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PER 1001 > Periodontal Disease > Flashcards

Periodontal Disease Flashcards

1
Q

Name 1-6

A

Review This
1. Gingival Margin
2. Free gingiva
3. Ginigival groove
4. Attached gingiva
5. Mucogingival junction
6. Alveolar mucosa
7. Intern dental gingiva

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2
Q

The root of the tooth is covered by?

A

Cementum

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3
Q

Union of the cementum and enamel

A

CEJ

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4
Q

What percent of indv do cementum and enamel not meet?
What does it result in?

A

5-10%
* More sensitivity

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5
Q

Why do older people experience less sensitivity than younger?

A

tertiary dentin which is more compact and closed channels which means they have less sensitivity compared to an 18 year old.

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6
Q

below the free gingiva is where you probe 1-3mm is healthy, 3-10mm is disease

A

GIngival Sulcus

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7
Q

What is the parameter for pocket depth?

A

Gingival Margin

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8
Q

Non-keratinized tissue

A

Sulcular Epithelium

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9
Q

at the base of the sulcus and connective tissues attachment

A

Junctional Epithelium

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9
Q

Keratinized

A

Outer Epithelium

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10
Q

Characteristic of Healthy Periodontum

A
  • 10% or less bleeding
  • No bone loss
  • Attached gingiva
  • Normal Subclinical inflmmation
  • 1-3mm probing
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11
Q

WHat does this shwo?

A

Healthy periodontum, no bone loss noted

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12
Q

Inflammation and infection of gums, reversible! 1st.

A

GIngivitis

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13
Q

Bones loss, decrease in clincal attachment, gingival recession. Irreversible

A

Periodontitis

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14
Q

What are the 2 elements of periodontal diseases?

A
  1. GIngivitis
  2. Periodontitis
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15
Q

What is the most common
Periodontal disease?

A

Gingivitis associated with or without Biofilm

Intial, moderate, severe

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16
Q

What is the best peramete for periodontal disease?

A

BOP= bleeding or probing

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17
Q

What are the parameters of localized gingivitis?

A

10-30% sies with BOP

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18
Q

What are the parameters of generalized gingivitis?

A

Greater than 30%

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19
Q

Why is the 30% rule important?

A

Helps classify gingivitis to general vs localized

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20
Q

What is the etiology of Periodontal disease?

Cause

A

Dental Biofilm Bacteria

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21
Q

What was the objective of the 1965 study of gingivitis?

A

Produce gingivitis in pt. with healthy gingiva and to study the sequence of changes in the microbiota and in the gingiva

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22
Q

GI

A

Gingival Index

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23
Q

PI

A

Plaque Index

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24
Q

WHat were the clincal results of the 1965 gingivitis study?

A

when oral hygine stopped
* Increased PI
* Increased GI (lots of bleeding)
* All subjects developed gingivitis
* GIngivitis start at 5th day, developed within 15-21 days

when oral hygine re-started
* GIngivits revered in 1 week

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25
Q

Explain bacteriological results of the 1965 study when gingivitis at the start when OH stopped?

A

G+ cocci & short rods (90-100%) little inflmmation, imediate increase of:
* cocci
* Desquamated epithelial cells
* Small increase in PMNL (neutrophils)

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26
Q

Increase in Polumorphnuclear Leukocytes results in what?

A

Inflmmation!

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27
Q

Explain bacteriological results of the 1965 study at 2-4 days post stopping OH

A
  • Increase in filamaents
  • Increase in slender roods
  • Cocci stil there
  • Increase in PMNL
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28
Q

Explain bacteriological results of the 1965 study at 6-10 days post stopping OH

A

Gradual transtion to:
* Vibrios
* Spirochetes
* Cocci, rod, filaments still there
* HEAVY PMNL accumilation

Shift from good to harmful bacteria

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29
Q

Explain bacteriological results of the 1965 study when health restablished?

A

Return to predominance of cocci and short rods. Two patients still had filaments present.

No more: spirochetes or vibrios.

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30
Q

What wasthe conclusion of the 1965 gingivitis study?

A

Mass of plaque buildup = gingival inflmation
* Removal of plaque can revert gingivitis symptoms

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31
Q

Explain Non-specific theory

A

Mass of plaque results in gingival inflamation

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32
Q

What 2 complexes inn the socransky are considered early colonzers?

A

Green and Orange

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33
Q

How to the early colonizing bacteria necessary for other bacteria assc. with periodontal disease?

A

They adhere to the pellicle and are necessary for the colonization of other bacteria associated with periodontal disease.

act as a base

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34
Q

The bacteria in the orange complex act as what?

A

A bridging species between bacteria int he green and red.

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35
Q

What are orange complex bacteria assocated with?

A

increased pocket depth and and progressive attachment loss

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36
Q

P. intermidia is what complex?

A

Orange

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37
Q

The Red complex and Aa complex are what?

A

final bacteria that colonize and lead to the **destruction of the periodontium. **

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38
Q

What occurs if the green and orange complex bacteria are not present int he mouth?

A

the red complex bacteria are rarely able to colonize.

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39
Q

What di the socransky complex disprove from teh 1965 gingivitis study?

A

A **mass of plaque is not required **for the establishment of gingivitis and periodontisits.

Sepcific bactera are what cause destruction

40
Q

What is the specific theory?

A

Specific bacteria causes the destruction (red complex)

41
Q

What is the current etiology of periodontitis?

A

Periodontitis is a multifactorial inflammatory disease caused by a dysbiotic (Unbalanced) microbiota

42
Q

Does calculus cause disease?

A

NO!
* mineralized plaque, no active bacteria
BUT it perpetuates the disease by **allowing plaque biofilm to adhere to it. **

43
Q

What is the dysbiosis of periodontisits characterized by?

A

the microbial shift that occurs in the biofilm
* decrease in beneficial symbionts
* and/or an increase of pathobionts, as microorganisms become pathogenic when host-microbe homeostasis breaks down.

44
Q

Interaction between host immune system and microbiome resulting in damage to self tissue

A

Host microbiome homeostasis breakdown

45
Q

What is associated with an oral mucrobiota dysbiosis and disease progression?

A

Host & enviromental factors

46
Q
  • smoking tobacco
  • poor oral hygiene
  • diabetes mellitus
  • pregnancy
A

modifiablerisk factors

Can be altered

47
Q
  • age a
  • heredity, including genetic diseases
A

non-modifiablerisk factors,

You cant change

48
Q

What does polymicrobial synergy and Dybiosis model?

A

Questioned the Red complex, some pathogens are incapable of pathogenicity alone. They require a commmunity to become pathogenic.

49
Q

What are the 3 fundamental pre-reqs for periodontal pathogens to emerge as pathogenic?

A
  1. Formationof a diverse community with appropriate receptor
  2. Each rep in a community is co-operative and harmonious
  3. The community will withstand host immunity and add to inflammation of periodontal tissue
50
Q

What is a virulence factor of periodontal pathogens?

A

Adhesion & receptors

51
Q

What are the 2 new emerging periodontal pathogens?

A

2 gram (+) anerobic bacteria
* Filifactor alocis
* P. Stomatis

52
Q

What is the virulence factor of the 2 new periodontal pathogens

A

Manipulate neutrophil effector functions
* even if engulfed by neutrophil they are NOT destroyed through phagocytosis
* F. alocis, P. Stomatis

53
Q

After dysbiosis of the host and pathogen occurs, and PAMPS are recognized what 2 paths can be taken?

A
  1. Pattern recogntion & cytokiene release
    OR
  2. Complement protiens

both lead to reqruitment & activation of neutrophil and macrophages and inflmmatory response and then tissue damage

54
Q

What is a PAMP on gram - bacteria?

A

Lipopolysachrides (LPS)

55
Q

What are the histopathologic events and types of cells involved in the initiation and progression of inflammatory periodontal disease?

A
  1. Inital Lesion (2-4 days rev)
  2. Early lesion (4-10 days rev)
  3. Established lesion (14-21 days rev)
  4. Advanced Lesion (Time depends on pt. Irreversible)
56
Q

Explain the intial lesion.

A
  • Develops 2-4 days post accumulation of plaque
  • Low grade inflamamtion
  • neutrophil & monocytes migrate through connective tissue into the sulcues
  • GFC (transudate) flow increases to try and flush bactera out of crevice.
57
Q

What Lesion?

Classic accute exudative ____ with loss of perivascular collage in gingival tissue, acute injury

A

Vasculitis, Initial Lesion 2-4 days

Dialation of blood vessels, shift from symbiotic to pathobiotic bacteria

58
Q

Most individuals will develop gingivitis in response to an

A

accumulation of plaque

59
Q

____ is fundamental for determining which individuals may progress (some stay with initial, some progress depending on strength of immune system)

A

Host immune system

60
Q

Explain the early lesion

A
  • Develops between day 4 - 10 after continued plaque accumulation
  • Corresponds with early stages of gingivitis
  • The gingiva becomes erythematous (red, lots of RBC) in appearance due to a proliferation in capillaries, the opening of microvascular beds and continued vasodilation
61
Q

What cells are associtated with early lesions?

A
  • Lymphocyes
  • Neutrophils
62
Q

What lesion?

Dense inflitrate of lymphocytes and other mononuclear cells, fibroblast morphology alteration, initiation of connective tissue loss.

A

Early lesion (4-10 days)

63
Q

What 3 things occur during early lesion?(4-10 days)

A
  • Fibroblast degenerate
  • Collagen destruction
  • Basal cell proliferate
64
Q

Early Lesion

What does fibroblast degeneration result in?

A

increases the ability for leukocytes to increase infiltration

65
Q

Early Lesion

Where does collagen destruction occur?

A

In the areas apical and lateral to the junctional epithelium and sulcular epithelium

Note destruction, more whiteness apical and lteral to the dark purple JE

66
Q

Early Lesion

What is the purpose of basal cell layer proliferation?

A

to maintain an intact barrier against the bacteria

67
Q

Explain an established lesion

A
  • Occurs approximately 14 to 21 days
  • Progression depends on:
    . Plaque challenge
    . Host susceptibility factors
    . Risk factors
  • Inflammatory cell infiltrate occupies a considerable volume of the connective tissues
  • Plasma cells predominate in older subjects
  • Lymphocytes predominate in younger subjects

Revesible

68
Q

What does establish lesion progression depend on?

A
  • Plaque challange
  • Host suseptibility factos
  • Risk factros
69
Q

In an established lesionw what cells can be see? How does this differ with age?

A
  • Lymphocytes in younger pt.
  • Plasma cells in older pt.
70
Q

Is there bone loss during established lesions?

A

No, plasma cells predominate but bone remains stable until it converts to an edvanced lesion.

Gingivitis.

71
Q

what occurs in collagen levels with established lesions?

A

Collagen depeletion continues with further proliferation of epithelium into the connective tissue space

72
Q

WHat accumulates during the established lesion phase? What does this result in?

A

neutrophils accumulate
in tissues and release lysosomal contents extracellularly which kills bacteria but also increases further tissue destruction

73
Q

What occurs in the Sulcus epithelium during the established lesion phase?

A
  • Lining becomes saturated with neutrophils
  • Highly permeable to substances inot or out of underlying connecitve tussves
  • SE begins to ulcertate, increases bleeding.

inflammation & damage is STILL reversible

74
Q

Explain Advanced lesion

A
  • Transition from gingivitis to periodontitis
  • Collagen destruction that now extends into the periodontal ligament and into the alveolar bone
  • Neutrophils predominate in the epithelium
  • Plasma cells predominate in the connective tissue

Irreversible!

75
Q

What cells predominate in an advanced lesion? Where?

A
  1. Neutrophils predominate in the epithelium
  2. Plasma cells predominate in the connective tissue

Connective tissue is no longer dense!

76
Q

what occurs in collagen in advanced lesion?

A

Collage destrcution extends into the PDL and Alveolar bone.

bone loss and PDL loss, pockets!

IRREVERSIBLE

77
Q

Define a periodontal pocket

A

The pathological apical migration of the junction epithelum.

Advanced lesion, to evade attacks

78
Q

What do osteoclast do during an advanced lesion?

A

begin toresorb bone as a defense mechanism to prevent the spread of bacteria into the bone

79
Q

The seperation of the gingiva and deepining of the JE forms a?

A

Periodontal Pocket

80
Q

Where does periodontisis (adavanced lesion) usually being?

A

Interproxmally!

81
Q

Explain this photo

A

Look!

82
Q

In an advanced lesion what occurs as the pocket deepens?

A

creates a protected, warm, moist anaerobic environment
* Encourages more bacterial growth (anerobic)
* Cycle continues until bacteria is removed or tooth is lost

83
Q

What occurs once teeth are cleaned post an advanced lesion?

A

Interproximal bone loss & cleanincal attachment loss remains, but inflmmation & bleeding goes away/

84
Q

Summary

A

Summary

85
Q
A
85
Q

What new development has come up about neutrophils?

A

They are in both acute and chronic phases of inflammation

86
Q

Explain how periodontisis can predispose people to cardiovascular disease?

A

people with periordontal pockets
have oral pathogens that can migrate to the heart

87
Q

Explain Nosocomial Pneumonia and how people can be predisposed to this through periodontitis

A

Pneumonia that you get in the hospital. People with periodontitis that are intubated can allow bacteria to travel to the lungs and cause this.

Respiratory Tract Infection
and Pneumonia

88
Q

Explain how periodontisis can predispose people to adverse pregnancy outcomes?

A

Inflmmator yreaction of pregnant women in the mouth can travel travel to the plaenta and cause early fetal birth

89
Q

Explain how periodontisis can predispose people to Type 2 diabetes & insulin resistance?

A

Its a cycle, diabetes promotes more periodontisits, vise versa.
Periodontisis common in diabetic pt. Also more prone to periodontal abscesss

90
Q

What are other things that periodontis can predispose you too?

A
  • Gastrointestinal disease
  • Oral & colorectal cancer
  • Lupus
  • Rheumatoid arthrisis
91
Q

Explain relationship of alzhimers & periodontitis

A

In 2017, P. gingivalis found in necropsies of 1 pt. with Alzheimer disease.

92
Q

The gingiva is always in a state of ____ due to the presence of bacteria.

A

mild inflammation

93
Q

Bacteria are required, but ____ to initiate the onset of periodontal disease.

A

not enough alone

94
Q

A few novel pathogens that play a role in the ____ have recently been discovered.

A

onset and disease progression

95
Q

____ is a part of the bigger picture.

A

Host susceptibility

96
Q

The ____ microbiome can overwhelm the host defenses. This may lead to further inflammation and eventual bone loss (periodontitis).

A

dysbiotic microbiome

PER 1001 (9 decks)

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