The inflammatory periodontal lesion #2 Flashcards
1
Q
- plaque-induced
- inflammation (edema + BOP)
- No destruction of PDL & bone
- No apical migration of epithelial attachment
A
Gingivitis
2
Q
Epithelial attachment =
A
junctional epithelium
3
Q
- plaque-induced
- inflammation (edema + BOP)
- destruction of bone
- apical migration of epithelial attachment
A
Periodontitis
4
Q
What do we mean when we say “periodontitis is host-related”?
A
susceptibility of host plays a role in progression of gingivitis to periodontitis
5
Q
What model of disease progression states that “continuous through out life at same rate of loss” i.e. everyone gets perio disease:
A
continuous model
6
Q
What model of disease progression states “progressive loss overtime of some sites; no destruction in others; time of onset and extent vary among sites”
A
Progressive model
7
Q
saying “periodontal disease affects mainly posterior teeth” would align with:
A
progresive model
8
Q
What model of disease progression states “activity occurs at random at any site; some sites show no activity; some sites have one or more bursts of activity; cumulative extent of destruction varies among sites
A
Random burst model
9
Q
Saying “periodontitis is different in various sites in the same individual and it is difficult to predict attachment loss” aligns with:
A
random burst model
10
Q
What model of disease progression states “several sites have one or more bursts of activity during one period of life; prolonged period of inactivity = remission; cumulative extend of destruction varies among sites; some sites don’t develop attachment loss; bursts due to risk factors:
A
Asynchronous multiple burst model
11
Q
What does asynchronous mean in the asynchronous multiple burst model?
A
not occurring at same time
12
Q
Signs of inflammation:
A
- rubor (redness)
- calor (heat)
- dolor (pain)
- tumor (swelling)
- function laesa (loss of function)
13
Q
Inflammation is a _____ phenomenon
A
vascular
14
Q
Inflammation includes what two components?
A
- Vasculitis
- Leukocyte migration
15
Q
Describe the components of vasculitis (3)
A
- dilation
- venous stasis (congestion)
- increased permeability
16
Q
First defense = _____ immunity
A
innate
17
Q
How does innate immunity work?
A
kills by phagocytosis
18
Q
What cells are involved in innate immunity?
A
- PMNs
- Monocytes
- Macrophages
19
Q
Describe innate immunity:
A
non-adaptive; genetic
20
Q
Second defense = _____ immunity
A
adaptive
21
Q
How does adaptive immunity work?
A
production of immunoglobulins by antibodies
22
Q
What cells are involved in adaptive immunity?
A
- B-cells
- T- cells
- plasma cells
23
Q
What are the plasma cells in adaptive immunity responsible for?
A
produce specific antibodies to individual antigens
24
Q
Activated B-cells become:
A
plasma cells
25
Plasma cells produce:
immunoglobulins
26
T lymphocytes ar edeveloped in the:
thymus
27
List the functions of T-lymphocytes
1. antigen presentation
2. help b-cells divide
3. destroy virally infected cells
4. can down-regulate immune response
28
T-cells an differentiate into 2 major forms including:
Cd4 and Cd8 cells
29
MHC class II molecules =
CD4 cells (helper t-cells)
30
MHC class I molecules =
CD8 (cytotoxic T-cells)
31
List the roles of helper T-cells:
1. help B cells
2. control leukocyte development
3. activate innate cell lining
32
List the roles of cytotoxic T cells:
destroy virally infected target cells
33
List cells that function in immunity: (4)
1. PMNs
2. Macrophages
3. B- Cells
4. T-cells
34
What immune cell is being described below?
- phagocytosis
- produce lysosomal enzymes
PMNs
35
What immune cell is being described below?
- phagocytosis
- process antigens
- cytokine secretion
macrophages
36
What immune cell is being described below?
- produce antibodies
B-cells (plasma cells)
37
What immune cell is being described below?
- Helps b-cells divide
Helper T cells (CD4)
38
What immune cell is being described below?
- down-regulates T and B cells
Supressor T-cells (Cd8 & Cd25)
39
What immune cell is being described below?
- Kills virally-infected cells
Natural Killer T cells (CD56)
40
What immune cell is being described below?
- Destroys infected cells
Cytotoxic T- cells (Cd8)
41
What immune cell is being described below?
- Kills infected cells
Killer T-cell (Cd28)
42
What are the main two components of humoral immunity?
1. antibodies
2. complement
43
Antibody that is the 1st responder and largest in size:
IgM
44
Antibody that is the 2nd responder, most abundant, and can cross the placenta:
IgG
45
Antibody that is found in saliva, and also a dimer:
IgA
46
Antibody that is co-expressed with IgM and unsure of role:
IgD
47
Antibody on mast cells & involved in allergic reactions:
IgE
48
Part of both of the innate and adaptive immune systems; a biochemical cascade that helps clear pathogens by lysis, opsonization, blinding, and clearance of immune complexes:
Complement
49
Portion of the immunoglobulin that is specific for antigen binding:
Fab
50
Constant portion of the immunoglobulin:
Fc
51
Antibody promotes phagocytosis:
opsonization
52
Antibody prevents bacterial adherence:
neutralization
53
Antibody activates complement enhancing opsonization and lysis
complement activation
54
Also called t-regulatory cells that down-regulate T and B cells and prevent autoimmune disease:
T-supressor cells
55
Mononuclear cells that kill cells sensitized with antibody (via Fc receptors):
Killer cells
56
Kill virally infected and transformed target cells that have not been previously sensitized:
NK cells
57
Activation in connective tissue; will become macrophages:
Monocytes
58
48 hr lifespan in the blood with migration to sites for phagocytosis:
Neutrophils
59
Cause damage by exocytosis (e.g. histamine release)
Eosinophils
60
Contain mediators of inflammation (histamine, prostaglandins, leukotrienes, and cytokines); involved in allergic reactions:
Mast cells
61
Cells that are in some way functionally similar to mast cells:
basophils
62
Soluble, locally active polypeptides; regulate cell growth, differentiation, & function; produced by cells of the immune system:
Cytokines
63
Specific cytokines may have different biologic properties dependent on: (4)
1. their concentration
2. the cells that produce them
3. the cells being attracted and acted upon
4. presence and extent of ECM
64
What cytokine is being described?
- pro-inflammatory: stimulates osteoclasts, fibroblasts, & macrophages
IL-1
65
What cytokine is being described?
- pro-inflammatory: stimulates T and B cells
IL-6
66
What cytokine is being described?
- pro-inflammatory: attracts & activates PMNs
IL-8
67
What cytokine is being described?
- pro-inflammatory: activates osteoclasts
TNF
68
What cytokine is being described?
- Vasodilation
- Pyrogenic
- Releases mediator from mast cells
- Cell-mediated cytotoxicity
PGE2
69
What growth factor is being described below?
- Stimulates epithelial cells & fibroblasts
TGF
70
What growth factor is being described below?
- stimulates fibroblasts
PDGF & FGF
71
What growth factor is being described below?
- stimulates epithelial cells
EGF
72
Can we accurately predict which patients with gingivitis will develop periodontitis?
NO- but we can assess risk factors such as habits and systemic disorders
73
List some mechanical (plaque retention) factors that modify the inflammatory response: (5)
1. calculus
2. caries
3. defective restorations
4. prosthesis
5. tooth anatomical factors
74
List some systemic factors that modify the inflammatory response: (4)
1. Diabetes
2 . Hormonal (puberty & pregnancy)
3. HIV/AIDS
4. Medications
75
List some genetic factors that modify the inflammatory response: (2)
1. Leukocyte Adhesion Deficiency (LAD)
2. Hypophosphotasia
76
The "initial lesion" develops in:
2-4 days
77
With the initial lesion, cells of _____ are present
acute inflammation
78
What is increased with the initial lesion?
GCF
79
What starts to form with the initial lesion?
pseudopocket
80
What are considered "cells of acute inflammation" that are present with the initial lesion?
PMNs
81
What are considered "cells of chronic inflammation"?
lymphocytes & with increased chronicity eventually plasma cells
82
What are the two types of virulence factors that are released into the periodontal tissues following the deposition of plaque?
1. stimulation of host defense systems
2. degradation of host tissues
83
When bacteria from the plaque utilize virulence factors that function to stimulate the host defense systems, what is occurring?
- cells are stimulated to release cytokines and chemoattractant factors (IL-8)
- inflammatory cells are signaled in
84
When bacteria from the plaque utilize virulence factors that function to degrade host tissues they use enzymes such as:
1. collagenase
2. trypsin-like enzymes
3. keratinase
4. phospholipase A
85
The following are clinical features of the ____.
1. increased GCF flow
2. sulcus increases from 0 to 3 mm by formation of a pseudopocket
3. alveolar bone is normal on the radiograph
Initial lesion
86
PMN diapedesis: _____ "slow" the PMNs and cause them to "roll". Cytokines activate ______ on the endothelial cells for PMN attachment.
Selectins; ICAM receptors
87
Put the following steps in order:
- adherence
- chemotaxis
- phagocytosis
- diapedesis
- killing + digestion + aggregation
1. diapedesis
2. chemotaxis
3. adherence
4. phagocytosis
5. killing + digestion + aggregation
88
The "early lesion" appears within:
4-7 days
89
- Acute inflammation persists with the initial lesion
- increased GCF
- Pseudopocket formation
- cells of chronic inflammation appear and then dominate
Early lesion
90
Do cells of chronic inflammation appear with the early lesion?
yes
91
What shift in cells do we see with the initial to the early lesion?
Acute cells of inflammation (PMNs) to chronic cells of inflammation (T-cells)
92
In an early lesion ____ loss continues and ____ activation begins
Collagen; MMPs
93
How is collagen lost with the early lesion?
Microbial factors (LPS & antigens) stimulate the release of cytokines and ALSO activations and release of MMPs
94
MMPs:
matrix metalloproteinases
95
includes 28 metal-dependent endopeptidases (proteases) with activity against most, if not all, extracellular matrix macromolecules (used for normal tissue remodeling)
MMPs
96
Important sub-class of MMPs:
interstitial collagenases
97
With the early lesion, collagen loss is up to:
70%
98
What causes collagen destruction in the early lesion?
1. PMNs products
2. cytokines
3. MMPs
(so a combination of bacterial products and host's defense system cause the destruction)
99
In what type of lesion do we see proliferation of JE rete pegs and the T-cell lesion?
Early lesion
100
Is there bone loss with the early lesion?
no (but we do have loss of collagen in the CT)
101
