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Periodontal Disease > Pathogenesis of Periodontitis > Flashcards

Pathogenesis of Periodontitis Flashcards

1
Q

Healthy gingiva is reflective of superb ___, the ___ epithelium is attached to enamel, and the ___ epithelium appears to be continuous with the JE. Inflammation is virtually ___.

A

hygiene; junctional; oral; absent

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2
Q

What are the tissue volume ratios in gingival health?

A

10% juncitonal epi
30% oral epi
60% CT

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3
Q

T/F. In gingival health, there are many PMNs present in the outer portion of the JE.

A

False, In gingival health, there are FEW PMNs present in the outer portion of the JE.

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4
Q

The JE is ___ (thin/thick), epithelial ridges (rete pegs) are ___ (present/absent), and ___ tissue is dense with prominent collagen fiber bundles.

A

thin; absent; connective

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5
Q

The ___ plexus with capillary ___ provides nutrients to the oral epi and the ___ of loops is constant.

A

subepithelial; loops; number

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6
Q

What does the supepithelial anastomose with?

A

supraperiosteal blood vessels from bone and PDL

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7
Q

T/F. Dentogingival plexus venules have no loops in health.

A

True.

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8
Q

What defense factors are in place that allows clinically healthy gingiva to avoid becoming clinical ginigvitis?

A
  1. intact barrier provided by junctional epi
  2. regular shedding of epi cells into oral cavity
  3. positive flow of fluid to the gingival crevice, which may wash away unattached microorganisms and noxious products.
  4. the presence in GCF of antibodies to microbial products
  5. the phagocytic function of neutrophils and macrophages
  6. Protective effect of Ab (detrimental effect of complement on the microbiota_
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9
Q

What are the four histopathological stages in the development of gingivitis and periodontitis?

A
  1. initial lesion
  2. early lesion
  3. established lesion
  4. advanced lesion
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10
Q

Match the lesion stage with its diagnosis.

  1. initial lesion
  2. early lesion
  3. established lesion
  4. advanced lesion

A. subclinical stage of gingivitis
B. clinical early stage of gingivitis
C. chronic gingivitis
D. progression to periodontitis

A
  1. -A
  2. -B
  3. -C
  4. -D
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11
Q

The initial lesion occurs within ___-___ days of inflammation.

A

1-4

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12
Q

Explain how increased permeability causes carbon particles and serum proteins to leak out of vessels.

A

When carbon particles are injected intravenously they become trapped in the open endothelial junctions due to increased permeability.

Decreased perivascular collagen in the basement membrane around venules allows venules to be leaky

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13
Q

Increased permeability causes an infiltration of ___ and ___ in the JE and ___ in CT.

A

JE - PMNs; monocytes (5%)

CT- lymphocytes (5%)

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14
Q

Dilation of vessels of the ___ plexus is induced by vasoactive mediators (___, ___, ___). ___ form between capillary endothelial cells resulting in increased permeability. Increased ___ ___ fluid will make the tissue edematous and swollen.

A

dentogingival; histamine; IL-1; TNF; Gaps; gingival crevicular

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15
Q

T/F. The initial lesion is visible clinically.

A

False, this stage is NOT detectable clinically.

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16
Q

GCF is a plasma ___ (health) or inflammatory ___ (disease).

A

transudate; exudate

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17
Q

How is GCF collected? Why would you want to collect it?

A

GCF passes through the periodontal tissues and can be collected from within or at the orifice of the gingival crevice.

GCF constituents indicate inflammatory changes and bacterial colonization.

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18
Q

GCF flow rates ___ during clinical inflammation.

A

increases

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19
Q

What protein marker is used to indicate GCF volume?

A

ninhydrin stain

20
Q

What up-regulates adhesion molecules in teh dentogingival vasculature? Where do PMNs migrate? What induces their migration?

A
  1. cytokine-mediated
  2. migrate through JE to gingival sulculs
  3. host factors (IL-8, C5a) and molecules released by bacteria (fMetLeuPhe)
21
Q

When does an early lesion occur?

A

4 to 7 days of plaque development

22
Q

Where are lymphocytes and PMNs located in early lesions? Are there any plasma cells?

A

Lymphocytes and PMNs are subjacent to JE

Few plasma cells present

Together they constitute 15% of infiltrated connective tissue

23
Q

Fibroblast undergo ___ ___ in an early lesion, where they make enzymes that break down collagen. This contributes to a loss of the ___ portion of the JE. Why does collage destruction occur?

A

cytopathic alterations; coronal

it creates space for infiltrate

24
Q

When does inflammation become clinically evident?

A

in an early lesion

25
Q

___ cells of the JE and SE proliferate and epithelial ___ ___ invade the coronal portion of the lesion.

A

Basal; rete pegs

26
Q

The ___ plexus remains dilated and is extremely permeable following minor trauma or inflammation. As JE invades the CT, the previously inactive capillary bed opens up and proliferates into the CT ___.

A

dentogingival; papillae

27
Q

What events continue to take place in the established lesion phase?

A
  1. increased swelling clinically evident
  2. increased fluid exudation, leukocyte migration
  3. collagen loss continues as infiltrate expands
28
Q

Are plasma cells seen in an established lesion?

A

plasma cells increase around blood vessels and in coronal CT

In addition to macrophages and serum proteins, T and B cells and plasma cells are present

29
Q

Activated T Cells produce ___ and ___ substances, plasma cells produce ___ and ___, and fibroblasts produce ___ and ___.

A

cytokines; chemotactic; Ig; cytokines; MMPs (metaloproteinases); TIMPs (tissue inhibitor of metaloproteinases)

30
Q

As the JE and sulcular epithelium proliferate deeper into the CT, the sulcus deepens and the coronal portion of teh JE is converted into permeable ___ epithelium (PE).

A

pocket

31
Q

T/F. Pocket epithelium is attached to the tooth surface and only contains a few PMNs.

A

False, the PE is NOT attached to the tooth surface and contains MANY PMNs.

32
Q

T/F. Although there is proliferation and lateral extension of the JE, there is no apical migration of JE and no bone loss at the established lesion stage.

A

True.

33
Q

During the advanced lesion, there is a switch from ___ to ___ cell predominance and this signals the conversion from gingivitis to ___.

A

T: B: periodontitis

34
Q

What is the first clinical sign of periodontitis?

A

destruction of CT attachment to root surface and apical migration of epithelial attachment.

35
Q

Where does bone destruction begin?

A

around communicating blood vessels along the crest of septum.

36
Q

At the advanced lesion stage, will removal of plaque resolve the inflammatory response?

A

Yes, but it will not reverse attachment loss.

37
Q

Is there any apical migration of the JE during the advanced lesion stage?

A

Yes, there is formation of a periodontal pocket and apical migration of JE from CEJ

38
Q

Is diabetes mellitus a risk factor for periodontitis? If a diabetic patient has periodontitis, what can it do to his/hers insulin resistance?

A

Yes

Periodontitis increases insulin resistance

39
Q

T/F. The incidence and severity of periodontitis is greater in poorly controlled diabetes.

A

True.

40
Q

There is an increase in bacteria in diabetics and the host response is impaired. For example, ___ ___ ___ (AGE) products create destructive phenotype of macrophages.

A

advanced glycation end products

41
Q

How does periodontal treatment affect stable diabetics?

A

the same as non-diabetics

42
Q

During pregnancy, puberty and menopause, what does estrogen affect?

A
  1. salivary peroxidases
  2. increase collagen metabolism, angiogenesis
  3. increase vascular response and inflammatory mediators
  4. gingival inflammation increased
  5. increase in bleeding during menstrual cycle
43
Q

Gingivitis is seen in ___-___% of pregnancies. Gingival inflammation is highest during ___ and ___ trimesters. It is best to perform periodontal treatment during ___ trimester and avoid ___ during pregnancy.

A

35-88%; 2nd; 3rd; 2nd; antibiotics

44
Q

What is the second risk factor for periodontitis?

A

tobacco smoking

45
Q

What problems will smoking patients have upon clinical examination?

A
  1. deeper probe depths and larger number of deep pockets
  2. more attachment loss, including recession
  3. more alveolar bone loss
  4. more tooth loss
  5. less gingivitis and bleeding on probing
  6. more teeth with furcation involvement
46
Q

Why do smokers have a low BOP?

A

because there is decreased inflammation and a decrease in blood vessels but an increase in keratinization

47
Q

T/F. Smoking is associated with better reduction in probing depth, better attachment gain in nonsurgical treatment, and better response to periodontal surgical treatments.

A

Smoking is associated with POORER reduction in probing depth, POORER attachment gain in nonsurgical treatment, and POORER response to periodontal surgical treatments.

Periodontal Disease (11 decks)

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