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infection and immunity > periodontal diseases > Flashcards

periodontal diseases Flashcards

1
Q

Gingival health:

A

Plaque reduction → Reduced inflammation → Low gingival crevicular fluid flow, high redox → Mostly G+ bacteria facultative anaerobes

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2
Q

Gingivitis:

A

Plaque accumulation → Increased inflammation → High gingival crevicular fluid flow, low redox → Mostly G- bacteria obligate anaerobes

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3
Q

What bacteria dominate in periodontal health?

A

Gram-positive cocci

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4
Q

What bacteria species dominate in periodontal health? (SONVV)

A
  • Streptococcus sanguis
  • Streptococcus oralis
  • Actinomyces naeslundii
  • Actinomyces viscosus
  • Veillonella spp
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5
Q

Are there a few spirochetes or motile rods in periodontal health?

A

Yes

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6
Q

What percentage of cells are gram-positive in chronic gingivitis?

A

About 55%.

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7
Q

Are spirochetes present in gingivitis?

A

Yes, but only occasionally.

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8
Q

What bacteria are common in chronic gingivitis? (SMNIICFV)

A
  • Streptococcus sanguinis
  • Streptococcus milleri
  • Actinomyces naeslundii
  • Actinomyces israelli
  • Prevotella intermedia
  • Capnocytophaga spp
  • Fusobacterium nucleatum
  • Veillonella spp
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9
Q

What triggers the inflammatory response in the crevice?

A

Natural plaque accumulation.

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10
Q

What does increased GCF flow provide?

A

Host molecules for Gram-negative anaerobes to catabolize.

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11
Q

What happens to healthy crevice species during disease progression?

A

Gram-negative anaerobes suppress Gram-positive facultative anaerobes, causing a population shift.

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12
Q

What causes tissue destruction in periodontal disease?

A

Virulence factors from periodontopathic flora.

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13
Q

What do periodontopathic flora produce during disease?

A

Virulence factors that overwhelm host defenses.

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14
Q

What is the result of virulence factor production?

A

Episodic tissue destruction and disease activity.

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15
Q

What is the Keystone Pathogen Hypothesis?

A

Low-abundance microbes like P. gingivalis trigger periodontitis.

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16
Q

How does P. gingivalis cause periodontal disease?

A

By altering the composition and increasing the quantity of normal oral microflora.

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17
Q

Gram-Positive: Facultative (MSV)

A

Streptococcus mutans
Streptococcus sanguinis
Actinomyces viscosus

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18
Q

Gram-Negative: Facultative (ACEC)

A

Aggregatibacter (Actinobacillus) actinomycetemcomitans
Capnocytophaga species
Eikenella corrodens

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19
Q

Gram-Negative: Anaerobic (PGFPITFC)

A

Porphyromonas gingivalis
Fusobacterium nucleatum
Prevotella intermedia
Tannerella forsythia
Campylobacter rectus

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20
Q

Spirochetes: Anaerobic

A

Treponema denticola
(Other Treponema species)

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21
Q

What happens in the initial lesion of gingivitis?

A

Within 4 days of plaque accumulation: GCF and PMNLs in the junctional epithelium with no clinical changes.

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22
Q

What occurs in the early lesion stage of gingivitis?

A

After 7 days:
- Lymphocyte infiltration
- clinically evident inflammation.

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23
Q

What defines the established lesion in gingivitis?

A
  • B cells and neutrophil predominance
  • leading to periodontal pocket formation if untreated.
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24
Q

What bacteria dominate in the initial lesion of gingivitis?

A

Gram-positive and facultative bacteria (e.g., streptococci).

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25
Q

What bacteria increase in the early lesion of gingivitis?

A

Actinomyces spp.
Capnocytophaga spp.
obligate anaerobic Gram-negative bacteria.

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26
Q

What bacteria dominate in the established lesion of gingivitis?

A

Black-pigmented bacteria:
- Porphyromonas gingivalis
- Prevotella intermedia

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27
Q

What causes the increase of black-pigmented bacteria in established lesions?

A

Increased bleeding.

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28
Q

How long can chronic marginal gingivitis persist?

A

10 yrs

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29
Q

Periodontitis-Predisposing Conditions neutrophil-based disorders:

A
  • Diabetes mellitus
  • Downs syndrome
  • Chediak-Higashi syndrome
  • Cyclic neutropenia
  • Drug-induced agranulocytosis
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30
Q

Does periodontal diseases Usually develops from preexisting gingivitis?

A

Yes But NOT ALL cases of gingivitis lead to periodontitis

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31
Q

Two main groups of periodontal diseases

A

Chronic periodontitis (the most prevalent form)
Aggressive periodontitis (localized or generalized)

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32
Q

What percentage of bacteria in chronic periodontitis are gram-negative?

A

About 75% (90% are strict anaerobes).

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33
Q

What types of bacteria are prominent in chronic periodontitis?

A

Motile rods and spirochetes.

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34
Q

Name some key bacteria involved in chronic periodontitis. (PGPIFTFAASCS)

A
  • Porphyromonas gingivalis
  • Prevotella intermedia
  • Fusobacterium nucleatum
  • Tannerella forsythia
  • Actinobacillus actinomycetemcomitans
  • Selenomonas spp
  • Capnocytophaga spp
  • Spirochetes
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35
Q

What percentage of bacteria in aggressive periodontitis are gram-negative bacilli?

A

About 65-75%.

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36
Q

How many spirochetes or motile rods are present in aggressive periodontitis?

A

Few spirochetes or motile rods.

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37
Q

What factors may be associated with aggressive periodontitis?

A

Cellular immune or genetic defects.

38
Q

Name some key bacteria involved in aggressive periodontitis. (AACPGPI)

A
  • Actinobacillus actinomycetemcomitans
  • Capnocytophaga spp
  • Porphyromonas gingivalis
  • Prevotella intermedia.
39
Q

Name some gram-negative bacteria in chronic periodontitis. (TFFPGPLCT)

A
  • T. forsythia
  • F. nucleatum
  • P. gingivalis
  • Prevotella loescheii
  • Campylobacter rectus
  • Treponema spp.
40
Q

What type of environment is ideal for bacteria in periodontal pockets?

A
  • Anaerobic
  • basic pH (shift from 7.4 to 7.8)
  • protein-rich fluid.
41
Q

What virulence factors are produced by bacteria in aggressive periodontitis?

A

Proteases and cytotoxins.

42
Q

What are the Host defense factors in aggressive periodontitis?

A

polymorphonuclear leukocytes (PMNLs) - AKA a bunch of neutrophils that are polymorphic

43
Q

How do PMNL numbers differ in healthy vs. active disease?

A

Healthy = low numbers
Active Disease = high numbers.

44
Q

What happens to neutrophils during active disease?

A
  • Neutrophil autolysis occurs
  • releasing lysosomal enzymes like collagenase, which can damage tissue.
45
Q

How do neutrophils combat bacteria in aggressive periodontitis?

A

Through proteolytic and hydrolytic enzymes, and cell-derived agents like hydrogen peroxide and lactic acid.

46
Q

What types of antibodies are elevated in aggressive periodontitis?

A

IgG, IgA, IgM from B cells.

47
Q

What cytokines are elevated in aggressive periodontitis?

A

Elevated cytokines from T cells.

48
Q

How can elevated antibodies protect the host in aggressive periodontitis?

A

Antibodies bind to periodontal pathogens and promote their killing.

49
Q

How can elevated antibodies be damaging in aggressive periodontitis?

A

They can cause hypersensitivity to host tissues, leading to further damage and disease progression.

50
Q

Specific host factors of aggressive periodontitis

A
  • b and t lymphocytes
  • antibodies (IgG, IgA, IgM)
  • proteases
  • lysozyme
  • lactoferrin
  • oral cleaning mechanisms
51
Q

NON Specific host factors of aggressive periodontitis

A
  • PMNLs
  • Macrophages
  • Complement system
  • salivary bacterial inhibtory substances
52
Q

How can periodontitis be characterized in relation to the immune system?

A

As a disruption of homeostasis, allowing infectious and inflammatory conditions to progress destructively.

53
Q

What type of bacteria are associated with periodontitis?

A

Inflammophilic bacteria, which are evolved to endure and take advantage of inflammation.

54
Q

How does inflammation help periodontitis-associated bacteria?

A

Inflammation provides tissue breakdown products like collagen peptides and heme (iron compounds) as nutrients.

55
Q

attachment to host tissue

A

fimbrae

56
Q

evasion of host defenses

A
  • capsule
  • neutrophil receptor blockers
57
Q

direct tissue damage

A

collagenase

58
Q

indirect tissue damage

A

prostaglandins

59
Q

“Red Complex” Bacteria

A

Porphyromonas gingivalis
Tannerella forsythia
Treponema denticola

60
Q

In what percentage of subgingival plaque samples is P. gingivalis found in chronic periodontal disease?

A

More than 85%.

61
Q

Where else can P. gingivalis be found in the body?

A
  • Liver or joint after it has already invaded the oral cavity
  • Detected in brains of patients with Alzheimer’s disease
62
Q

What unique enzyme does P. gingivalis produce?

A

Peptidylarginine deiminase (PPAD).

63
Q

What is the function of PPAD in P. gingivalis?

A

It alters protein structure and function, aiding in biofilm growth and colonization.

64
Q

What type of bacterium is P. gingivalis?

A

Gram-negative, strict anaerobe.

65
Q

What type of metabolism does P. gingivalis use?

A

Asaccharolytic, meaning it doesn’t rely on sugars for energy.

66
Q

What essential element does P. gingivalis require for survival?

A

Iron

67
Q

Where does P. gingivalis colonize in the mouth?

A

It reaches the sulcus/pocket, where it is a late colonizer.

68
Q

How does P. gingivalis survive in biofilm?

A

It relies on other species to reduce oxygen levels.

69
Q

Where does P. gingivalis reside in the mouth?

A

On the root surface, in Gingival Crevicular Fluid (GCF), and on the surface of gingival epithelial cells.

70
Q

Is P. gingivalis present in patients with or without periodontal disease?

A

Yes, it can be found in both cases.

71
Q

What other areas can P. gingivalis be found in the mouth?

A

Tonsillar area, tongue, and buccal mucosa.

72
Q

What are the lipopolysaccharide mode of actions?

A

Endotoxic activity
- stimulates host
- inflammatory response
- significant immunological activity
- antiphagocytic activity

73
Q

Fimbriae(virulence factor of p.gingivalis mode of action?

A

adhesions and invasion to epithelial cells

74
Q

Why is P. gingivalis extensively studied?

A

Due to its ability to infect distant tissues and organs in many systemic diseases beyond periodontal disease.

75
Q

How is P. gingivalis cultured in the lab?

A

It is easily grown and can be genetically manipulated.

76
Q

What is a key feature of P. gingivalis colonies?

A

It forms dark purple-black pigmented colonies on blood agar plates.

77
Q

Disease initiation and progression of periodontitis

A
  • Plaque close to gingival margin
  • Host defenses overcome
    Gingival inflammation (gingivitis)
  • Periodontal inflammation and attachment loss (periodontitis)
78
Q

Multifactorial disease of periodontal

A
  • Host factors
  • Microbial factors
79
Q

Gingiva cells

A

consists of stratified squamous epithelium; based on function and morphology is divided into three parts including oral or outer, sulcular and junctional epithelium

80
Q

Periodontal ligament and root cementum cells

A

consists of several different cell types including fibroblasts, cementoclasts/blasts and osteoclasts

81
Q

Alveolar bone cells

A

consist of several different cell types including osteoblasts and osteoclasts

82
Q

Cementoblasts

A

produce organic matrix of cementum while cementoclasts are responsible for the breakdown of cementum

83
Q

Osteoclast

A

multinucleated cells that degrade and reabsorbs bone; involved in the turnover of bone along with osteoblasts

84
Q

Fibroblasts

A

involved in collagen turnover since these cells produce new collagen and destroy “old” collagen

85
Q

Osteoblasts

A

produce organic matrix of bone

86
Q

Host Immune System in Periodontitis

A

Periodontal bacteria induce host inflammatory responses that cause damage to host tissues

87
Q

What type of infection is a periapical abscess?

A

A polymicrobial (endogenous) infection, involving a mixture of 3 or 4 different species.

88
Q

What type of bacteria are predominant in periapical abscesses?

A

Strict anaerobes

89
Q

What type of microbial interactions are important in the severity of periapical abscesses?

A

Synergistic microbial interactions.

90
Q

Facultative anaerobes in periapical abscesses

A

Streptococcus milleri
Streptococcus sanguis
Actinomyces spp.

infection and immunity (11 decks)

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