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Periodontics > Lecture 4 > Flashcards

Lecture 4 Flashcards

Bacteria and Oral Biofilms

1
Q

bacterial infections

A

gingivitis and periodontitis

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2
Q

bacteria

A

replicate/adapt quickly to environmental changes
tough cell membrane
gram + or gram -

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3
Q

gram + periodontal microorganisms

A

facultative cocci: streptococcus sanguis, streptococcus mitis, streptococcus salivarius
facultative rods: actinomyces viscosus
obligate rods: eubacterium lentum

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4
Q

gram - periodontal microorganisms

A

facultative rods: aggregatibacter actinomycetemcomitans
obligate anaerobic rods and cocci: P. Gingivalis, P. Iintermedia, V. Alcalescens
anaerobic spirochetes: treponema denticola

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5
Q

intercellular matrix of dental plaque

A

organic: polysaccharides, proteins, glycoproteins, lipid material and DNA

inorganic materials: calcium and phosphorus with sodium, potassium and fluoride

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6
Q

supragingival dental plaque

A

gram positive cocci and rods
nutrients from saliva and diet

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7
Q

subgingival dental plaque

A

gram -, anaerobic, motile rods and spirochetes
nutrients from GCF and blood

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8
Q

subgingival bacterial attachment zones

A

tooth-associated: adhere to the tooth surface
tissue associated: adhere to the epithelium
free floating: unattached, not part of the biofilm

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9
Q

tooth associated plaque

A

densely packed and strongly adherent to the tooth surface
gram + rods, cocci and filamentous bacteria
facultative aerobic or facultative anaerobes

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10
Q

tissue associated plaque

A

loosely packed, loosely adherent to soft tissue wall
gram -, motile, anaerobic spirochetes
bacteria can invade the gingival CT and be found within the deeper perio tissues

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11
Q

unattached bacteria

A

free swimming in pocket
gram -, motile, anaerobic
spirochetes and others

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12
Q

what is the source of inorganic components of supragingival plaque

A

saliva

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13
Q

calculus is frequently found in areas of the dentition adjacent to

A

salivary ducts

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14
Q

the inorganic components of subgingival plaque are derived from

A

crevicular fluid

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15
Q

materia alba

A

white cheeselike accumulation
salivary proteins, bacteria, desquamated epithelial cells
lacks structure
displace with water

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16
Q

dental plaque

A

clear to yellow-grayish substance
bacteria in a matrix of salivary glycoproteins and extracellular polysaccharides
a biofilm
impossible to remove by rinsing or water

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17
Q

calculus

A

hard deposit that forms via the mineralization of dental plaque
covered by a layer of unmineralized dental plaque
impossible to remove by rinsing or water

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18
Q

plaque biofilms

A

a matrix enclosed bacterial population adherent to each other and/or to surfaces or interfaces
structurally organized

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19
Q

life cycle of a biofilm

A

attachment: bacteria attach to a surface
growth: attract other bacteria, rapid multiplication, ECM for protection and maintain attachment
detachment: clumps break free to attach to new surfaces

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20
Q

phase 1

A

initial attachment
acquired pellicle formation
protein film forms within minutes after cleaning tooth surface
derived from salivary glycoproteins, antibodies, GCF
protect enamel from acid
gram + facultative bacteria

21
Q

phase 2

A

irreversible attachment
additional bacteria colonization
coaggregation, gram negative colonizers adhere to bacteria
attract other free-floating bacteria

22
Q

phase 3

A

maturation
formation of extracellular protective matrix
bacterial secretion
provides anchorage and protection for the attached bacteria from antimicrobials, antibiotics and immune system

23
Q

phase 4

A

maturation phase II
bacteria microcolonies form mature biofilm
complex collection of different bacteria
increased numbers of gram neg/anaerobic bacteria

24
Q

phase 5

A

dispersion
microbes disperse from the biofilm colony allowing biofilms to spread to new tooth surfaces

25
Q

dental plaque - colonization

A

different bacteria species join the biofilm in a particular sequence
-early colonizers: nonpathogenic/gram +
-intermediated colonizers: specific cell-cell adhesion
-late colonizers: gram - bacteria join biofilm

26
Q

why is physical/mechanical disruption so important for individuals with periodontitis

A

adequate disruption causes the entire process of bacterial succession to begin again
the cleaner the tooth surface, the less complex the bacterial formation

27
Q

dental plaque biofilm development always begins _____ and progresses _______

A

supragingivally and progresses subgingivally

28
Q

the clinical signs of inflammation may appear within

A

4-14 days

29
Q

non-specific plaque hypothesis

A

accumulation of bacterial biofilms lead to periodontal destruction

30
Q

specific plaque hypothesis

A

specific pathogenic bacteria lead to periodontal destruction

31
Q

host response hypothesis

A

it is the host’s inflammatory and immune response, not the type of bacteria, which determines if periodontal destruction progresses

32
Q

contemporary perspectives

A

despite plaque biofilm causing the initial inflammatory response, it is not sufficient for periodontal destruction to occur
it is the host inflammatory and immunes responses that determine whether gingivitis progresses to periodontitis

33
Q

virulence factors

A

endotoxins
microbial invasion
enzyme production

34
Q

endotoxins

A

in gram negative bacteria cell membranes are released when bacteria die or break apart
initiates inflammation
can kill pmns

35
Q

microbial invasion

A

ability to penetrate tissue to avoid host defense cells

36
Q

enzyme production

A

break down collagen and host proteins (basic structure of periodontium)

37
Q

bacteria synthesize and release… and these do what

A

toxic by products (ammonia, hydrogen sulfide)
these increase the permeability of epithelium/toxic to cells and tissues

38
Q

biochemical mediator in periodontitis include

A

cytokines
chemokines
prostoglandins
metalloproteinases

39
Q

cytokines

A

initiate tissue destruction and bone loss

40
Q

chemokines

A

attract additional immune cells

41
Q

prostoglandins

A

cause bone destruction

42
Q

metalloproteinases

A

cause collagen destruction of periodontal tissues

43
Q

proteins, lipids, enzymes released by leukocytes activate

A

inflammatory response
attracts additional immune cells and increase vascular permeability
contributes to tissue destruction

44
Q

4 histologic stages in development of periodontal disease

A
  1. initial lesion: healthy but mild inflammation
  2. early lesion: acute inflammation/gingivitis
  3. establish lesion: chronic gingivitis
  4. advanced lesion: transition to periodontitis
45
Q

initial lesion

A

corresponds with clinically healthy gingival tissues/mild inflammation
develops 2-4 days after supragingival plaque accumulation
gram neg bacteria initiates immune response
pmns pass from blood vessels to CT into sulcus, cytokines destroy healthy tissue
tissue destruction easily repaired after infection fought
lesion is not seen clinically and is reversible with adequate OH

46
Q

early lesion

A

corresponds with acute gingivitis, evident clinically
biofilm maturation continues 4-14 days
bacterial toxins penetrate junctional epithelium
JE cells release cytokines attracting larger # of PMNs
cytokines cause localized destruction of connective tissue
macrophages are recruited to the connective tissue (release biochemical mediators which recruit additional immune cells)
epithelial ridges appear in sulcular epithelium and adjacent CT
this lesion is reversible with adequate OH

47
Q

established lesion

A

corresponds with chronic gingivitis
within 2-3 weeks of plaque accumulation
coronal portion of JE detaches from tooth surface
macrophages and lymphocytes are most numerous in tissue, PMNs most numerous in sulcus
lymphocytes produce large numbers of antibodies
macrophages produce cytokines with initiate collagen destruction
epithelial ridges extends deeper into the connective tissue
lesion is still reversible
periodontal instrumentation and patient education are helpful

48
Q

advance lesion

A

transition from gingivitis to periodontitis
state of chronic inflammation
immune response is so strong it begins to harm the periodontium
biochemical mediators produced by PMNs/macrophages destroy CT and PDL fibers
apical migration of the JE occurs (periodontal pocket forms)
clinically- BOP, alveolar bone loss, furcation involvement, mobility
tissue destruction is not reversible

Periodontics (11 decks)

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