucleatum
A. a
C. recta
43
Q

What is the name of the rare bacterium that is gram- and a facultative anaerobe, and what are other characteristics about it?

A

A. a - Aggregatibacter Actinomycetemmcotans
Small, non-motile, gram negative, facultative anaerobe, saccharolytic, coccobacillus, small convex colonies with a star-shaped center, increased frequency in aggressive cases.
Prevalence near 90% in localized adolescent periodontitis (LAP). Prevalence near 30-50% in adult periodontitis.
Many serotypes, B is most common with LAP.
Has the ability to invade host epithelial cells, it releases a good amount of exotoxins: extracellular substances produced by bacteria which are toxic to certain cells and tissues of the body, botulinum, tetanus, leukotoxins. Leukotoxin produced by A.a. is thought to kill PMNs and monocytes from blood and PMNs from the pocket.

44
Q

What are the characteristics of LPS, the endotoxin?

A

Lipopolysaccharide is is a virulence factor associated with many gram-negative bugs.
• Unlike exotoxins, LPS is an integral part of the outer membrane. Once released, the cell can exert a variety of activities that promote tissue damage.
LPS is only released once the bacteria dies, whereas exotoxins are released while the bacteria is alive and is continuous. Most bacteria die very rapidly and only live from minutes to hours
- So bacteria is always dying and always growing

45
Q

What are the three factors that stimulate LPS release?

A
  1. Cytotoxic effects
  2. Complement activation
  3. Bone resorption (direct or indirect)
46
Q

Characteristics of P. Gingivalis:

A 
Porphyromonas Gingivalis
•  Gram-negative
•  anaerobic
•  non-motile
•  asaccharolytic
•  rod shaped (bacillus)
•  black pigmented Bacteroides
47
Q

Characteristics of T. Forsythia:

A 
Tannerella Forsythia
•  Gram negative
•  anaerobic
•  Spindle-shaped
•  Pleomorphic
•  Growth shown to be enhanced by co- cultivation with F. Nucleatum
•  Formerly known as Bacteroides forsythus and Tanerella forsythensus
•  ***invades epithelial cells***
48
Q

Characteristics of P. Intermedia:

A

Prevotella Intermedia

• Black pigmented Bacteroides

49
Q

Characteristics of F. Nucleatum:

A 
Fusobacterium Nucleatum
•  Gram negative
•  Anaerobic
•  Spindle shaped rod
•  Most common isolate from sub-gingival samples!!!!!!!
50
Q

Characteristics of C. Rectus:

A 
Campylobacter Rectus
•  Gram negative
•  Anaerobic
•  Short, motile vibrio
•  Forms small convex spreading
51
Q

Characteristics of P. Micros:

A 
Peptostreptococcus Micros
•  Gram positive (this is the only perio pathogen discussed today that is gram positive!!!!!!!!)
•  Anaerobic
•  small coccus
•  Asaccharolytic
52
Q

Characteristics of Spirochetes:

A

• Gram negative
• anaerobic
• Helical shaped • related to NUG (ANUG)


53
Q

What measurements establish an active site in terms of pathogenesis?

A

A site shows attachment loss greater than 2-2.5mm in 2 months.

54
Q

From health to periodontitis. Histo + Clinical of Initial Lesion (2-4 days)

A

Histo - Classic vasculitis of vessels subjacent to the junctional epithelium (j.e.)
Exudation of fluid from the gingival sulcus
Increased migration of leukocytes into the j.e. and gingival sulcus
Presence of serum proteins, especially fibrin, extra vascularly
Alteration of the most coronal portion of the j.e.
Loss of perivascular collagen
Clinical - Appears clinically healthy
No periodontal pocket
No radiographic evidence of bone loss

55
Q

From health to periodontitis. Histo + Clinical of Early Lesion (4-7 days)

A

Histo - Accentuation of features of the initial lesion
Accumulation of lymphoid cells subjacent to j.e.
Cytopathic alterations of fibroblasts
Further loss of collagen fiber network of the marginal gingiva
Beginning proliferation of basal cells of j.e.
Clinical - Gingivitis (acute form)
changes in gingival color, contour, consistency and BOP
no periodontal pocket
no radiographic bone loss

56
Q

From health to periodontitis. Histo + Clinical of Established Lesion (2-3 weeks)

A

Histo - Persistence of the manifestations of acute inflammation
Predominance of plasma cells without appreciable bone loss
Presence of immunoglobulins extravascularly in the c.t. and j.e.
Continuing loss of connective tissue noted in the early lesion
Proliferation, apical migration and lateral extension of j.e.
early pocket formation may or may not be present
Clinical - Gingivitis (chronic form)
changes in gingival color, contour, consistency an BOP
no periodontal pocket
no radiographic bone loss

57
Q

From health to periodontitis. Histo + Clinical of Advanced Lesion (>3 weeks)

A

Histo - Persistence of features described for the established lesion
Extension into alveolar bone and PDL with significant bone loss
Continued loss of collagen subjacent to the pocket epithelium
Cytopathically altered plasma cells
Formation of periodontal pockets
Periods of quiescence and exacerbation
Conversion of distant bone
m arrow into fibrous connective tissue
W idespread m anifestations of inflam m atory/im m unopathologic reactions
Clinical - Periodontitis
Changes in gingival color, contour, consistency and bleeding on probing
Periodontal pocket
form ation
Alveolar bone loss as shown on radiographs

Periodontics I (7 decks)

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