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Oral Microbiology > Lecture # 11-12 Opportunust oral pathogens & the Immunobiology of Perio > Flashcards

Lecture # 11-12 Opportunust oral pathogens & the Immunobiology of Perio Flashcards

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1
Q

What are the major risk factors of PERIODONTAL DISEASE?

A

1) Tobacco use
2) Some systemic diseases (diabetes)
3) medications (many)
4) crooked teeth, ill fitting bridges
5) pregnancy
6) infected w. more pathogenic bacteria (red complex: P. gingivalis, T. forsythia, T. Denticola)
7) Hereditary approx. 1/3 population at increased risk
8) Age
9) Poverty

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2
Q

What is periodontitis?

A

A plaque-induced inflammation of gingival tissues that results in destruction of the periodontal ligament, loss of alveolar bone, and migration of the junctional epithelium.

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3
Q

Is periodontitis a reversible or irreversible process?

A

IRREVERSIBLE

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4
Q

What does active periodontal disease cause?

A

Destruction of tooth attachment leading to periodontal pocket formation; loss of collagen attachment fibers and loss of collagen attachment fibers & loss of alveolar bone that persists after the active disease process has stopped.

Note: Hard to MEASURE b/c it goes inactive.

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5
Q

What does attachment loss mean in periodontitis?

A

Attachment does NOT indicate if disease is ongoing or occurred earlier, with loss being a combination of SLOW GRADUAL and/or burst of more rapid activity

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6
Q

More severe periodontistis occurs only in what?

A

A minority of the population more commonly in older individuals.

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7
Q

Most periodontist is due to what?

A

Due to loss over a lifetime becoming more obvious and easier to MEASURE in older individuals

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8
Q

What factor plays a major role ?

A

Genetic (up to 18x over “normal” patients)

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9
Q

_____________ defects are commonly associated w/ rapid disease in patients that are younger than 10 yrs old.

A

Neutrophil

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10
Q

What dramatically exacerbates the development of periodontitis ?

A

-Smoking increases the likelihood ~ 4x over non-smokers

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11
Q

Why is the mechanism of active periodontitis not clear?

A

1) Bacterial products alone cam directly cause tissue damage
2) host inflammatory factors induced by bacteria can cause host tissue damage
3) Too many bacteria factors or FEW HOST defense factors could destroy balance leading to attachment loss
4) Non of the currently described bacteria appear to be a single direct cause of perio disease. (DOES NOT FULFILL KOCH’s postulates)

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12
Q

Peridontitis could be the result of what mechanisms?

A

Result of a VARIETY of DISEASE MECHANISMS

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13
Q

In adult periodontitis the most common suspected pathogens are present in?

A

Small proportions of the active lesions

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14
Q

Unique combinations of organisms along with ______ ______ may lead to disease.

A

Malfunctioning immunity

***This is the MOST popular idea

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15
Q

In HIV patients who are immunosuppresed, does the causative agents in perio patho occur in all of the active lesions?

A

No, which makes it difficult to pin-point the exact causes.

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16
Q

What two causes lead to host tissue damage ?

A

1) Inflammatory host processes and immune hypersensitivity mechanisms I-IV
2) Bacteria can damage tissue via many distinct mechanisms

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17
Q

What are the 3 major hypotheses for perio disease?

A

1) A specific bacterium
2) Specific mechanism, multiple bacteria
3) Multiple mechanisms, multiple bacteria

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18
Q

What is the nonspecific Plaque Hypothesis and the Specific Plaque Hypothesis ?

A

1) Nonspecific Plaque Hypothesis:
All plaque is BAD. Small amounts of plaque are neutralized by host. Large amounts of plaque produce disease. Plaque control is treatment. Much clinical treatment is still based on this THEORY.

2) Specific Plaque Hypothesis:
Only certain plaque is pathogenic. CERTAIN Bacteria within the plaque produce MORE substances that cause the destruction pf periodontal tissues

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19
Q

What are the major suspected periodontal pathogens, proposed by countless experiments (following Socransky’s Modified Postulates) ?

A

1) Prophyromonas gingivalis (inactive lesions)
2) Tannerella forsythia
3) Treponema denticola
4) Prevotella intermedia (inactive lesion)
5) Aggregatibacter actinomycetemcomitans (both in active and inactive lesions)

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20
Q

what is the mechanism behind the most popular hypothesis (#3) ?

A
  • Damaging microbe products
  • Defense inhibitors
  • Inflammatory agents
  • Type I-IV immune hypersensitivity
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21
Q

What is the Damaging microbe products for perio disease?

A
  • Exoenzymes
  • Exotoxins
  • Toxic metabolites
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22
Q

What is the Defense inhibitors for perio disease?

A

-DECREASE PMN Migration
-DECREASE T/B Function
-

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23
Q

What is the Inflammatory agents for perio disease?

A
  • LPS massive potential

- Wall lipids

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24
Q

What is the Type I-IV immune hypersensitivity for perio disease?

A
  • Ag = ?

- Ag-Ab complexes

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25
Q

Which bacteria are apart of the “RED COMPLEX”

A

1) Prophyromonas gingivalis
2) T. Denticola
3) T. a forsythia

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26
Q

In a healthy condition which species of bacteria are mostly present in perio disease?

A

-Gram (+) cocci and rods
w/ FEW spirochaetes or motile gram (-) rods

Ex: S. sanguis

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27
Q

In the “chronic gingivitis” condition which species of bacteria are mostly present in perio disease?

A

-55% Gram (+) w/ occasional spirochaetes & gram (-) motile rods

Ex: A. israeli, S. sanguis, Prevotella intermedia

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28
Q

In the “chronic periodontitis” condition which species of bacteria are mostly present in perio disease?

A

-75% gram (-) (90% ANAEROBES). Motile rods & spirochaetes are prominent

Ex: Tannerella forsynthia

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29
Q

In the “AGGRESSIVE periodontitis” condition which species of bacteria are mostly present in perio disease?

A

-70% Gram (-) rods. FEW spirochaetes or mobile rods.
Associated w/ IMMUNE or GENETIC defects

Ex: Prevotella intermedia

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30
Q

Which 2 Perio Pathogens are best studied?

A

1) A. actinomycetemcomitans

2) P. Gingivalis

31
Q

Aggregatibacter actinomycetemcomitans

  • Gram + or -
  • Metabolism?
  • Oxygen requirement
  • Catalase + or -
  • pH?
  • Sugar metabolism?
  • Growth w/ steroids?
A
  • GRAM - ROD
  • CAPNOPHILIC (CO2)
  • FACULTATIVE (ANAEROBE)
  • Catalase +
  • pH= 7-8, 7.5* (inflamed pocket = 8!)
  • SACCHAROLYTIC
  • INCREASE Growth w/ steroid hormones
32
Q

What is the major virulence factors for Aggregatibacter actinomycetemcomitans ?

A

1) Fimbrae bind

2) LPS Vesicles (BLEBS)

33
Q

What does the FIMBRAE BIND include for Aggregatibacter actinomycetemcomitans ??

A

1) Epithelial cells
2) Matrix protein
3) Salivary proteins
4) F. nucleatum

34
Q

What does the LPS Vesicles include for Aggregatibacter actinomycetemcomitans ??

A

1) LPS activates MACROPHAGES
* 2) Filled with LEUKOTOXIN = PORE PROTEIN (** “CYTOTOXIC EXOTOXIN “ for PMNs & Macrophages)
3) Bone resorption STIM. PROTEIN —> STIM Osteoclasts

35
Q

_________of Aggressive adult periodontitis is associated with A. a

_______________ of Aggressive Juvenile periodontitis is associated w/ A.a

A
  • 30-50%

- 90%

36
Q

What is the effect of the LPS blebs that are released by A. a (virulence factor) ?

A

Can diffuse throughout gingival tissue and induce significant pathology by activating inflammatory response

37
Q

Porphymonas Gingivalis:

  • Gram + or -
  • Metabolism?
  • Oxygen requirement
  • pH?
  • Sugar metabolism?
A
  • GRAM (-) ROD
  • ANAEROBIC
  • NEEDS HEMIN ***
  • pH = 7.5- 8.5 (higher than A.a)
  • ASACCHAROLYTIC (unlike A.a)
38
Q

What are the MAJOR Virulence Factors for Porphymonas Gingivalis:

A

1) CHO Capsule
2) Fimbrae
3) Secretes many Enzymes (proteases)
4) LPS
5) Toxic Products
6) LPS Blebs

39
Q

What does the CHO CAPSULE, virulence Factor for Porphymonas Gingivalis involve?

A

-Multiple Ag types (Ab MAY NOT opsonize new strains)

40
Q

What does the FIMBRAE, virulence Factor for Porphymonas Gingivalis involve?

A
  • Binds Bacteria & Tooth
  • Bind host cells
  • DECREASE IL-8 PRODUCTION by epith.
41
Q

What does the Secreted Enzymes, virulence Factor for Porphymonas Gingivalis involve?

A
  • Ig
  • LACTOFERRIN
  • Complement
  • Collagen Matrix
  • Fibrin
42
Q

What does the LPS, virulence Factor for Porphymonas Gingivalis involve?

A
  • 100-1000X LESS inflmamtory
  • DECREASE MARGINATION
  • DECREASE TNF, IL-1 and NOxide PRODUCTION
  • May SHUT DOWN PMNs

Note: **Unique LPS exception “stealthy attack” is NOT VERY INFLAMMATORY AT ALL!
(Opposite from A.a)

43
Q

What does the Toxic Products, virulence Factor for Porphymonas Gingivalis involve?

A
  • H2S

- NH3

44
Q

Compare and contrast A.a and P.g

A
  • BOTH RARE in HEALTH
  • A.A spread among family (caregiver) at young age
  • P.G spread among ADULTS, more COMMON
  • A.A found at FEW sites of mouth
  • P.G if present, found at MOST sites of mouth
  • P.G Chronic generalized perio (GCP)
  • A.A localized AGGRESSIVE perio (LAP)
45
Q

In progressive periodontitis sire what is the % for AA and PG?

A 
AA= < 4% Flora
PG = > 25% Flora
46
Q

Both Porphyromonas Gingivalis and Prevotella Intermedia have which 2 colonization factors?

A

1) Capusles

2) Pili

47
Q

Both Porphyromonas Gingivalis and Prevotella Intermedia have which 3 Host Defense factors?

A

1) Ig A proteases
2) Ig G proteases
3) SOD (superoxide dismutase)

48
Q

PMNs are the major leukocyte to do battle w/ disease causing bacteria in the sulcus.
True or False

A

True

49
Q

PMNs major function as it is everywhere, is to remove the insult that is causing inflammation?

A

True

50
Q

A.a is mostly implicated w/ localized aggressive perio, while P.g and P.i are mostly implicated with generalized chronic perio?

A

True

51
Q

What are some of the host protective mechanisms against gram (-) bacteria?

A

1) Oral PMNs (10 ^ 10/ Day)
2) resistant to LPS toxicity
3) can function anaerobically
4) Detoxify area

52
Q

A.a has leukotoxins porins, strong LPS , anti-phagocytic capsule and is facultative?

True or False?

A

True

53
Q

P.g and P.i have enzyme proteases, WEAK LPS (blocks chemotaxis) , anti-phagocytic capsule and is Anaerobic?

A

True

54
Q

Since the sulcular ecology is unique what happens when oxygen makes it to this area?

A

-It is quickly removed by reaction with organism molecule producing an ANAEROBIC ENVIRONMENT

55
Q

What do low levels of saliva & food residue to these areas require that most of the bacteria uses what as theri substrate?

A

Proteins instead of sugar

56
Q

The slow of fluid and absence of salivary washing ___________ the role of bacterial adhesion as an important colonization factor?

A

-DECREASE

Note: Many of the organisms here are HIGHLY MOTILE

57
Q

Why is this sulcular environment more complex?

A

Because of the different surfaces available

(i.e tooth pellicle, gingival epi) & the WALL of NEUTROPHILS which migrate to this site

58
Q

__________ can remove LPS detoxifying this potent bacterially-derived inflammatory endotoxin

A

-PMNs

***MAJOR FUNCTION OF PMNs

59
Q

What increases the potential mechanisms for both immunity and host collateral damage?

A

1) Steady stream of dilute plasma exudate w/ Complement
2) Ig G antibody
3) various cytokines

60
Q

Since most of these SUBGINGIVAL flra are Gram (-) the concentration of LPS will be high RESULTING in what?

A

A massive activation of CYTOKINE PRODUCTION by Macrophages in gingiva and which activates OSTEOCLASTS causing BONE LOSS, and act on FIBROBLASTS = Collagen degradation

61
Q

What direction is the loss of attachement mechansim under?

A

Under LOCAL gingival Th cell direction

62
Q

What gives way to a final strategy of removing the inflammatory site?

A

The slow maintenance, replacement, and repair

63
Q

Losing the infected tooth will do what benefit ?

A

Lose the inflammatory insult and keep the infection from going systemic at all costs

64
Q

Some bacteria may penetrate into individual junctional epi cells and modify alert mechanisms, while other can produce __________ (e.g, A.a) and some possess __________ that doesnt alert the keratinocytes (e.g. P.g) adequately

A
  • Leukotoxins

- LPS

65
Q

What happens when a massive B-cell buildup occurs w/ increased B-cell presentation of Ag and Ab formation?

A

-Large #’s of plasma cells appear

Note: Role of b-cells is not well understood

66
Q

a switch in fibroblast function from production of collagen to the production of collagenase and PGE2 is triggered by what?

A

-Macrophage IL-1

67
Q

A switch from the repair of bone to osteoclast activation and the loss of bone is due to what ?

A

IL-1, TNF- alpha and PGE2

68
Q

A cariogenic diet high in simple sugars will select for an increase in what bacteria?

A

Increase # of supra-gingival cariogenic bacteria like S. mutans, Lactobacilli species, and Actinomyces species.
= Acids and cause Caries

69
Q

What bacteria does “unhealthy” plaque contain?

A

-Anaerobic areas (both supra- and sub gingivally) have more Gram (-) asaccharolytic (eats protein) especially Subgingival.

70
Q

Since the sub-gingival Grm (-) bacteria produce proteolytic enzymes, toxins, toxic molecules, LPS blebs and may be invasive what does this induce in the HOST RESPONSE?

A
  • Inflammation! Sends cervical fluid and PMNs thru “leaky” junctional epi to do battle w. subgingival plaque microbes.
  • B & T cells, and macrophages brought into the gingiva itself to protect the tissue form invasion. If THIS balance is tipped significantly = Attachment & bone loss –> PERIODONTAL DISEASE
71
Q

Since Periodontal disease is an inflammatory, immunologic process, the infection induces what?

A
  • Local inflammation w/ many macrophages infiltrating the underlying gingival tissues.
  • LPS and cytokines from T cells cause the macrophages to become SUPER-MACs
72
Q

What do these SUPER MACs (b/c of LPS and cytokines from T cells) do to bacteria?

A
  • Engulf bacteria and their products that entered gingival tissue.
  • DROOL destructive enzymes and oxygen radicals onto surrounding tissues.
  • Secrete inflammatory mediators & CKs

Note: IF this continues for long, attachment loss occurs

73
Q

The decoupling of the osteoblast-osteoclast activity can occur by regulating osteoclast. What happens if this goes on for long?

A

Bone structure that holds the tooth is lost and ultimately the tooth will also be lost.
*Which is the goal of inflammation anyway…. to remove the insult.

74
Q

What therapies can help eliminate or reduce the perio disease?

A
  • Reducing bacterial load = reduce imuno stimulus

- BMP( bone morph proteins) encourages osteoblast activity to help bone structure regenerate

Oral Microbiology (11 decks)

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