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Perio I > 5. Microbiology of Periodontal Disease > Flashcards

5. Microbiology of Periodontal Disease Flashcards

1
Q

Periodontal Diseases Have Microbial Etiology

* Stop brushing/flossing > gingivitis (\_\_\_\_)
* 10% > periodontitis (\_\_\_\_)
* Gumline > increase in volume of gingival margin (due to inflam cells/fuids) and then loss of atatchment, PDL and bone (in perio)
A

reversible

irreversible

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2
Q

Contemporary Model of Pathogenesis of Periodontitis

* Amount of plaque and content of plaque changes as you go to disease
* \_\_\_\_ (low biomass, and content is of bacteria that is beneficial) in clinical health > protect the sites to prevent colonization
* Gingivitis > high \_\_\_\_, and bc of changes you select for diff bacteria > lead to diff outcomes; host fighting the bacteria
* \_\_\_\_ and \_\_\_\_ that affect bacteria levels > modulating the biofilm to affect composition and behavior
A

symbiosis
biomass
smoking
diabetes

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3
Q

Different Oral Habitats Harbor Different Biofilms

• Oral cavity - \_\_\_\_ sq/cm2 (palm of hand); soft and hard tissue
• Bacterium > prefer to stay on teeth, \_\_\_\_ surface; close to gingival margin has a lot of "food" for you
• \_\_\_\_ is how we subdivide the bacteria
• Take samples form each area, they are different from each other and group differently > some bacteria are better at binding to some areas than others
	○ The closer two of the names are the more similar > \_\_\_\_ and \_\_\_\_ more similar to each other
• 1ml of saliva = \_\_\_\_ microbial cells; each areas has different profile due to physical characteristics of each area
A 
220
non-shedding
areas
subgingival
supragingival
10^8
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4
Q

• More advantageous to live in ____ than in a ____; more difficult to treat for clinicians

A

biofilm

planktonic state

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5
Q

Biofilm: a Bacterial Lifestyle
• Carpentier & Cerf (1993): “a community of microbes embedded in an organic polymer matrix, adhering to a surface”
• Elder et al (1995): “a functional consortium of microorganisms organised within an extensive exopolymer matrix”
• Costerton et al (1999): “a structured community of bacterial cells enclosed in a self-produced polymeric matrix and adherent to an inert or living surface

* \_\_\_\_ - father of biofilm biology in dentistry
* Commonalities, necessary for biofilm formation > \_\_\_\_, \_\_\_\_ and an ideal \_\_\_\_
* Oral cavity > different areas with diff communities and diff surfaces
A

costerton
matrix
community
ideal surface

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6
Q

COMPONENTS OF A BIOFILM

• Require a \_\_\_\_ that bring bacteria in, and taking the waste out, bring nutrients and substrate
	○ Tooth, soft tissue, implant, composite, a lot
• Fluids > saliva and GCF
	○ Saliva - \_\_\_\_, GCF - \_\_\_\_
A

bulk fluid
carbs
proteins

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7
Q

Advantages of Biofilm Lifestyle
• Protection from ____ system
• Protection from antibiotics and antimicrobials
• Bacteria: ____ of the dry weight; ____ is matrix of polysaccharides, salivary proteins and glycoproteins
• ____: maintains integrity of the community
• ____: 75-80% of volume, concentration of enzymes
• Enzymes produced by bacteria can be concentrated in the glycocalyx
• Cells at the bottom of a biofilm are alive but metabolically ____: metabolic activity in outer layers

• Tolerance to antibiotics > dose, and the target bacteria is down further in the biofilm; and, resistant bacteria on the outside, and can also conduct gene transfer of \_\_\_\_ genes
• Bacteria ry to bind electrostatic and van der waals at first, and have appendages \_\_\_\_, fimbrarie > as soon bind, they change their \_\_\_\_ > secreting matrix (and exopolysacc's)
	○ You have viruses, yeast and archaea as well
• \_\_\_\_ > formation of food webs
A 
immune
70%
30%
exopolysaccharides
glycocalyx
inactive
resistance
pilliae
behaviors
cross-feeding
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8
Q

Biofilm Structure

* \_\_\_\_-like colonies
* Within biofilm > \_\_\_\_ system (bring fluid, oxygen, nutrient, substrate)
* \_\_\_\_ > outside of biofilm > clusters that are detaching that try to go colonize elsewhere
A

mushroom
primitive circulatory
streamer

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9
Q

The Biofilm Life Cycle

1: ____ attachment
2: ____ attachment
3: Maturation I
4: Maturation II
5: ____

* Saliva > glycoproteins; antibodies (\_\_\_\_) cover the surface > bacteria come to adhere, but only specific bacteria for glyco's > multiply and secrete \_\_\_\_ > spread \_\_\_\_ and then \_\_\_\_ > form mushroom-like colonies > dispersion (release of planktonic)
* Behave differently in biofilm vs planktonic; as soon as bacteria attaches and change \_\_\_\_ expression (up to \_\_\_\_ of genetic changes)
A 
reversible
irreversible
dispersion
IgA
exopoly
lateral
vertical
gene
30%
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10
Q 
Dental Plaque Development
Pellicle formation
Initial colonization
Horizontal spread and co-aggregation
Vertical growth
Climax community (niches)
* Pellicle formation immediately after porphy > initial colonization (good at binding glycoproteins, \_\_\_\_, \_\_\_\_ [early]) > horizontal spread > secrete matrix and coaggregate > bacteria tthat bind these bugs (coagg) > vertical growth > channels formed > more layers, change the types of bacteria that are here, and they are ammenable to binding more bacteria; each layer has diff \_\_\_\_, etc.
* \_\_\_\_ > no more microbial change; 
* Cell-cell communication > \_\_\_\_ > way for bacteria to sense population and do not need to proliferate anyway
A 
streptococcus
actinomyces
metabolisms
climax community
quorum sensing
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11
Q

Dental Biofilm Development

* As it accumulates, occurs at \_\_\_\_, and it is \_\_\_\_
* Grows first laterally, and then vertically
* In rougher areas of tooth, why gingival margin? GCF, high protein food
A

gingival margin

self-limiting

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12
Q

Patients Present Different Rates of Plaque Formation

• Difference in plaque \_\_\_\_ rates
• \_\_\_\_ that promote plaque growth
	○ Properties of tissue, microbiome, etc.
A

formation

factors

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13
Q

Microbial Ecology
Study of relationships of microorganisms with one another and with the environment

* Relationships that affect plaque
* Conditioning film/pellicle > only bugs that can bind will stay
* Resistance > some bacteria may be resistant > can xfer \_\_\_\_ genes, and they also have \_\_\_\_ of resistance (protect surrounding bac)
* Quorum signaling
* Gene transfer
* Coadhesion/coagg > some bugs that bind bug who bind bugs to surface
* Antagonims > \_\_\_\_ so they establisht hemsvles
* \_\_\_\_ > xhcnaged of metabolic activity
A

resitant
radius
bacteriocins
cross-feeding

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14
Q

Bacterial Interactions

Early and late colonizers do not ____, but they all aggregate with ____

A more ____ state is conducive to shift towards gram negative anaerobes

Streptococci are less sensitive to ____. Modify environment to more ____ state

Receptors on non shedding surface; recognized primarily by ____

• Streptococci, best at binding pellicle (v specific, receptor to mucins, etc.)
• 2nd wave > bugs bind strepto > actinocyes > veinoella > propenma > early colonizers > change environment > consume oxygen and sugar > create new environment for late colonizers
• Pathogenic bacteria
• F. nucleatum > bridges early and late colonizers
	○ \_\_\_\_; p gingi is small \_\_\_\_
A 
co-agg
f. nucleatum
reduced
air
reduced
streptococci

filamentous
rod

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15
Q

HUMAN SUPRAGINGIVAL
PLAQUE

* Crown with epoxy > observed accumulation
* Different \_\_\_\_, and some mushrooms and channels
A

shapes

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16
Q

Experimental Gingivitis

• Plaque accumulate for \_\_\_\_ days
• Most changed in \_\_\_\_ days > gingivitis
	○ Change in color, contour, texture and consistency
• \_\_\_\_ migration of epithelium due to inflam cells and edema
A

21
10-11
coronal

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17
Q

Early vs. Mature Supragingival Plaque

* Gram and shapes only
* Day 0 > most \_\_\_\_ cocci and rods
* Progression of time > losing streptococcus, in expesnse of \_\_\_\_ cocci rods and then \_\_\_\_
A

gram+
gram-
spirochetes

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18
Q

HUMAN SUBGINGIVAL PLAQUE

* Subgingival plaque > root surface, and GCF, and you have multiple surfaces > protected area
* Content of microbiome > 3 types of biofilm > \_\_\_\_-attached, \_\_\_\_-attached, \_\_\_\_-attached biofilm
* Type of bugs in eachaarea are \_\_\_\_; in coronal portion > actinomyces, (yellow = streptocuss), purple = veionella, these all like oxygen and metabolize sugar; in apical portion > orange (connect early and late colonizers), and then at bottom > red complex (p gingiv, trepmone, tener forsythia) > need heme to grow
* these areas are \_\_\_\_ > \_\_\_\_ and \_\_\_\_ comes to feed them
A 
tooth
epithelium
loosely
different
ulcerated
GCF
blood
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19
Q

Non-Specific Plaque Hypothesis

Periodontal Diseases result from plaque accumulation, ____ of the species present within the dental plaque

A

irrespective

20
Q

Acute Necrotizing Ulcerative Gingivitis (ANUG)

* This brough back \_\_\_\_ theory
* Trench mouth, from WWII
* Areas of necrosis and papillae > \_\_\_\_ and smells, all gingival and no loss of \_\_\_\_
* Was not about amount of plaque, and bugs > \_\_\_\_ and \_\_\_\_ mostly > immune response
A 
specific
paifnul
bone
fuso
spirochetes
21
Q

Aggressive Periodontitis (Localized) - LJP

* \_\_\_\_
* \_\_\_\_ and \_\_\_\_
* Limited amount of \_\_\_\_
A

plaque
first molars
incisors
plaque

22
Q

Specific Plaque Hypothesis

____ species of bacteria cause different forms of gingival and periodontal diseases

A

specific

23
Q
  • Studied using culture > take samples, petri and grow and identify
    • Comparing: dx has more ____ and more ____(prevotella, and p gingivalis); normal has compatible healty colonies
    • Use ____ > numbers and shapes of bacteria; right is dx (filaments and spirochetes, and more of them)
A

colonies
black
phase contrast

24
Q

Checkerboard DNA-DNA Hybridization

* Before microarrays, think of this as a \_\_\_\_
* Some bugs more \_\_\_\_ than others (40)
* DNA probes targeting bacteria; attached to \_\_\_\_ molecule; when probe is denatured (half of DNA strand with reporter)  finds complement on bacteria > light/signal
* Can compare to \_\_\_\_, so you can figure out how many bugs you have in each sample
A

macroarray
common
reporter
standards

25
Q

Microbial complexes

Blue: \_\_\_\_
Yellow: \_\_\_\_
Purple: \_\_\_\_ and \_\_\_\_
Green
Orange: \_\_\_\_
Red: \_\_\_\_, \_\_\_\_ and \_\_\_\_
A 
actinomyces
streptococcus
v. parvula
a. odontolyticus
f. nucleatum
p. gingi, t. forsythia, t. denticola
26
Q

Early Biofilm Formation
Pellicle

* 0, 2, 4, 6 hours and analyze for bugs
* At 0 > you have bacteria, and you had more and more as time goes on
* Best at growing at this stage > \_\_\_\_ and \_\_\_\_
* Specificity > copmoisiton of saliva is different from the plaque (saliva is red)
A

yellow

actinomyces (blue

27
Q

Experimental Gingivitis

* Over 21 days
* 0 - 21 : increases in bacteria, most significant in \_\_\_\_
* Also confirms that you can restore \_\_\_\_ even better than before
A

orange

health

28
Q

Ecological Plaque Hypothesis

* Focuses on \_\_\_\_
* Takes into consideration, mass, content, behvaior and influence of host and evniroenmtn
* A little biofilm > a little inflam > not a lot of CGF > gram+, \_\_\_\_ compatbiily
* A lot of biofilm > inflam > a lot of GCF, bleeding, higher \_\_\_\_, higher \_\_\_\_ > anaerobic, like GCF
* \_\_\_\_ increases GCF levels
* Factors that tip balance
A 
dysbiosis
health
pH
temp
smoking
29
Q
  • Smokers > red; non-smokers > green
    • Visualize how similar and different samples are; closer together in space are more similar in microbial composition, etc
    • Reds are ____, greens are ____; different from one another
    • Smoking chages ____
A

clumped
clumped
microbiome

30
Q

Smoking Favors a Pathogenic Microbiome

* Used a checkerboard
* All sites > orange, red; also seen in deep and \_\_\_\_ sites
* Sites that look clinically healthy, but they have a more \_\_\_\_ microbiome bc of the environemental pressure that \_\_\_\_ represents
A

shallow
pathogenic
smoking

31
Q

Ethnicity Modulates the Oral Microbiome

* Ethnicity, AA, chinese, latinos, whites
* Some level of \_\_\_\_, but they had core \_\_\_\_ that distinguish them from each other
* \_\_\_\_ can influence, not just ethinicity
A

commonality
bacteriotype
diet

32
Q

What Does Microbiome Mean?

* Collection of microorgs in oral cavity; including \_\_\_\_, yeast, but usually just the bacteria
* Couldn't culture some bugs back then; but then 2000's that allowed \_\_\_\_ to culture bacteria > went to knowing we had \_\_\_\_ bacteria  that could colonize (not 700 all at once, etc.)
* Develop database > look into 700 > \_\_\_\_ cultivated, \_\_\_\_% that cannot be cultivated and we don’t know much about that may be pathogens (\_\_\_\_ unnamed)
A 
viruses
DNA
700
50%
35%
15%
33
Q

• Firstly Looked at ____, sizes and colnines [only few ____ at a time] > many bacteria at once > complexes how we go from health to disease > in 2000’s+ ____ techniques that didn’t need cultivation, only need the ____ (can look at ____, fungi, etc.)

A 
shapes
samples
molecular
DNA
viruses
34
Q

Periodontal Microbiome in Health and Disease

• Good to explore, and to confirm that these bugs were pathogens actually
• People healthy, and perido people, and within that , some from sahllow and some from deep
• Plotted in \_\_\_\_ order of relative abundance
• Red - deep, green is shallow, blue is healthy
• In disease > p gingiv, trepnoma, tanneroma forsythia; also see other bugs; and \_\_\_\_ organisms
	○ All bugs are high in disease, and low in health and \_\_\_\_ in shallow
• \_\_\_\_ in dx patients are diff from shallow in healthy (have more pathogenic bacteria) > these shallow sites will p\_\_\_\_
A 
decreasing
uncultivated
intermediates
shallow
progress to disease
35
Q

Periodontal Diseases Result from Dysbiotic Communities
• ____: shifts in the resident microbiota of certain body sites that lead to disease
• Biofilms as a whole cause and perpetuate chronic infections
– “Pathogenic ____”,
– “Pathogenic ____ community”,
– “The community as ____”

* Pathogen here, the bugs we already have them in our mouth (diff from other diseases)  part of resident microbiota > pathogen \_\_\_\_
* Just presence of pathogens do affect community as whole > introduce p gingi > the community behaves \_\_\_\_ (not just pathogen being bad and influencing the community)
A

dybiosis
synergy
microbial
pathogen

synergy
differently

36
Q

Classical vs. Opportunistic Infection

• \_\_\_\_, can be pathogenic but they can live in harmony (the case here in periodntitis)
A

pathobionts

37
Q 
Identification of Pathogens
• Over \_\_\_\_ species
• \_\_\_\_ species
• \_\_\_\_ sample
• Identification of \_\_\_\_ sites
• Periodontal disease activity resulting from different species
• Need numbers of active sites in order to observe
A

700
uncultivable
representative
active

38
Q

Identification of Pathogens

  • Clinically similar Diseases
  • Bacteria that grow as a result of the disease process
  • ____ Infections
  • ____ state
  • ____ strains
    • ____ state > people with perio, but had pathogens for a number of years, but something happened so they develo
    • Different strains > strains may not be as ____ (not as much LPS); not taken into consideration
A

mixed
carrier
virulent

carrier
virulent

39
Q

Identification of Periodontal Pathogens: Koch’s Postulates Modified
by Socransky

* How to tell whether pathogen > \_\_\_\_ postulates
* \_\_\_\_ > preence/numbers in disease cased
* \_\_\_\_ >
* Host response > immunogenic
* \_\_\_\_ factors > intent to do harm
* Animal sutides > reproduce here
* Done in \_\_\_\_, \_\_\_\_, \_\_\_\_ and \_\_\_\_ (hard to study), this why they're classical pathogens
A 
koch's
association
elimination
virulence
AA
PG
TF
spirochetes
40
Q

Virulence Factors

  • ____; coagg, multiplication
  • ____ (LPS) on surface and in vesicles
    • Interbacterial relationships - together they’re ____, more potent
    • Bacterial enzymes: collagenases, proteases - i.e., some proteases that degrade ____
    • Overcome host defense mechanisms - when go from health–> gingivitis–> periodontitis, either ____ bacterial action ex. LPS but a lot of damage (loss of fibers, bone) is due to the host response to that bacterial insult- ____.
    • Factors resulting in tissue damage:
    – Indirect : caused by the immune response, upon bacterial stimulus
    – Direct: caused by the bacteria
A 
adhesins
endotoxins
stronger
IgA
direct
indirect
vesicles
41
Q

TABLE OF ACTIONS OF LPS!

A

YA

42
Q

This is a number of examples of these virulence factors in some of the most common pathogens: P. Gingivalis and AA. So both of them have ____.

P. Gingivalis has ____ that releases blebs with LPS, ____ to attach, ____ to penetrate tissues, ____ to degrade CT, trypsin like proteases.

AA. primary virulence factor is ____ which kill leukocytes but also has LPS, ____, bacteriocins, ____.

A 
LPS
capsules
fimbrae
invasins
collageneases

leukotoxin
adhesins
invasins

43
Q

Kissing???!

This study ruined kissing for everyone..looked into French kissing and to see what happened to microbiome.
Couples said how many times and how kiss and had them kiss.

Control group gave probiotics- ____. Then kissed again. For priobiotics group, knew what bacteria they gave, saw after kiss how much bact. the person gave the other: ____ M bacteria

But these bugs ____. Kissing could influence the microbiome but was the ____ of kissing. Basically its not because you were exposed to some new bug that is now part of our microbiome. But if you are exposed multiple times–> part of ____.

A 
lactobacillus bravis
80
transient
frequency
microbiome
44
Q

Take Home Messages

Oral Cavity is Unique in the Human Body:
• ____ Environment
• ____ Host-Microbial Interaction
• Etiologic agents reside within a biofilm that is located outside the body (double protection)
• Pathogens are part of the ____ microbiota: found in health for long periods prior to disease initiation
• Provides ____ surfaces: natural microbial colonization
• Multiple ____ for pathogens beyond the periodontal pocket

A 
open
dynamic
indigenous
non-shedding
reservoirs
45
Q
  • There are clear differences in the development and composition of ____ and ____ biofilms (plaque).
  • ____ (saliva/GCF), ____ (tooth, soft tissue, restorations) and ____ are key determinants of biofilm formation and composition.
  • Bacterial colonization is initiated by colonization by ____cocci and rods, followed by ____ cocci and rods. Then ____ and ____ and finally ____ are detected.
A 
supragingival
subgingival
bulk fluid
surface
bacteria
gram+
gram-
fusobacteria
filaments
spirochetes
46
Q
  • There are clear clinical differences between periodontal health, gingivitis and periodontitis
  • Gingivitis and periodontitis result from microscopic changes in the underlying periodontal structures
  • These changes result from interactions between the ____ and the local ____ and can be modulated by certain ____ and ____ factors
  • Gingivitis is widespread in populations, while periodontitis is somewhat less common
  • Periodontitis is preceded by gingivitis, but not all cases of ____ lead to periodontitis
A 
host
microbiota
local
systemic
gingivitis
47
Q
  • Factors such as ____, diet, ____ and ethnicity can shape the oral microbiome
  • The ____ plaque hypothesis provide the framework for the current understanding of the etiology of periodontal diseases
  • Certain microbial complexes are associated with periodontal health and others to disease: their colonization follows a ____ pattern
  • The modified ____ are the basis for the classification of pathogens
  • The health-associated microbiome is composed primarily of ____ and ____ (yellow and blue complexes) whereas the disease-associated microbiome is enriched for ____, ____ (orange complex), ____ and ____ (red complex)
  • Adherence capability, ____ and ____ are some of the most important virulence factors of periodontal pathogens
A 
smokiing
genetics
specific
specifc
koch's postulates
streptococci
actinomyces
prevotella
fusobacterium
porphyromonas gingivalis
treponema denticola

LPS
enzymes

Perio I (10 decks)

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