09/03 - Periodontal Microbiology Flashcards

1
Q

How were studies on plaque formation conducted?

A
  • adhesive tape samples from the tooth surface
  • plaque grown on epoxy resin crowns worn for different time periods
  • in vitro studies of attachment and aggregation between different bacterial species
  • experimental gingivitis models
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2
Q

Early studies of oral microbiology were based on: ___ and ___.

A

cultivation and microscopy

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3
Q

What is the great plate anomaly?

A

when you look under a microscope, you see 100 species, but on a plate, only 50 grows; not everything you see will grow

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4
Q

What is the “we know what we can grow” bias?

A

all studies focused on cultivable species, but there are so many more species in the mouth

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5
Q

What approaches to study oral microbiolgy revolutionized species identification?

A

molecular (DNA, RNA) approaches

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6
Q

How many distinct oral species are there? What % have never been cultured?

A
  • more than 700 distinct oral species
  • +60% never have been cultured
  • includes exotics (ex. Archea) like termite guts and other extreme environments
  • fungi and viruses may also play a role in disease
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7
Q

What is the definition of a plaque biofilm?

A

organized cooperating community of organisms with specific inter-bacterial and host-bacterial interactions

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8
Q

What is atopic dermatitis?

A

“Purell disease”; children who are not exposed to bacteria when they are young begin making autoantibodies; 1st world problem (seriously!)

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9
Q

In the attachment stage of biofilm formation, planktonic bacteria adhere to ___ which is made up of ___ and ___. There is an alteration in ___ and ___.

A
  • acquired pellicle
  • salivary glycoproteins
  • antibodies
  • surface charge
  • free energy
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10
Q

What is the difference between rapid attachers and slow attachers?

A
  • rapid attachers: specific attachment structures (fimbrae, extracellular polymers, glycocalyx)
  • no specific mechanism
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11
Q

How do bacterial characteristics change following attachment?

A
  • synthesis of new outer membrane proteins

- active cellular growth

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12
Q

What is the difference between co-aggregation and co-adhesion during the growth phase of biofilm formation?

A
  • co-aggregation: cell-to-cell recognition of genetically distinct cell types; mediatedby protein or glycoprotein receptors on one cell and carbohydrates on the other; all cells are suspended; “clumps” form which then attach to the pellicle
  • co-adhesion: interactions between suspended and already adhering microorganisms; influenced by temperature and lactose
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13
Q

What two factors affect co-adhesion?

A
  • temperature: no co-adhesion at higher than 37 degrees

- lactose: inc lactose, dec co-adhesion

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14
Q

What 3 things occur during biofilm maturation?

A
  • increase in diversity
  • replication and matrix formation
  • ecological succession
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15
Q

What are the 3 categories of bacteria in ecological succession?

A
  • tertiary colonizers: gram negative
  • secondary colonizers: bridge species
  • primary colonizers: gram positive and some negative
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16
Q

Which bacterial colonizers are usually beneficial? Which are usually pathogenic?

A
  • beneficial: primary colonizers

- pathogenic: tertiary colonizers

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17
Q

Name examples of tertiary, secondary, and primary colonizers.

A
  • tertiary: Porphyromonas gingivalis, A. actinomycetemcomitans
  • secondary: F. nucleatum
  • primary: S. sanguis
18
Q

S. sanguis is found in large numbers in deep, active periodontal pockets. Through scaling and root planing of a deep periodontal pocket will most likely result in increased numbers of A. actinomycetemcomitans.

State whether each statement is true or false.

A

both are false

19
Q

When a biofilm increases in thickness, what changes?

A
  • difficulty in diffusion in and out of the biofilm
  • an oxygen gradient develops
  • completely anaerobic (no oxygen) conditions emerge in the deeper layers
  • reverse gradients of fermentation products develop as a result of bacterial metabolism
20
Q

How does the nutrition in the biofilm differ between the supragingival plaque and subgingival plaque?

A
  • supragingival plaque: dietary products dissolved in saliva
  • subgingival plaque: periodontal tissues and blood (“clavicular fluid”); bacterial hydrolytic enzymes breakdown host macromolecules into peptides and amino acids
21
Q

What makes up 15-20% of a biofilm? What makes up the remaining biofilm?

A
  • microcolonies (15-20%)

- interbacterial matrix

22
Q

What are the 3 sources of the biofilm matrix?

A
  • dead bacterial cells
  • saliva
  • gingival exudate
23
Q

Are there voids/water channels in a bacterial biofilm? What makes up the backbone of the biofilm?

A
  • yes

- exopolysaccharides

24
Q

Compare the lower layer, loose layer, and fluid layer of the biofilm.

A
  • lower layer: dense microbes, polysaccharide matrix, tightly bound together, steep diffusion gradients
  • loose layer: irregular in appearance, extends into surrounding media
  • fluid layer: stationary sublayer, fluid layer in motion, nourishes the biofilm by molecular diffusion
25
Q

Do shear forces determine the colony shape in supra or subgingival plaque? What do colonies with low shear force look like? With high shear force?

A
  • supragingival plaque
  • low shear force: towers or mushrooms
  • high shear force: elongated colonies capable of oscillation (like seaweed)
26
Q

Describe the difference between a gram-positive matrix and gram-negative matrix.

A
  • gram-positive: very fibrillar, due to dextrans and levans
  • gram-negative: very regular; contains tri-laminar vesicles; filled with endotoxins and proteolytic enzymes; probably involved in adherence
27
Q

Describe the structure of subgingival plaque.

A
  • cuticle forms primary attachment
  • structure similar to supragingival plaque
  • bacterial layers near sulcular epithelium different from tooth-attached (no inter-bacterial matrix, more spirochetes and flagellated bacteria)
28
Q

What are the 3 bacteria mentioned as an example of bacterial collaboration? How do they collaborate?

A
  • Streptococcus cristatus: 1st colonizer; facultative species (can live with or without O2); uses up O2 when available
  • Fusobacterium nucleatum: 2nd colonizer; robust anaeriobe; binding to Strep improves survival when O2 is present
  • Porphyromonas gingivalis: 3rd colonizer; microaerophilic, obligate anaerobe; coagregation essential to survival when O2 is present
29
Q

How did F. nucleatum and S. cristatus interact during the tissue culture experiment?

A
  • F. nucleatum invades epithelial cells
  • S. cristatus does not invade cells
  • after coaggregation, S. cristatus is carried inside by F. nucleatum
30
Q

What are the advantages to biofilm living?

A
  • DEFENSE: presence of concentrated bacterial enzymes; inter-bacterial matrix
  • PROTECTION FROM EXTERNAL CHANGES: diffusion minimal in interior regions; antibiotic and antimicrobial resistance; protection from friction and shearing forces; attachment
  • TRANSFER OF INFORMATION AND GENETIC MATERIAL: signaling (quorum sensing); conjugation; transformation; plasmid transfer; trasposon transfer
31
Q

What is the definition of quorum sensing?

A

regulation of expression of specific genes through accumulation of signaling compounds that mediate intercellular communication

32
Q

Describe the process of quorum sensing between commensal and pathogenic bacteria.

A
  • auto-inducer (AI) 1 or 2 turns on in response to cell density
  • commensal bacteria produce and respond to low levels of AI-2
  • pathogens produce AI-2 in high levels
  • Al-2 may determine the switch from commensal to pathogenic community
33
Q

What are the 3 reasons why biofilm bacteria are more resistant to antibiotics?

A
  • BIOFILM BACTERIA GROW MORE SLOWLY (antibiotics depend on cell turnover for efficacy; slow-growers express “non-specific defense mechanisms”; slow growers make more exo-polymers)
  • EXO-POLYMERS RETARD DIFFUSION (ion-exchange mechanism prevents highly charged molecules from reaching deeper zones; extracellular enzymes inactivate antibiotics)
  • BIOFILM BACTERIA EXPRESS DIFFERENT GENES (gene transfer; phenotypic expression of biofilm existence)
34
Q

Why don’t oral pathogens fit the usual model of a pathogen?

A
  • oral pathogens are normally present throughout life

- damage requires presence in large numbers

35
Q

The ecological concept of oral microbial diseases states…

A
  • ecological shifts lead to changes in proportions
  • balance shifts in favor of “pathogens”/disease
  • periodontal disease is an example of “ecological catastrophe”
36
Q

Which of the following is NOT a reason why growth of a microbe is different in nature compared to pure culture?

a. limited nutrients in natural environment
b. poor nutrient distribution in natural environments
c. not optimal temperature in natural environments
d. lack of competition in natural environments

A

d. lack of competition in natural environments

37
Q

What is the clinical significance (3) of biofilm formation?

A
  • tooth-brushing has an effect on where the biofilm is located (interproximal, fissures, etc.) and non-contact brushing can remove towers and mushrooms by shear forces
  • antibiotic resistance
  • translocation and transmission of bacteria
38
Q

What are the 2 targets of therapy in the prevention of biofilms?

A
  • AI-2

- vaccines that target common resistance genes

39
Q

What are the different ways bacteria can translocate in the mouth?

A
  • periodontal probe can translocate pathogens from pockets to healthy sites
  • drug-resistant strains can translocate to neighboring teeth
  • teeth act as reservoirs for colonization of implants
  • bacteria can infect membranes in GTR
40
Q

What is Leuven’s “one-stage full-mouth disinfection”?

A
  • full-mouth scaling and root-planing within 24 hours
  • subgingival irrigation with 1% chlorhexedine
  • tongue brushing
  • oral antimicrobial rinse
41
Q

True or false: Plaque cannot form on implant abutments.

A

FALSE; plaque can form on implant abutments

42
Q

Implants that fail have a microbial composition similar to ___.

A

periodontal disease