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perio exam 2 > microbial etiology of perio disease > Flashcards

microbial etiology of perio disease Flashcards

1
Q

what’s the etiology of perio disease?

A

a complex interaction between bacterial plaque and host response, modified by local anatomic factors of both natural and iatrogenic origin and by systemic factors

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2
Q

path of periodontitis

A

plaque (anatomical, iatrogenic, behavioral) + host response (smoking, systemic disease, genetics)=inflammation, connective tissue loss+ bone loss

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3
Q

non-specific plaque hypothesis

A

quantity or biomass of dental plaque

basis of conventional therapy–oral hygiene, mechanical removal of deposits by scaling and surgery

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4
Q

specific plaque hypothesis

A

association of specific bacteria with perio disease

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5
Q

dental plaque

A

soft deposits that form the biofilm adhering to the tooth and other oral surfaces

  • supragingival
  • subgingival
  • composed predominantly of microorganisms
  • intercellular matrix=0-25% of plaque mass subgingival, much more (80%) supragingival
  • clinically cannot remove by water spray
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6
Q

formation of biofilm

A

starts clean/just in saliva

  1. molecular adsorption
  2. single organisms
  3. multiplication
  4. sequential adsorption of organisms
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7
Q

dental pellicle formation

A
  • phase 1 of biofilm formation
  • forms within minutes by selective adsorption
  • glycoprotein (mucins) and antibodies
  • origin: supragingival–saliva and subgingival–crevicular fluid
  • coats enamel and other oral surfaces
  • functions to prevent desiccation, lubrication
  • provides substrate for bacterial colonization
  • forms within minutes
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8
Q

what does dental pellicle contain?

A
  • substrate for bacterial attachment
  • fimbriae (adhesive)
  • antibodies
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9
Q

initial bacterial colonization contains?

A

facultatively anaerobic G+ cocci and rods

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10
Q

secondary colonization & plaque maturation

A

takes days
co-aggregation
G - bacteria attach to pre-existing G+ bacteria

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11
Q

initial colonizer

A

streptococcus sanguis
24 hour plaque
some actinomyces

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12
Q

second phase colonizer

A

actinomyces viscosus dominates

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13
Q

third phase contents

A

G - bacteria attach to G +

  • prevotella intermedia
  • fusobacterium nucleatum
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14
Q

fourth phase contains

A
  • increased heterogeneity and pathogenicity
  • prevotella intermedia
  • capnocytophaga species
  • fusobacterium nucleatum
  • **porphyromonas gingivalis
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15
Q

what is the developing plaque ecosystem influenced by?

A
  1. bacterial interactions:
    - attachment/adherence
    - exchange of nutrients
    - bacteriocins
  2. substrate characteristics
    - smooth surface vs pit and fissure
    - supra-gingival vs sub-gingival
  3. bacteria–host interactions
    - inflammation: blood and gingival crevicular fluid
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16
Q

layers of dental plaque

A

lower layer: dense microbes and matrix
loose intermediate layer
fluid superficial layer

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17
Q

how do nutrients penetrate plaque?

A

by molecular diffusion

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18
Q

how does the bacteria get O2

A

steep diffusion gradients

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19
Q

bacteria in deeper layers are protected from what?

A

antimicrobial agents

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20
Q

whats the advantage of biofilm formation vs planktonic growth?

A
  • protects from competing organisms, host defense, and toxic environmental agents (antibiotics)
  • processing and uptake of nutrients
  • development of appropriate physico-chemical environment (pH, oxidation-reduction potential)
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21
Q

attachment of bacteria in biofilms

A
  • fimbriae (actinomyces, strep, Pg)

- fibrils (strep, Pi)

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22
Q

structure of biofilms

A
  • 20% bacteria and 80% matrix
  • bacteria not randomly distributed
  • water channels for passage of nutrients
  • matrix=water + exopolysaccharides
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23
Q

what does the biofilm matrix do?

A
  • maintains integrity of biofilm
  • prevents dessication
  • binds nutrients
  • buffers
  • reservoir of extracellular enzymes
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24
Q

physiological heterogeneity of biofilms

A
  • bacteria in different physiological states in different locations within the biofilm
  • increase respiratory activity and protein synthesis in outer layer of biofilm
  • pH varies between microcolonies in biofilm
  • bacteria in biofilms produce beta-lactamase, catalase, superoxide dismutase, elastase, cellulase
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25
Q

quorum sensing

A
  • dependent on cell density
  • involves regulation and expression of specific genes thru accumulation of signaling compounds
  • signaling compounds detected for Pg, Pi, and Fn
  • way the bacteria communicate
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26
Q

bacteria grown in biofilms are more resistant to what compared to plantonic suspension?

A

biofilm bacteria are more resistant to antibiotics

27
Q

structure of supra-gingival dental plaque

A
  • acquired pellicle
  • G+ cocci bacteria
  • G+ rods
  • matrix–derived from microorganisms, saliva, and ging crevicular fluid; proteins and carbs like fructans/levans, glucans/dextrans, from dietary sucrose
28
Q

structure of sub-gingival dental plaque

A
  • cuticle–electron-dense layer, epithelial origin
  • pellicle
  • G+ cocci and G+ rods
  • loosely-adherent superficial layer–spirochetes, motile bacteria
  • no intermicrobial matrix
29
Q

calculus

A

hard deposit that forms by mineralization of dental plaque and is generally covered by a layer of non-mineralized plaque

30
Q

calculus formation

A
  • depends on presence of plaque and salivary gland secretions
  • supra-ging correlates with salivary gland ducts
  • subgingival contains products of blood and gingival crevicular fluid
  • attaches to tooth surface via surface irregularities in enamel and cementum
31
Q

supra-gingival calculus

A
  • averages 37% mineral
  • consists of different calcium phosphate crystals:
  • -brushite (recent, 2 weeks old)
  • -octa calcium phosphate (superficial layers of calc)
  • -hydroxyapatite (inner layers of old calc)
  • -whitlockite (small proportions)
32
Q

subgingival calculus

A
  • 58% mineral

- mostly whitlockite with some hydroxyapatite

33
Q

calculus is a ______ for periodontitis?

A

secondary etiologic factor

provides a surface that facilitates plaque formation and compromises efficiency of plaque removal

34
Q

what happens if calculus forms in germ-free animals?

A

-doesn’t result in periodontitis but when perio pathogen is added, periodontitis results

35
Q

whats the primary etiology of periodontal disease?

A

dental plaque

36
Q

how many different microorganisms can colonize the mouth?

A

500

37
Q

how many different species can be in one individuals mouth?

A

150+

38
Q

range of bacterial count

A
  • 103 in health sulcus
  • > 108 in deep perio pockets
  • 109 in supra-gingival plaque on a single tooth
39
Q

ecological relationship between plaque bacteria and host is usually _____

A

benign

40
Q

the tooth as a feature of perio infection

A
  • exposed to oral cavity
  • enamel surface does not shed like epithelium
  • bacteria in contact with tissues for long periods
  • biofilm not accessible to host defense system
  • surface irregularities are sanctuaries for bacteria
41
Q

arguments against specific plaque hypothesis

A
  • why is tissue destruction localized?
  • why don’t all patients with heavy plaque have disease?
  • why do some patients with good oral hygiene have disease?
42
Q

koch’s postulates

A
  • bacteria must be isolated from diseased tissues
  • pure cultures must be obtained
  • organisms must cause disease in animals
  • same organisms must be obtained from experimental animals
43
Q

modified koch’s postulates for periodontics

A
  • putative pathogens in large numbers in diseased sites
  • absence of pathogens in health
  • demonstrated immune response to putative pathogens
  • virulence factors can often be demonstrated
  • animal models should simulate human disease
  • elimination of organisms leads to clinical improvement
44
Q

aggregatibacter actinomycetemcomitans

A
  • formerly actinobacillus actinomycetemcomitans
  • elevated in aggressive periodontitis, chronic perio and active sites
  • elimination Aa results in successful therapy
  • elevated host antibody in serum and saliva
  • virulence factors: leukotoxin, collagenase, endotoxin, epitheliotoxin–invades epithelial cells
45
Q

porphyromonas gingivalis

A
  • elevated in chronic perio and active sites
  • elimination of Pg results in successful therapy
  • elevated host antibody in serum and saliva
  • virulence factors: collagenase, proteolytic trypsin-like activity, gingipains (lysine and arginine), endotoxin (TLR2/TLR4), fibrinolysis and hemolysin, fimbriae invades epithelial cells, endothelial cells, dendritic cells
46
Q

tannerella forsythia

A
  • elevated in chronic periodontitis, active sites abscesses
  • elimination of Tf results in successful therapy
  • elevated host antibody in serum
  • virulence factors: endotoxin, induces apoptotic cell death, induces production of inflammatory mediators by host, invades epithelial cells
47
Q

treponema denticola

A
  • spirochete
  • elevated in necrotizing ulcerative periodontitis, deep pockets
  • decrease numbers reported with successful therapy
  • virulence factors: motile organism, invades epithelial cells
  • difficult organism to culture and differentiate
  • rare
48
Q

prevotella intermedia

A
  • elevated in necrotizing ulcerative gingivitis, chronic periodontitis and active sites
  • decreased numbers with successful therapy
  • virulence factors: collagenase, endotoxin, invades epithelial cells
49
Q

association of bacteria in mixed biofilms is not what?

A

random

50
Q

***six microbial complexes in periodontal disease

A
  1. actinomyces
  2. yellow complex (strep)
  3. green complex (capnocytophage, Aa-a, E corrodens, campylobacter concisus)
  4. purple complex (V parvula, actinomyces odontolyticus)
  5. orange complex (campylobacter gracilis, c rectus, eubacterium nodatum, F nucleatum, P intermedia)
  6. red complex (T forsythia, P gingivalis, T denticola)
51
Q

top three microbes in etiology of perio disease

A

T forsythia
P gingivalis
t denticola
(red complex)

52
Q

factors affecting composition of biofilm

A
  • perio disease state

- local environment–supraging, subging, pocket depth

53
Q

red complex at lower level in what?

A

supragingival

54
Q

what has higher numbers of red complex?

A

in periodontitis and subgingival plaque

55
Q

what is in deep pockets?

A

red complex bacteria (Pg, Tf)

orange complex bacteria (Fn, Pi)

56
Q

what bacteria are not effected by pocket depth?

A

s. sanguis and actinomyces sp

57
Q

requirements for perio disease initiation and progression

A
  • host must be susceptible
  • presence of bacterial pathogens
  • pathogen must achieve sufficient numbers
  • environment conducive to expression of virulence factors by the pathogen
58
Q

host defenses against perio disease

A
  • flow of saliva and gingival crevicular fluid
  • mech displacement by chewing
  • substances in saliva and GCF (antibodies, nonspecific blocking agents, lysozyme, lactoperoxidase, lactoferrin)
  • desquamation of epithelial cells
  • antibody
  • PMNs
59
Q

host susceptibility factors

A
  • defects in PMN levels or function
  • immunocompromised states
  • diabetes
  • smoking
60
Q

S sanguis and actinomyces naeslundii inhibits ____

A

Aa while Aa produces bacteriocins against S sanguis and actinomyces naeslundii

61
Q

bacterial factors that cause tissue damage

A
  • substances that damage tissue cells
  • LPS (gram - bacterial cell wall)
  • causes host cell release of inflamm mediators (IL1, prostaglandin, TNF)
  • substances that degrade intercellular matrix (collagenase, ARG-gingipain, LYS-gingipain)
  • leukotoxins
62
Q

most of the tissue destruction in perio is caused by what?

A

host-induced inflammation, rather than direct effect of bacterial products
-bacteria cause inflammation but host enzymes damage tissue

63
Q

dysbiosis

A

commensoral organisms becoming accessory

perio exam 2 (4 decks)

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