09/12 - Pathogenesis of Periodontitis Flashcards
(56 cards)
1
Q
In healthy gingiva, the tissue volume ratios are: ___% JE, ___% OE, and ___% CT.
A
- 10% JE
- 30% OE
- 60% CT
2
Q
In healthy gingiva, the JE is how many cell layers thick?
A
10-20 cell layers
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
4
Q
The subepithelial plexus contains anastomoses of ___ blood vessels with vessels from ___.
A
- supraperiosteal
- bone and PL
5
Q
What capillary plexus has no loops in health?
A
dentogingival plexus
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
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
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
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
10
Q
True or false: The initial lesion stage is detectable clinically.
A
FALSE: It is not detectable clinically.
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
12
Q
In health, GCF is ___, but in disease, it is ___.
A
- plasma transudate
- inflammatory exudate
13
Q
The GCF constituents indicate ___ and ___. GCF flow rate ___ (increases/decreases) with clinical inflammation.
A
- inflammatory changes
- bacterial colonization
- increases
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)
15
Q
True or false: An initial lesion is an early response to plaque accumulation.
A
true
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
17
Q
Initial Lesion Summary:
- ___ present extravascularly
- alteration of the ___ portion of JE
- loss of ___
A
- serum proteins
- most coronal portion
- perivascular collagen
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
19
Q
True or false: Inflammation is clinically evident in an early lesion.
A
true
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
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)
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
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
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.
- is
- increased
- plasma cells
- collagen
26
In an established lesion, in addition to macrophages and serum proteins, what other cells are present?
T and B cells and plasma cells
27
In an established lesion, what do activated T cells produce? Plasma cells? Fibroblasts?
- T cells: cytokines and chemotactic substances
- plasma cells: Ig and cytokines
- fibroblasts: MMPs and TIMPs
28
During an established lesion, what important conversion takes place? Describe this change.
- 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
True or false: PE is attached to the tooth surface.
FALSE: PE is not attached to the tooth surface.
30
True or false: PE is loaded with PMNs.
true
31
Established Lesion Summary:
- persistence of features of ___
- increased proportion of ___
- presence of ___ in CT, JE, and gingival sulcus
- continuing loss of ___
- acute inflammation
- plasma cells
- extravascular immunoglobulins
- collagen and matrix
32
Established Lesion Summary:
- proliferation and lateral extension of ___
- early ___ formation may be evident
- no apical migration of ___ and no ___ at this stage
- JE
- pocket
- JE and no bone loss
33
When does an advanced lesion occur?
beginning and duration are not known
34
How is an advanced lesion different from an established lesion? (AKA what is the evidence of periodontitis?)
- 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
In an advanced lesion, where does bone destruction begin? How does it continue?
- 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
Advanced Lesion Summary:
- persistence of ___ features
- increased proportion of ___ cells (approx. 50%)
- extension of lesion into ___ with significant ___
- established lesion features
- plasma cells
- alveolar bone and PL
- bone loss
37
Advanced Lesion Summary:
- continued loss of ___ subjacent to PE
- formation of ___ and apical migration of ___ from CEJ
- collagen fibers and matrix
- periodontal pocketing
- JE
38
What are the 3 common modifying factors of periodontitis?
- diabetes
- pregnancy/puberty/menopause
- smoking
39
What 5 things can modifying factors of periodontitis influence?
- susceptibility to gingivitis and periodontitis
- plaque growth and composition
- clinical presentation
- disease progression
- response to periodontal therapy
40
What are the 4 oral and periodontal effects of diabetes mellitus?
- xerostomia
- candida infections
- periodontitis
- multiple periodontal abscesses
41
Is the incidence and severity of periodontitis greater in well-controlled or poorly-controlled diabetes?
poorly-controlled
42
True or false: Periodontitis decreases insulin resistance.
FALSE: Periodontitis increases insulin resistance (glycemic control improved after periodontal therapy; diabetics with severe periodontitis have proteinuria and cardiovascular problems).
43
What are the effects of diabetes on bacteria?
- Spirochetes increase in poorly-controlled diabetes
- P. intermedia, C. rectus, P. gingivalis in Type II diabetes
- Capnocytophaga predominance in Type I diabetes
44
What are the effects of diabetes on host response?
- 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
True or false: The effect of periodontal treatment on stable diabetics is the same as non-diabetics.
true
46
What are the (5) effects of estrogen in pregnancy, puberty, and menopause?
- 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
When is gingival inflammation the highest during pregnancy? What is pregnancy's effect on the microbiota?
- during 2nd and 3rd trimesters
| - increases P. intermedia; naphthoquinones from steroids used by Pi; increase in spirochetes
48
What are the effects of pregnancy on the host that relate to periodontitis?
- increase in vascular permeability, resulting in increased gingival exudate
- decrease in keratinization
- decrease in PMN chemotaxis and phagocytosis, antibodies, T-cell response
49
When is periodontal treatment best during pregnancy? Should antibiotics be used?
- during 2nd trimester
| - best to avoid use of antibiotics during pregnancy
50
What syndrome does menopause lead to in 30% of women? What is this syndrome due to? How does this affect periodontal disease?
- 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
What is the second risk factor for periodontitis?
tobacco smoking
52
How does tobacco smoking effect the pockets? What other effects does it have on the periodontia?
- 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
True or false: Tobacco smoking leads to less gingivitis and bleeding on probing.
true!
54
What is the effect of tobacco smoking on bacteria?
- smokers have more plaque
| - increase in AA, Tannerella forsythia, P. micros, P. gingivalis, C. rectus, and P. intermedia
55
What is the effect of tobacco smoking on the host that relates to periodontitis?
- lower BOP (decreased inflammation, decrease in blood vessels, increase in keratinization)
- lower amounts of GCF in gingivitis
- decreased PMN functions (migration, phagocytosis, ICAM)
56
How does smoking affect the response to treatment?
- 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
