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OMC I, Module II > 3. Periodontal Microbiology I > Flashcards

3. Periodontal Microbiology I Flashcards

1
Q

What is Periodontal Disease?
“The term periodontal disease has been given different meanings and is used rather ____. It is used in a general sense to encompass all diseases of the periodontium in much the same way as the terms
liver disease and kidney disease are used.” Fermin A. Carranza
Clinical Periodontology 8th Edition

A

ambiguously

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2
Q

Classification of Periodontal Diseases and Conditions*

▪ ____ Diseases

  • –• Plaque-Induced Gingival Diseases
  • –• ____-Induced Gingival Lesions

▪ Chronic Periodontitis
▪ ____ Periodontitis
▪ Periodontitis as a Manifestation of Systemic Disease
▪ ____ Periodontal Diseases
▪ Abscesses of the Periodontium
▪ Periodontitis Associated with ____ Lesions
▪ Developmental/Acquired Deformities and Conditions

*1999 International World Workshop for the Classification of Periodontal Diseases

A

gingival
non-plaque

aggressive
endodontic

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3
Q

Periodontal Disease

DIGC > ____, ____ channels (gingival hyperplasia)

A

cyclosporine

calcium

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4
Q

Plaque-Induced Periodontal Diseases

Periodontitis Inflammation and destruction of the
____.

Gingivitis Inflammation of the ____.

Erythema/edema of gingival margins > gingivitis (restricted to ____)

Periodontitis > soft tissue is inflamed, but inflammatory lesion has spread to attachment apparatus (____, ____ and ____) > bone resorption and teeth becoming loose and falling out

A

attachment apparatus
gingiva
soft tissue

cementum
alveolar bone
PDL

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5
Q

Structures of the Periodontium

Cementum, alveolar bone and PDL anchor teeth within jaws; and soft tissue is anchored to teeth via ____ and ____

A 
epithelial attachment (JE)
collagen fibril bundles
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6
Q

Plaque-Induced Periodontitis

Severe > ____ teeth, and danger of losing ____

A

loose

teeth

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7
Q

Plaque-Induced Periodontal Diseases

How do we know that ____ plaque has a role in the pathogenesis of these diseases?

Etiology is ____ in nature

A

bacterial

bacterial

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8
Q

The Etiology of Periodontal Disease

Written records from as far back as ____ years BC describe conditions that today would be diagnosed as periodontal disease. Many of them attribute the disease to collections of “material” on the surfaces of the teeth.

“Occasionally there is deposited in the inner and outer surfaces of the teeth or between the gums, large and rough concretion: the teeth take on a black, yellow or green color, following which the gums become altered and the teeth become very unsightly.”

A

3000

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9
Q

The Etiology of Periodontal Disease

Very early on it was shown that the condition could be treated by removing these “concretions” from teeth.

____ are the concretions that were found on teeth

Treatment > ____ teeth, remove, and you would see resolution; treatment has not changed much since then

A

tartar/calculus

scrape

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10
Q

____ is a risk factor for failing implants and susceptibility to periodontal disease

A

smoking

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11
Q

Generalized aggressive periodontitis

Tartar is not the inciting agent, it is the ____ that forms that is the inciting agent

A

plaque

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12
Q

“History” of Periodontal Microbiology

From specific infection (bacterial) > non-specific plaque hypothesis (nothing to do with what was in plaque, but as to how much plaque you had)

In 1960’s > sophisticated microscopy and how to grow anaerobic bacteria in vitro and then evaluate > molecular techniques, collectively led to renewal of specific infection into the ____ hypothesis (unique bacteria are responsible for causing distinct types of periodontal disease) > ____ hypothesis (herpes viruses were implicated in playing a role) > ____ and ____ pathogens

A

specific plaque
ecologic plaque
dysbiosis
keystone

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13
Q

Evidence Supporting the Bacterial Etiology of Periodontal Disease
1. Animal Studies
• ____ animals
• ____-induced diseased

A

germ-free

ligature

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14
Q

Ligature-Induced Murine Model of Periodontitis

Ligature placed on molar of mouse > allow plaque formation > over time, bone loss occurs on ____ and ____ aspects of teeth > reproducibly lead to bone loss as a result of ____

A

buccal
palatal
inflammation

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15
Q

Evidence Supporting the Bacterial Etiology of Periodontal Disease

  1. Human Studies
    • ____ gingivitis model
    • treatment studies
    - efficacy of ____

Cannot do animal studies in humans due to ____ reasons

A

experimental
antibiotics
ethical

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16
Q

Experimental Gingivitis Model

Initial study conducted by ____ and his colleagues in Aarhus, Denmark.

Purposes:

  1. “To attempt to produce ____ in patients with healthy gingiva by withdrawing all active efforts directed towards oral cleanliness, and
  2. to study the sequence of ____ in the micro- bial flora and in the gingivae thus produced.”
A

Harold Loe
gingivitis
changes

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17
Q

Experimental Gingivitis Model
Materials and Methods:

• There were 12 subjects: 9 ____ dental students,
1 periodontology “teacher” and 1 lab technician.
• At the outset of the experiment subjects were scored for their levels of gingival ____, amounts of
____ on their teeth and ____ composition of the plaque.
• Subjects were then instructed to cease all methods of ____ after which they were periodically evaluated.

A 
first year
inflammation
plaque
microbial
oral hygiene
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18
Q

Experimental Gingivitis Model

Materials and Methods (continued):
• At the first signs of inflammation, measurements were taken and the subjects immediately given ____ instructions and told to start cleaning their teeth.
• Subjects were then followed until ____ and ____ were no longer detectable.

A

oral hygiene
inflammation
plaque

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19
Q

Experimental Gingivitis Model

____: formation of dental plaque

A

day 3

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20
Q

Experimental Gingivitis Model

Can identify individual BV (BOP) by ____

A

day 15

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21
Q

Experimental Gingivitis Model

3 days post-OH

A

YAY

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22
Q

Experimental Gingivitis Model

Clinical Results:
• At the outset of the experiment, subjects exhibited minimal gingival inflammation/plaque accumulation.
• ____ subjects developed gingivitis upon cessation of of oral hygiene.
- 3 subjects developed gingivitis within ____ days - the other 9 subjects developed gingivitis within
____ days.
• Following recommencement of oral hygiene the inflammation was resolved within ____ days.

A

all
10
15-21 days
7

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23
Q

Experimental Gingivitis Model

Microbiologic Results:
• On day 0 minimal numbers of bacteria were present most of which were ____ and ____.
• Soon after cessation of oral hygiene (OH) there was a dramatic increase in the numbers of ____.
• ____ and slender ____-shaped bacteria were detected 2 to 4 days following cessation of OH.
• ____ organisms were detected at day 10 such that by the time gingivitis developed a dramatic shift in the bacterial composition of the plaque had taken place.

A 
gram-positive cocci
rods
cocci
filamentous
rod
spirochetal
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24
Q

Experimental Gingivitis Model

So oral hygiene is very effective in controlling PAC (?) and also can reverse gingivitis. What they concluded from this:
(in this case, they didn’t know exactly what the bugs were) but they knew that they were gram-negative and they
knew the morphology of these bugs, so the appearance of ____ shaped organisms and ____
corresponded with the onset of gingival inflammation.
• What they concluded from this is is that it’s this group of bugs (____) that are responsible
for inducing the gingival inflammation.

[MORE FROM AMI’S NOTES]

A

gram-negative rod
spirochetes

gram-negative rod/spirochetes

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25
Q

Experimental Gingivitis Model

Conclusions:
• ____ is essential for the development of gingivitis.
• The presence of certain bacteria at the onset of gingival inflammation suggests that there may be specific organisms acting as periodontal pathogens.
• Individuals are ____ susceptible to developing gingivitis; some develop the disease more quickly than others.
• Removal of plaque leads to ____ of gingivitis.

A

bacterial plaque
differentially
resolution

26
Q

Experimental Gingivitis Model

Conclusions:
• ____ is essential for the development of gingivitis.
• The presence of certain bacteria at the onset of gingival inflammation suggests that there may be specific organisms acting as periodontal pathogens.
• Individuals are ____ to developing gingivitis; some develop the disease more quickly than others.
• Removal of plaque leads to ____ of gingivitis.

• At this time, people were arguing the non-specific plaque… this argued that and claimed that there may be some specificity in bacteria
A

bacterial plaque
differentially susceptible
resolution

27
Q

Evidence in Support of the Specific Plaque Hypothesis

  1. Animal Studies
    • primates
    • dogs
    • rodents
  2. Human Studies
    • ____ observations
    • experimental gingivitis model
    • ____ of the microbiota in
    supragingival verus subgingival plaque
    • association between distinct forms of periodontal
    diseases and with specific species of bacteria• Came from animal studies (pathogens from humans, into animals) - and if it induced something that looked like human periodontitis - there was some ____ of bacteria
A

clinical
characterization/comparison

specificity

28
Q

Evidence in Support of the Specific Plaque Hypothesis

  1. Clinical Observations: the amount of plaque on an individual’s teeth and the severity of disease is not always directly ____.

i.e. • Clean mouth, but very ____ disease - argues against ____ bacterial theory
○ Something unique about the bugs in her mouth that made her present like this…

A

correlated
extensive
non-specific

29
Q

Evidence in Support of the Specific Plaque Hypothesis

  1. Longitudinal microbiologic studies utilizing the experimental gingivitis model, indicate that the presence of certain morphotypes ( i.e., ____, ____, etc.) is associated with disease.• ____ bugs in general…
A

filaments

spirochetes

30
Q

Evidence in Support of the Specific Plaque Hypothesis

These studies did not determine the exact identity of the apparently “important” organisms!

• Just looking at \_\_\_\_ and \_\_\_\_of the organisms, could'n't tell the actual organisms
A

shapes

gram-stain

31
Q

Evidence in Support of the Specific Plaque Hypothesis
3. ____ of the microbiota in supragingival versus subgingival plaque.

* Gram-positive turn into \_\_\_\_
* Facultative anaerobes into \_\_\_\_
* Some specificty with the onset of \_\_\_\_
* We don't actually know that the bugs directly cause the disease, but they're \_\_\_\_
A

characterization/comparison

gram-negative
anaerobes/capnophilic
gingivitis/periodontitis
associated

32
Q

Evidence in Support of the Specific Plaque Hypothesis

4. Associations between the presence of ____ bacterial organisms and the ____ of unique forms of disease.

A

specific

presence

33
Q

Complexity of the Oral Microbiome

• Composition of characters doesn't change, but the \_\_\_\_ of characters do

Which of the organisms that have been detected in dental plaque are ____
to the pathogenesis of periodontal disease?

A

frequency

relevant

34
Q

Koch’s Postulates

  1. The microorganism must be found in abundance in all organisms ____ from the disease, but should not be found in ____ organisms.
  2. The microorganism must be isolated from a diseased organism and grown in ____.
  3. The cultured microorganism should cause disease when introduced into a ____ organism.
    -or in an
    experimental
    model, because
    we won’t give
    this to humans)
  4. The microorganism must be ____ from the inoculated, diseased experimental host and identified as being ____ to the original specific causative agent.
A

suffering
healthy

pure culture

healthy

reisolated
identical

35
Q

Problems Connected with the Application of Koch’s Postulates to the Study of Periodontal Disease

  1. ____ difficulty in isolation and characterization of organisms.
  2. Gingival microbiota composed of a ____ mixture of organisms derived from at least 600 species of bacteria capable of inhabiting the human oral cavity.
  3. The existence of multiple forms of ____ disease.
  4. Presence of putative pathogens isolated from both ____ and ____ individuals.• Periodotnal doesn’t fit into medicine - it’s ____
    • Dr. Sokransky - identifying potential pathogens for periodontal disease - but koch’s postualtes there are problems because [reads list]
    • Four is a really big problem
    ○ Most of us have the ____ pathogens in our mouths rn
A 
technical
complex
"periodontal"
diseased
healthy

polymicrobial
putative

36
Q

Problems Connected with the Application of Koch’s Postulates to the Study of Periodontal Disease

  1. Unclear as to whether the presence of the organism actually ____ the disease or is simply the result of favorable ____ conditions induced by the disease.
    • X = strict anaerobic; this enviornment is oxygen-containing
    • C = adhesins; allow to attach to acquired pellice (X cannot do)
    • D and A
    • X has virulence potential that can cause damage
    • C can bind to acquired pellicle, and has receptors on surface that can interact with X, which is how it can bind to the matrix
    • D is a ____ anaerobe - makes the oxygen poor enviornemnt that is supportive of X
    • A can inhibit host resposne (toxin that kills neutrophils)
    • X can now colonize site, envior supports growth, and host systme will not remove
    • Which is the etiologic disease now? We cannot tell
A

causes
environmental
facultative

37
Q

Problems Connected with the Application of Koch’s Postulates to the Study of Periodontal Disease

  1. Lack of an ____ model that accurately depicts the human condition.
A

animal

38
Q

Socransky’s Modifications of Koch’s Postulates

  1. The ____ pathogen must be associated with disease as evident by increases in the numbers of at diseased sites
  2. The ____ of the organism should arrest the progression of the disease.
    • You may find bugs in healthy sites, but at ____ levels - these organisms, when numbers exceed threshold, they are capable of inducing disease
    • Big problem with second modification - no therapies that allow us to target ____ bacteria
A

putative
elimination
low
specific

39
Q

Socransky’s Modifications of Koch’s Postulates

  1. The organism should exhibit ____ relevant to the initiation and progression of the disease.
  2. The cellular/humoral immune responses to the organism should be ____ of it’s unique role in the pathogenesis of the disease.
  3. The organism must be capable of causing a similar disease in ____ models.
A

virulence factors
suggestive
experimental animal

40
Q

How do these organisms cause periodontal disease?
Virulence Factors
____
Invasion
____
Tissue Damage
— Or figure out mechanisms that are ____ to survival of host cells - many orgs are capable of directly causing damage to host themselves

A

colonization
immunoevasion
deletrious

41
Q

Techniques Used for the Isolation and/or Idendtification of Potential Periodontal Pathogens

Dark Field Microscopy

Immunologic Assays
____ - Anaerobic/aerobic
Biochemical Assays

Nucleic Acid Probes/PCR

Molecular Genetic Approaches

  • ____ RNA sequencing and ____
  • Next-generation sequencing technologies

Biogeography

A

bacterial culturing
16S ribosomal
phylgenetics

42
Q

Bacterial Culturing

• Hard to grow samples in a laboratory
Would sample pocket w/ \_\_\_\_, sit with 15 secs, put into a vial that contains \_\_\_\_ transport media, and sent to lab, techs take sample and innoculate petri dishes (\_\_\_\_  and \_\_\_\_)
A

paper point
anaerobic
selective
non-selective

43
Q

Bacterial Culturing

• Placed into \_\_\_\_ culturing chamber, sit in week
• Based on \_\_\_\_, use of \_\_\_\_, they can tell what organisms are in patients mouth
	○ But cannot grow a lot of bacteria from oral cavity bc they're ungrowable
• Can tell which \_\_\_\_ the orgs are sensitive to, and base choices based on studies
A

anaerobic
colony morph
antibodies
antibiotics

44
Q

Associations Between Specific Bacteria and Unique Forms of Periodontal Disease

Necrotizing Ulcerative Gingivitis:
• \_\_\_\_ onset
• characteristic “\_\_\_\_”, crater-like
depressions at the apex of the interdental
papillae
• \_\_\_\_ over involved tissue 
• \_\_\_\_ gnawing pain
• \_\_\_\_ lymphadenopathy and mild fever
• \_\_\_\_, foul taste
• commonly seen in subjects under some
form of \_\_\_\_
* Psueudomembrane - painful and white
* Students during \_\_\_\_ will present with this
A 
acute
punched out
pseudomembrane
constant
local
metallic
emotional stress
finals
45
Q

Necrotizing Ulcerative Gingivitis

In the past, this condition has been referred to as: - Acute Necrotizing Ulcerative Gingivitis (____)

  • Vincent’s Disease
  • ____
    • Initially called trench mouth from WWI
    • Gingiva doesn’t look ____, but the pseudomembrane, and punched out papillae
    • Different from ____ - these don’t hurt as much as this
A

ANUG
trench mouth
inflamed
gingi/periodontitis

46
Q

Necrotizing Ulcerative Gingivitis

____
____ species
____ species
____ intermedia

• These bugs don't cause, but they're \_\_\_\_ with the disease
A 
spirochetes
fusobacteria
selenomonas
prevotella
associated
47
Q

Associations Between Specific Bacteria and Unique Forms of Periodontal Disease

Localized Aggressive Periodontitis:
• formerly called localized \_\_\_\_ periodontitis 
• \_\_\_\_ onset
• \_\_\_\_ rate of progression
• typically involves \_\_\_\_ and first
\_\_\_\_
• \_\_\_\_ aggregation
• progression of disease may \_\_\_\_ 
• amounts of microbial deposits are often
\_\_\_\_ with the extent of attachment loss
• You see this disease at the time of puberty
• Age range of males vs females
	○ Females are a lot \_\_\_\_ than males - resulting in a \_\_\_\_ age range
	○ From \_\_\_\_ years of age
• Localized - permanent incisors and first molars
• Families - \_\_\_\_ component
• Self-arrest - break down quickly but once it happens it doesn't get \_\_\_\_
A 
juvenile
circumpubertal
rapid
permanent incisors
molars
familial
"self-arrest"
inconsistent
earlier
broad
9-21
genetic
worse
48
Q

Localized Aggressive Periodontitis

• No \_\_\_\_, no \_\_\_\_, but signiifcant \_\_\_\_ affecting first molars (or permanent incisors)
	○ We don't know why these!
• First to \_\_\_\_ - incisors and first molars - may have something to do with time of eruption
• Clinical burnout - see at 40/50 - looks the \_\_\_\_, doesn't get any worse!
A 
gingivl inflamamtion
plaque/calculus
bone loss
erupt
same
49
Q

Localized Aggressive Periodontitis

____

  1. ____ coccobacillus
  2. Microaerophilic (____)
  3. Non-____
  4. Non-____
    • Doesn’t cause! It’s ____ with disease
    • Closest correlation with single periodontal entity and a disease
    • ____ of dnetal plaque
A 
Aa
gram-negative
capnophilic
encapsulated
motile
associated
late colonizers
50
Q

Virulence Factors of
A. actinomycetemcomitans

* Lots of VF
* \_\_\_\_ - bone resportion [characterisitc of perio] and induces inflam
* \_\_\_\_ - kills leukocytes (PMNs)
* \_\_\_\_
A

endotoxin/LPS
leukotoxin
cytolethal distending toxin

51
Q

Virulence Factors of
A. actinomycetemcomitans
Leukotoxin (Ltx)

* Membrer of \_\_\_\_ toxins - \_\_\_\_ forming molecules - works similar to \_\_\_\_ udner some circumstacnes
* After incubated with toxin - PMNs have holes in surface - influx of fluid and undergoes \_\_\_\_ (a form of \_\_\_\_) (high cxn of toxin)
* Same cell line, to \_\_\_\_ conc., the cells undergo \_\_\_\_ (condensation of DNA along the nuclear membrane)
* Tropism is for \_\_\_\_ (neutrophils, T cells, B cells)
A 
RTX
pore
complement
osmotic lysis
necrosis
low
apoptosis
immune cells
52
Q

Virulence Factors of
A. actinomycetemcomitans

Cytolethal Distending Toxin (CDT)

• \_\_\_\_ protein chanis - monolayer of cells (CHO) and incubate with CDT - morphology of cells look \_\_\_\_ - they become \_\_\_\_
A

3
larger
distended

53
Q

Virulence Factors of
A. actinomycetemcomitans
Cytolethal Distending Toxin (CDT)

• CDT causes \_\_\_\_ arrest
• Under some circumstances it may induce \_\_\_\_
• Grow gingiva in culture
	○ After 24 hours, epi projections (oral epithelium)
	○ And incubated with toxin at 24 hrs, the structure appears \_\_\_\_, and the basal cells are \_\_\_\_
	○ This is same mag
• CDT affects the \_\_\_\_ that's provided by epithelial cells, that alters how bacterial cells pass the epithelium and induce damage
A 
cell cycle
apoptosis
larger
enlarged
barrier
54
Q

Associations Between Specific Bacteria and Unique Forms of Periodontal Disease

Chronic Periodontitis:
• most commonly seen in \_\_\_\_
• can be \_\_\_\_ or \_\_\_\_
• \_\_\_\_ rate of progression
• amount of microbial deposits \_\_\_\_
with extent of attachment loss
• \_\_\_\_ calculus is a common finding 
• can be modified by \_\_\_\_ and
“environmental” factors such as \_\_\_\_ and or \_\_\_\_
* Opposite of aggressive form
* Used to be called adult periodontitis
A 
adults
localized
generalized
consistent
subgingival
systemic disease
smoking
emotional stress
55
Q

Chronic Periodontitis

• \_\_\_\_, calculus, severe \_\_\_\_, lots of \_\_\_\_
A

plaque
infalmamtion
bone loss

56
Q 
Chronic Periodontitis
\_\_\_\_ gingivalis 
\_\_\_\_ forsythia
\_\_\_\_
\_\_\_\_denticola

____is most important

A

porphyromonas
tannerella
Aa
treponema

PG

57
Q

Chronic Periodontitis
Porphyromonas gingivalis

  1. ____ coccobacillus
  2. ____
  3. ____
  4. Non-____
A

gram-negative
obligate anaerobe
encapsulated
motile

58
Q

Virulence Factors of
Porphyromas gingivalis

* \_\_\_\_, same effects produced by AA
* \_\_\_\_
* Enzymes that degrade \_\_\_\_
* \_\_\_\_
A

endotoxin
colonization
ECM
cytotoxins

59
Q

Suspected Periodontal Pathogens: Consensus from culture-, DNA hybridization- and PCR- based approaches

* Red complex.- \_\_\_\_, \_\_\_\_, and \_\_\_\_
* Consensus - bugs that are thought ot be most important, \_\_\_\_ and \_\_\_\_
* Other relevants, important in secondary manner
* \_\_\_\_ viruses may be important in periodontitis… DEBATABLE
A

PG
tannerella forsythia
treponema denticola

herpes

60
Q

16S rRNA

• Much of everything we learned up to now are odler tehcniques
• State of art - utilizing primers that recognize 16S rRNA in species
• Sequences, analzye and compare genomes - identify organisms we know, and name organisms we don't even know
• Tells you everything that's there in the mouth…
• Comparing plaque from individual with perio and healthy
	○ Presence of different organisms and abundance
	○ A stark difference in composition of plaque between the two

Bacteria detected in subgingival plaque associated with disease:

  • Treponema socranskii
  • Filifactor alocis
  • Peptostreptococcus stomatis - Megasphaera spp.
  • Selenomonas spp.
  • Synergistetes spp.
  • MT7(Saccharibacteria)
  • Others

It is not know whether these organisms play an ____ role in the disease or are thriving in the environment resulting from ____ and/or ____ degradation.

A

active
inflammation
tissue

OMC I, Module II (8 decks)

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