microbiology of periodontal disease 1 Flashcards

1
Q

which Intraoral Surfaces represent ecosystems with distinct ecologic determinants?

A
  1. Supragingival surfaces
  2. Subgingival surfaces
  3. Epithelial surfaces
  4. Dorsum of the tongue
  5. Tonsils
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2
Q

what is dental plaque?

A

Dental plaque is primarily composed of bacteria in a matrix of salivary glycoproteins and extracellular polysaccharides

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3
Q

what is the progression of changes in biofilm?

A

bacteria at the gingival margin, epithelial cells and a few cocci (well cleaned mouth) –> then masses of cocci and short rods (no cleaning for 1 - 2 days) –> then filamentous, leukocyte, fusobacteria (no cleaning for 4 - 7 days) –> then vibrios and spirochetes (no cleaning for 1 - 2 weeks)

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4
Q

what is the progression of changes in biofilm?

A

bacteria at the gingival margin, epithelial cells and a few cocci (well cleaned mouth) –> then masses of cocci and short rods (no cleaning for 1 - 2 days) –> then filamentous, leukocyte, fusobacteria (no cleaning for 4 - 7 days) –> then vibrios and spirochetes (no cleaning for 1 - 2 weeks)

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5
Q

what did the experimental gingivitis in man by Loe H, Theilade E and Jensen SB. J Periodontol 1965;36:177-187
reveal?

A

Dental plaque is the main etiological factor causing periodontitis.

It was to attempt to produce gingivitis in patients with healthy gingiva by withdrawing all active efforts directed towards oral cleanliness, and to study the sequence of changes in the microbial flora and in the gingiva thus produced.

12 healthy individuals (10 male, 2 female)
Mean age = 23 y.o.
Gingival index (0-3)
Plaque index
Periodontal index
Bacteriological examinations

After examination subjects were instructed not to perform any plaque control
As soon as inflammatory changes were observed, the patients reinstituted plaque control
Plaque and gingival indexes assessed

Results

Three subjects developed gingivitis in 10 days
Nine subjects developed gingivitis in 15-20 days
Gingival inflammation resolved in 7-10 days after proper plaque control was reinstituted

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6
Q

what were the bacteriological results for the experimental gingivits in man?

A

pellicle –> early colonizers (S. oralis, s. mitis, s. giordonii, s. sanguinis then p. acnes etc.) –> bridging (fusobacterium nucleatum) –> late colonizers (A. actinomycetemcomitans, Eubacterium spp., P. gingivalis, P. intermedia, etc.) –> gingivits established and they all communicate with one another and are attached.

Then when you use plaque control again by brushing and maintaining good habits, you get bacterial reversion where they unattach from one another and go down layer by layer until you get to the pellicle again.

conclusions

Study demonstrated a cause and effect relationship
Gingivitis is a reversible disease process
Bacterial colonization sequence and composition

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7
Q

what are the elements of treatment for plaque-induced gingivitis?

A

individualized plaque control instructions
anti-plaque/anti-gingivitis dentrifice or rinse if necessary
professional removal of supra- and subgingival calculus
correction of defective restorations
restorations of carious lesions
re-evaluation at 4 to 6 weeks

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8
Q

what is specific plaque hypothesis?

A

Early on they thought that all bacteria in the mouth was bad and pathogenic. That was wrong and so they found this out.

Experimental transmission of periodontal disease in animals
New methods of microbial analysis

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9
Q

what are the periodontal pathogens?

A
Aggregatibacter actinomycetemcomitans
Porphyromonas gingivalis
Bacteroides forsythus (Tannerella forsythensis)
Spirochetes
Prevotella intermedia
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10
Q

how is plaque as a biofilm?

A

Organized structure
Microcolonies of bacterial cells non-randomly distributed in a shaped matrix
In the lower plaque layers, bacteria are bound together in a polysaccharide matrix with other organic and inorganic materials
Open fluid-filled channels running through the plaque mass

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11
Q

what is the effect of an antiseptic mouthrinse on a mature plaque biofilm?

A

In the well structured form, toothpaste and mouthwash will not penetrate into the mature biofilm. Maybe the initial layers of biofilm but not in the mature biofilm.

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12
Q

what are the five proposed mechanisms of increased biofilm tolerance to antimicrobials?

A

slow penetration, stress response, altered microenvironment, persisters

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13
Q

what is subgingival plaque biofilm like?

A

you have to have supragingival plaque before subgingival, then it starts to go down and you get PMNs

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14
Q

what is subgingival plaque biofilm like?

A

you have to have supragingival plaque before subgingival, then it starts to go down and you get PMNs

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15
Q

MAYBE TALK TO DR. OTERO TO SEE WHAT WE NEED TO LEARN FROM THE MICROBIAL COMPLEXES IN SUBGINGIVAL BIOFILM SLIDE

A

AL;SDJFALSD

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16
Q

What are bacterial virulence factors?

A

Ability to invade tissues
LPS: tissue destruction
exotoxins: destruction of leukocytes
enzymes: assist in tissue invasion

17
Q

What are bacterial virulence factors?

A

Ability to invade tissues
LPS: tissue destruction
exotoxins: destruction of leukocytes
enzymes: assist in tissue invasion