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AU14 - Periodontology Exam 1 > 09/12 - Pathogenesis of Periodontitis > Flashcards

09/12 - Pathogenesis of Periodontitis Flashcards

1
Q

In healthy gingiva, the tissue volume ratios are: ___% JE, ___% OE, and ___% CT.

A
  • 10% JE
  • 30% OE
  • 60% CT
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2
Q

In healthy gingiva, the JE is how many cell layers thick?

A

10-20 cell layers

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3
Q

What is the name of capillary loops in healthy gingiva? Are the number of loops constant?

A
  • subepithelial plexus

- yes, it is constant

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4
Q

The subepithelial plexus contains anastomoses of ___ blood vessels with vessels from ___.

A
  • supraperiosteal

- bone and PL

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5
Q

What capillary plexus has no loops in health?

A

dentogingival plexus

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6
Q

What are the (6) reasons for stability of healthy gingiva?

A
  • shedding of epithelial cells
  • intact epithelial barrier
  • positive flow of gingival crevicular fluid
  • complement system
  • PMNs and macrophages
  • protective effects of antibodies
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7
Q

What are the 4 histopathological stages in the development of gingivitis and periodontitis?

A
  • INITIAL LESION: subclinical stage of gingivitis
  • EARLY LESION: clinical early stage of gingivitis
  • ESTABLISHED LESION: chronic gingivitis
  • ADVANCED LESION: progression to periodontitis
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8
Q

When does the initial lesion form? When the permeability increases, what leaks out of the vessels? What cells are present in the JE and what are in the CT?

A
  • occurs within 1-4 days of plaque development
  • carbon particles and serum proteins leak out of vessels
  • PMNs and monocytes in JE
  • lymphocytes in CT
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9
Q

During the initial lesion, does the vascular density increase or decrease? The perivascular collagen? The gingival crevicular fluid volume?

A
  • vascular density increases
  • perivascular collagen decreases
  • gingival crevicular fluid volume increases
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10
Q

True or false: The initial lesion stage is detectable clinically.

A

FALSE: It is not detectable clinically.

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11
Q

Describe the vascular changes during the initial lesion.

A
  • dilation of vessels of the dentogingival plexus is induced by vasoactive mediators (histamine, IL-1, TNF)
  • gaps form between capillary endothelial cells, resulting in increased permeability
  • fluids and proteins move out of the capillary
  • gingival crevicular fluid flow rate increases
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12
Q

In health, GCF is ___, but in disease, it is ___.

A
  • plasma transudate

- inflammatory exudate

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13
Q

The GCF constituents indicate ___ and ___. GCF flow rate ___ (increases/decreases) with clinical inflammation.

A
  • inflammatory changes
  • bacterial colonization
  • increases
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14
Q

During the initial lesion, there is a cytokine-mediated up-regulation of ___ on endothelial cells. ___ adhere to the post-capillary venules and begin to migrate through the JE into the gingival sulcus. Chemotaxis is induced by ___ and ___.

A
  • adhesion molecules
  • PMNs
  • host factors (IL-8, C5a)
  • molecules released by bacteria (fMetLeuPhe)
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15
Q

True or false: An initial lesion is an early response to plaque accumulation.

A

true

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16
Q

Initial Lesion Summary:

  • ___ subjacent to JE
  • exudation of ___ into tissue and gingival sulcus
  • increased migration of ___ into the JE and gingival sulcus
A
  • vasculitis
  • fluid
  • leukocytes
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17
Q

Initial Lesion Summary:

  • ___ present extravascularly
  • alteration of the ___ portion of JE
  • loss of ___
A
  • serum proteins
  • most coronal portion
  • perivascular collagen
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18
Q

When does an early lesion occur? What cells are located subjacent to the JE and what cells are few in number? What cells undergo cytopathic alterations?

A
  • occurs within 4-7 days of plaque development
  • lymphocytes and PMNs subjacent to the JE
  • few plasma cells
  • fibroblasts
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19
Q

True or false: Inflammation is clinically evident in an early lesion.

A

true

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20
Q

In an early lesion, ___ destruction occurs which creates space for infiltrate. The ___ cells proliferate. ___ invade the coronal portion of the lesion.

A
  • collagen
  • basal cells of JE and SE
  • epithelial rete pegs
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21
Q

During an early lesion, the ___ plexus remains dilated. There is a ___ (small/large) number of venules. The plexus ___ (is/is not) permeable.

A
  • dentogingival plexus
  • large number
  • is (extremely)
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22
Q

In an early lesion, as the ___ invades the ___, the previously inactive capillary bed opens up and proliferates into the ___.

A
  • JE
  • CT
  • CT papillae
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23
Q

Early Lesion Summary:

  • accentuation of the features of ___
  • accumulation of ___ immediately subjacent to JE
  • cytopathic alteration in resident ___
A
  • the initial lesion
  • lymphoid cells
  • fibroblasts
24
Q

Early Lesion Summary:

  • further loss of ___
  • early proliferation of ___
  • inflammatory changes ___ (are/are not) clinically evident
A
  • collagen network
  • basal cells of JE
  • are
25
Q

In an established lesion, increased swelling ___ (is/is not) clinically evident. There is ___ (increased/decreased) fluid exudation and leukocyte migration. ___ cells increase around blood vessels and in coronal CT. ___ loss continues as infiltrate expands.

A
  • is
  • increased
  • plasma cells
  • collagen
26
Q

In an established lesion, in addition to macrophages and serum proteins, what other cells are present?

A

T and B cells and plasma cells

27
Q

In an established lesion, what do activated T cells produce? Plasma cells? Fibroblasts?

A
  • T cells: cytokines and chemotactic substances
  • plasma cells: Ig and cytokines
  • fibroblasts: MMPs and TIMPs
28
Q

During an established lesion, what important conversion takes place? Describe this change.

A
  • conversion of JE to PE (permeable pocket epithelium)
  • JE and sulcular epithelium proliferate and migrate deeper into the CT; the sulcus deepens and the coronal portion of the JE is converted into PE
29
Q

True or false: PE is attached to the tooth surface.

A

FALSE: PE is not attached to the tooth surface.

30
Q

True or false: PE is loaded with PMNs.

A

true

31
Q

Established Lesion Summary:

  • persistence of features of ___
  • increased proportion of ___
  • presence of ___ in CT, JE, and gingival sulcus
  • continuing loss of ___
A
  • acute inflammation
  • plasma cells
  • extravascular immunoglobulins
  • collagen and matrix
32
Q

Established Lesion Summary:

  • proliferation and lateral extension of ___
  • early ___ formation may be evident
  • no apical migration of ___ and no ___ at this stage
A
  • JE
  • pocket
  • JE and no bone loss
33
Q

When does an advanced lesion occur?

A

beginning and duration are not known

34
Q

How is an advanced lesion different from an established lesion? (AKA what is the evidence of periodontitis?)

A
  • switch from T- to B-cell predominance signals conversion from gingivitis to periodontitis
  • destruction of CT attachment to root surface and apical migration of epithelial attachment indicates first clinical sign of periodontitis
35
Q

In an advanced lesion, where does bone destruction begin? How does it continue?

A
  • bone destruction begins around communicating blood vessels along crest of septum
  • apical proliferation of PE into the deep CT; the PE is not attached to the tooth
36
Q

Advanced Lesion Summary:

  • persistence of ___ features
  • increased proportion of ___ cells (approx. 50%)
  • extension of lesion into ___ with significant ___
A
  • established lesion features
  • plasma cells
  • alveolar bone and PL
  • bone loss
37
Q

Advanced Lesion Summary:

  • continued loss of ___ subjacent to PE
  • formation of ___ and apical migration of ___ from CEJ
A
  • collagen fibers and matrix
  • periodontal pocketing
  • JE
38
Q

What are the 3 common modifying factors of periodontitis?

A
  • diabetes
  • pregnancy/puberty/menopause
  • smoking
39
Q

What 5 things can modifying factors of periodontitis influence?

A
  • susceptibility to gingivitis and periodontitis
  • plaque growth and composition
  • clinical presentation
  • disease progression
  • response to periodontal therapy
40
Q

What are the 4 oral and periodontal effects of diabetes mellitus?

A
  • xerostomia
  • candida infections
  • periodontitis
  • multiple periodontal abscesses
41
Q

Is the incidence and severity of periodontitis greater in well-controlled or poorly-controlled diabetes?

A

poorly-controlled

42
Q

True or false: Periodontitis decreases insulin resistance.

A

FALSE: Periodontitis increases insulin resistance (glycemic control improved after periodontal therapy; diabetics with severe periodontitis have proteinuria and cardiovascular problems).

43
Q

What are the effects of diabetes on bacteria?

A
  • Spirochetes increase in poorly-controlled diabetes
  • P. intermedia, C. rectus, P. gingivalis in Type II diabetes
  • Capnocytophaga predominance in Type I diabetes
44
Q

What are the effects of diabetes on host response?

A
  • PMN FUNCTION AND CHEMOTAXIS IMPAIRED: PMN enzymes beta glucornidase and elastase increase in poor control; collagenase increases
  • CYTOKINES, MONOCYTES, AND MACROPHAGES: increase in PGE, IL-1beta, and TNF-alpha; advanced glycation end products create destructive phenotype of macrophages
  • CONNECTIVE TISSUE: decrease matrix synthesis by fibroblasts and osteoblasts; reactive oxygen species cause cell damage; AGE creates thickening of vascular endothelium, synthesis of wound healing steroids
45
Q

True or false: The effect of periodontal treatment on stable diabetics is the same as non-diabetics.

A

true

46
Q

What are the (5) effects of estrogen in pregnancy, puberty, and menopause?

A
  • affects salivary peroxidases
  • increases collagen metabolism and angiogenesis
  • increases vascular response and inflammatory mediators
  • increased gingiva inflammation
  • increased bleeding during menstrual cycle in women with gingivitis
47
Q

When is gingival inflammation the highest during pregnancy? What is pregnancy’s effect on the microbiota?

A
  • during 2nd and 3rd trimesters

- increases P. intermedia; naphthoquinones from steroids used by Pi; increase in spirochetes

48
Q

What are the effects of pregnancy on the host that relate to periodontitis?

A
  • increase in vascular permeability, resulting in increased gingival exudate
  • decrease in keratinization
  • decrease in PMN chemotaxis and phagocytosis, antibodies, T-cell response
49
Q

When is periodontal treatment best during pregnancy? Should antibiotics be used?

A
  • during 2nd trimester

- best to avoid use of antibiotics during pregnancy

50
Q

What syndrome does menopause lead to in 30% of women? What is this syndrome due to? How does this affect periodontal disease?

A
  • osteoporosis
  • due to decreased absorption and increased elimination of calcium
  • osteoporosis may not cause periodontal disease, but may affect severity of pre-existing disease
51
Q

What is the second risk factor for periodontitis?

A

tobacco smoking

52
Q

How does tobacco smoking effect the pockets? What other effects does it have on the periodontia?

A
  • deeper pockets and larger number of pockets
  • more attachment loss, including recession
  • more alveolar bone loss
  • more tooth loss
  • less gingivitis and bleeding on probing
  • more teeth with furcation involvement
53
Q

True or false: Tobacco smoking leads to less gingivitis and bleeding on probing.

A

true!

54
Q

What is the effect of tobacco smoking on bacteria?

A
  • smokers have more plaque

- increase in AA, Tannerella forsythia, P. micros, P. gingivalis, C. rectus, and P. intermedia

55
Q

What is the effect of tobacco smoking on the host that relates to periodontitis?

A
  • lower BOP (decreased inflammation, decrease in blood vessels, increase in keratinization)
  • lower amounts of GCF in gingivitis
  • decreased PMN functions (migration, phagocytosis, ICAM)
56
Q

How does smoking affect the response to treatment?

A
  • smoking is associated with poorer reduction in probe depths and poorer attachment gain (without surgery)
  • smoking is associated with poorer response to periodontal surgical treatment
  • limited studies show that quitting smoking may lead to more favorable treatment outcome

AU14 - Periodontology Exam 1 (11 decks)

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