Exam 2 Flashcards

1
Q

what are the 5 methods of measuring gingivitis/periodontitis?

A

plaque index

gingival index

probing depth/pocket depth

gingival cervicular fluid

bleeding on probing

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2
Q

what is plaque index?

A

a measure of accumulated dental plaque on different surfaces of teeth, usually a score is calculated for an individual tooth

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3
Q

what is gingival index?

A

a measure is calculated for an individual tooth, using redness as an indicator of inflammation

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4
Q

what is probing depth/pocket depth?

A

increased depth is indicative of attachment loss, specifically referring to the PDL

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5
Q

what is gingival cervicular fluid?

A

an inflammatory exudate derived from periodontal tissues, composed of serum and locally generated materials such as inflammatory mediators and antibodies directed against dental plaque bacteria

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6
Q

what is bleeding on probing?

A

results from dilation, engorgement, and thinning of the epithelium, rupture more easily

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7
Q

what are the most subjective measures for gingivitis status?

A

plaque index

gingival index

probing depth

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8
Q

what are the best measures for gingivitis status?

A

bleeding on probing

gingival cervical fluid volume

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9
Q

What are the 3 major differences between Plaque Induced Gingivitis and Periodontitis?

A

1) there is no alveolar bone loss associated with gingivitis
2) here is no attachment loss of the PDL with gingivitis
3) gingivitis is reversible, unlike periodontitis

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10
Q

Can someone have attachment and or bone loss and still have gingivitis? If so under what condition?

A

you can have gingivitis associated with a site that has had previous bone or attachment loss but is not progressing

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11
Q

What type of bacteria benefit from primary colonizers and the increasing reduced environment of the developing biofilm (decreasing oxygen)?

A

Gram negative bacteria – facultative rod bacteria

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12
Q

1) Outline the Loe et al experiement:
2) What were the main results?
3) What was a limitation/caveat?

A

1)

  • Stopped oral hygiene (whole mouth) until inflammation was achieved (14-21 Days
  • Resumed brushing and interdental gingival massage until baseline measures were obtained
  • Bacterial assessment were obtained through impressions and using bacterial smears
  • Beginning of non-brushing period was associated with increases cocci bacteria
  • Days later filamentous and rod associated bacteria were overserved along with large amounts of cocci.
  • Near peak inflammation vibrios and spirochetes and some cocci were detected
  • in health, commensal organisms were gram positive cocci bacteria (like strep species)

2)

  • Plaque maturation produced changes in the environment that allowed new species of bacteria to grow
  • Accumulation of plaque was the cause of gingival inflammation

3)

  • Staining is not indicative of specific species, just types of bacteria
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13
Q

what were the major points of the Soc. et al 1998 study?

1) what had been already established?
2) what technique was developed?
3) result?
4) what was the caveat of this study?

A

1) It had been established that microbe complexes exist in subgingival plaque and were associated with varying levels of gingival health/diseases severity

2)

  • Socransky et al. developed a technique “Checkboard” DNADNA Hybridization in order to identify and classify microbial complexes associated with gingival health and disease
  • Use Specific digoxigenin-labeled whole genomic probes or 16S rRNA-based oligonucleotide probes directly conjugated to alkaline phosphatase (turns black when released – bound probe).

3) 5 major bacterial complexes associated with clinical measures

4) Caveat: Only probes for 43 different taxa were used and varied between Genus and Species from subjects with periodontitis

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14
Q

these two studies are foundational in gingival health and disease research. What evidence in your lecture suggests that they may be out of date?

A

they are older studies? (1965 and 1998)

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15
Q

What are the major shifts in types of bacteria from Healthy to Gingivitis?

A

as the biofilm matures the redox potential of the environment decreases

–> favors the growth of anaerobic and facultative bacteria species

–> increase in gram negative bacteria

–> emergence of gram negative facultative rod bacteria

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16
Q

What is significant about microbial complexes defined by Sorcransky?

1) What is the Orange complex associated with?
2) What is the Red Complex associated with?

A

1) orange = associated with gingivitis (more like red complex, but differenct clinical measures (BOP, PD))
2) red = associated with periodontitis

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17
Q

Is the epidemiology of gingivitis well established? Why or Why not?

A

Periodontal epidemiology is deficient

Most conditions are lumped together, as explained with the different types of gingivitis

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18
Q

describe gingivitis

A

reversible inflammation in the marginal periodontal tissues

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19
Q

decribe chronic periodontitis

A

severity of disease consistent with plaque and calculus. Slow to moderate progression of tissue destruction. Aggravated by systemic conditions (i.e. diabetes) or environmental factors (i.e. smoking).

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20
Q

describe necrotizing periodontal diseases

A

“Trench mouth”

painful condition with a fusospirochaetal etiology

different from other periodontitis because of PAIN

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21
Q

Describe the Koch’s Postulates and its limitations within the periodontal diseases.

A

1) The suspected pathogenic organism should be present in all casesof the disease and absent in healthy animals.
* Some perio pathogens present in healthy individuals and sites
2) The microorganism must be isolated from a diseased organism and grown in pure culture.
* Most oral species are fastidious and are difficult to isolate and cultivate in lab (i.e. Treponema)
3) The cultured microorganism should cause disease when introduced into a healthy organism.
* Lack of good animal model systems for perio

​4) The microorganism must be reisolated from infected host and shown to be the same as the original

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22
Q

describe specific plaque hypothesis

can be used to explain?

A

Pathogenicity of plaque depends on the presence of, or relative increase of, specific microorganisms

  • Not all plaque bacteria are equally pathogenic
  • Can be used to explain A. actinomycetemcomitans in localized aggressive periodontitis
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23
Q

describe non specific plaque hypothesis

A

Non-specific: Periodontitis caused by dental plaque as a whole, accumulating over time on the teeth.

  • All plaque bacteria equally capable of causing disease
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24
Q

describe ecological plaque hyposthesis

A

Ecological: Disease is a result of an imbalance in the total microbiome due to ecological stress, resulting in an enrichment of disease-related microorganisms

  • Consistent with specific plaque hypothesis in recognizing that different plaque bacteria have varying pathogenic potentials
  • Focused on ecological perturbation and emphasizes the microbiome as a whole
  • Disease can be prevented by targeting the putative pathogens and also by interfering with the environmental factors
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25
Q

Define keystone pathogen and its significance in disease progression. (Be prepared to provide examples).

A

keystone pathogen: a low abundance species which can disproportionately modulate the host response

  • When bacteria acts independently, it has little impact on the host
  • Overtime, bacteria assemble into heterotypic communities –> some cause disease, others don’t (can be pro inflammatory and produce toxic components), growth controlled by the host
  • If host is infected with keystone pathogen, it can disrupt the community –> becomes pathogenic (dysregulation of immune surveillance, altered composition and total counts, increased expression of virulence factors, overgrowth of pathobionts, disruption of tissue homeostasis)
  • Examples:
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26
Q

Understand the concept of homeostasis and dysbiosis in relation to health and disease

A

Combined synergy and dysbiosis is more severe than the sum of the individual species acting alone

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27
Q

what are the 5 common mechanisms of pathogenesis?

A

1) colonization and adhesion
2) invasion
3) enzymes
4) toxins and cell constituents
5) subversion of host immunity

28
Q

describe colonization and adhesion:

1) define colonization and what is used for it
2) define adhesion, auto aggregation, and co-aggregation

A

1) Colonization: Adherence to other bacteria or to host tissue cells

  • FimA fimbriae important for biofilm/binding onto things

2) Adhesion: mediated by protein adhesions on the outer membrane of bacteria

  • Auto-aggregation: cell to cell recognition and binding by selfrecognizing surface structures
  • Co-aggregation: cell to cell recognition of genetically distint microbial partners
29
Q

what are the 2 methofs of invasion? Define them and their details

A

1) By ruffling: direct uptake into otherwise non-phagocytic gingival epithelial cells

  • Examples: porphyromonas gingivalis (Pg), aggregatibacter actinomycetemcomitans (Aa)

2) By zipping of gingival epithelial cells by F, Nucleatum:

  • Attaches to the epithelial cell via FadA adhesion binding
  • Then uses “zipping” entry mechanism: direct contact between bacterial ligands and host cell receptors, which encircle the bacteria as a vacuole
30
Q

enzymes/proteases can degrade: (mechanism of pathogenesis)

A
  • Proteins
  • Iron and hemin sequestering molecules
  • Immune effector molecules
  • Structural components of tissue
  • Antimicrobial peptides
  • Ex: P. gingivalis protease gingipains
31
Q

mechanisms of pathogenesis: Toxins and cell constituents:

A.a makes what 2 toxins?

how do these work/details?

A

Aa produces leukotoxin, which kills human neutrophils and monocytes by causing pore formation in cell membranes and by inducing apoptosis

  • These leukotoxins can be packaged in vesicles which penetrate into tissues

Cytolethal distending toxin (Cdt)

  • A-B toxin – affect internal cell function, A=active, B=binding
  • DNase that induces cell cycle arrest, cytoplasmic distension, and sometimes followed by apoptosis
  • Activity against epithelial cells, fibroblasts, and lymphocytes
  • Aa strains that possess the cdt operon are more frequently isolated from patients diagnosed with LAP
32
Q

All, enrichment of specific pathogenic bacteria - what hypothesis?

A

ecological plaque hypothesis

33
Q

specific bacteria - what hypothesis?

A

specific plaque hypothsis

34
Q

all- what hypothesis?

A

traditional non specific plaque hypothesis

35
Q

specific bacteria and surrounding community - what hypothesis?

A

keystone

36
Q

all, difference in virulence - what hypothesis?

A

updated, non specific plaque hypothesis

37
Q

mechanisms of pathogenesis: Toxins and cell constituents:

What are other cell constituents besides toxins that bacteira use for pathogenesis?

A

LPS/Lipid A

  • these interact with monocytes/macrophages via TLR4 to induce production of cytokines and inflammatory mediators
38
Q

mechanisms of pathogenesis: Subversion of host immunity (P. gingivalis)

what are the 3 mechanisms and characteristics, and what do they all lead to?

A

1) Inhibit IL-8/chemokine paralysis:
* Neutrophils follow IL-8 gradient to site of infection –> Pg secretes SerB which inactivates NF kappa B –> no IL8 transcription –> no gradient –> neutrophils do not go to bacteria
2) Complement subversion:
3) TLR4 antagonism:

  • TLR4 recognizes LPS of gram – bacteria
  • P. gingivalis has many Lipid A structures –> some antagonize/turn off host inflammatory response vis turning off TLR4 –> LPS not recognized

these all lead to impaired host defense

39
Q

Describe “Ruffling” and identify the pathogens capable of this technique.

A

ruffling: direct uptake into otherwise non-phagocytic gingival epithelial cells

  • Examples: porphyromonas gingivalis (Pg), aggregatibacter actinomycetemcomitans (Aa)
40
Q

Describe the “Zipping” mechanism, the proteins involved, and the oral bacteria that does this.

A

zipping of gingival epithelial cells by F, Nucleatum:

  • Attaches to the epithelial cell via FadA adhesion binding
  • Then uses “zipping” entry mechanism: direct contact between bacterial ligands and host cell receptors, which encircle the bacteria as a vacuole
41
Q

define antagonisms

A

dampens host immune response, off switch, turns off inflammatory response

42
Q

define agonism

A

activation

43
Q

what are the unique characteristics of P. gingivalis LPS?

A

LPS is specific to gram – bacteria

Lipid A is a component of LPS

Interacts with different monocytes/macrophages via TLR4 (sole job is to recognize LPS) to induce production of cytokines and inflammatory mediators (gram – bacteria have LPS –> agitates host cells to cause inflammation)

44
Q

Provide at least two examples of the link between oral and systemic health/disease

A
  • 1) Perio and atherosclerosis – oral bacteria can be found inside the athero plaques in patients with periodontitis , bacteria in mouth get into blood stream –> activate endothelial cells and macrophages  cause plaque
  • 2) Perio and diabetes – periodontitis could have negative effect on glycemic control, inflammation is a central feature of the pathogenesis of diabetes and periodontitis
  • 3) Periodontitis and adverse pregnancy outcomes
  • 4) Perio and cancer – increase in overall cancer rates for patients with perio disease, oral cancer
  • 5) F nucleatum infection is prevalent in colorectal cancer
45
Q

summary of perio and systemic disease:

A

low grade bacteremia; spread/infection of oral bacteria to other tissues

increase in inflammatory burden systemically

autoimmune responses triggered by bacterial products

46
Q

Broadly describe protein signaling cascade that occurs after receptor binding and its final products within host cells

A
47
Q

why is type 2 diabetes related to periodontitis?

A

diabetic state induces inflammation

inflammation causes increased insulin resistance

48
Q

what 2 bacteria havwe a combined syndergy and dysbiosis that is more severe than the sum of the individual species acting alone?

A

Tannerella forsythia and fusobacterium nucleatum

49
Q

what pathogens are in the red complex?

A

P gingivalis

T forsynthis

T denticola

50
Q

Etiology of P. gingivitis

early gingivitis is more influenced by _______ which allows for ______

plaque indiced gingival disease is the result of:

A

supragingival plaque accumulation along the gingival margin which allows for a dysbiotic shift and colonization of the subgingival pocket

an interaction between the microorganisms found in the dental plaque biofilm and the tissues and inflammatory cells of the host

51
Q

Know health dynamics and disease imbalance with respect to cytokine expression

A

In disease there is an increase in cytokine expression// production

IL-1B and TNFa increase RANKL –> get more loss, increase in neutrophils

52
Q

What is a neutrophil and what is/are its functions?

A

It is a white blood cell, it engulfs and destroys bacteria and other pathogens

Active in initial stages of infection

Important in clearing bacterial infections

Direct actions against bacteria

53
Q

What is gingival crevicular fluid (GCF) and what is its role in health? e.g. what does it do for commensal bacteria and what does it due to potential invaders?

A

Its an inflammatory exudate from the periodontal tissues

flow of this fluid removes microbes, provides nutrition

54
Q

What are some of the ways you can increase GCF production? (Do any seem surprising?)

A

GCF production is NOT increased by trauma from occlusion

Mastication of course foods, tooth brushing and gingival massage, ovulation, hormonal contraceptives, smoking –> surprising because smoking shrinks blood vessels so you would think less plasma would be coming out

55
Q

What is the major host response factor in GCF?

A

inflammation

56
Q

What is the pattern recognition hypothesis?

A

The immune system evolved to discriminate infectious non-self from noninfectious self

57
Q

What is the role of lipopolysaccharide (LPS), lipoteichoic acid (LTA), and Peptidoglycan in pattern recognition?

A

It triggers bacterial recognition by the innate host response system

58
Q

Know which Gram + and Gram – have LPS, LTA, and Peptidoglycan

A

Gram Positive = LTA, peptidoglycan (thicker)

Gram Negative = LPS, peptidoglycan

59
Q

Know which Toll-like receptor recognizes LPS, LTA, and Peptidoglycan

TLR-2 =

TLR-4 =

A

TLR-2 = peptidoglycan, LTA

TLR-4 = LPS

60
Q

Know the difference between germ free mice and conventional (healthy) mice and how it affects the mucus layer. How does this impact health in relation to the microbiome?

A

Germ free = no microbes

conventional = has bacteria/microbes

Mucous layer is less vascularized/smaller capillary system in germ free, mucous layer is also smaller

61
Q

What chemokine is essential for neutrophil migration into periodontal tissue?

A

IL-8

62
Q

what are the 4 periodontal diseases?

delineation between _____ and _____ periodontitis has been eliminated

A
  • chronic
  • aggressive
  • necrotizing
  • system associated

agressive abd chronic

63
Q

P. gingivalis adhesions (3)

A

FimA (colonization)

Mfa1

hemagglutinins

64
Q

A. a Adhesion

A

Flp1

65
Q

F. nucleatum adhesions (3)

A

FadA (zipping)

FomA

RadA

66
Q

T. forsythia Adhesion

A

BspA