Pathogenesis Part 1 Flashcards
1
Q
what type of plaque casues gingivitis
A
supragingival plaque
2
Q
swelling =
A
edematous
3
Q
redness =
A
erthema
4
Q
what type of plaque is involved in periodontitis?
A
subgingival plaque
5
Q
what type of immunity is non-specific?
A
innate immunity- always there
6
Q
what stages of periodontal disease does BOP occur
A
bleeding on probing occurs in the early, established and advanced lesion (acute gingivitis, chronic gingivitis and periodontitis)
7
Q
what stage of periodontal disease does a periodontal pocket form?
A
advanced lesion-periodontitis
8
Q
what stage of periodontal disease does cytoplasmic alterations of fibroblasts occur?
A
early lesion - acute gingivitis
9
Q
what stage of periodontal disease do white blood cells migrate into the junctional epithelium and gingival sulcus?
A
initial lesion- clinically healthy
10
Q
what stage of periodontal disease does the proliferation, apical migration and lateral extension of junctional epithelium occur?
A
established lesion - chronic gingivitis - 2-3wks
11
Q
when do the basal cells of the junctional epithelium begin to proliferate?
A
early lesion - acute gingivitis - 4-7days
12
Q
what stage of periodontal disease are immunoglobulins (antibodies) present in the connective tissue and junctional epithelium?
A
established lesion - chronic gingivitis - 2-3wks
13
Q
what stage of periodontal disease does alveolar bone loss occur?
A
Occurs histologically in the advanced lesion from periodontitis- greater than 3 weeks
14
Q
what stage of periodontal disease do lymphoid cell accumulate?
A
early lesion - acute gingivitis - 4-7 days
15
Q
what stage of periodontal disease do plasma cell become cytopathologically altered?
A
advanced lesion- periodontitis
16
Q
what stage of periodontal disease does the loss of perivascular collagen begin?
A
initial lesion 2-4 days
17
Q
what stage of periodontal disease is distant bone marrow converted into fibrous connective tissue?
A
advanced lesion - periodontitis
18
Q
When does fluid begin exudation from the gingival sulcus?
A
initial lesion
19
Q
what stage of periodontal disease are there periods of quiescence and exacerbation?
A
advanced lesion - periodontitis
20
Q
what stage of periodontal disease is there a predominance of plasma cells with out bone loss?
A
established lesion- chronic gingivitis
21
Q
what can be stimulated to destroy collagen and ECM?
A
fibroblasts
22
Q
what are the 4 types of cells of the innate immune response?
A
- mast cells 2. acute phase proteins 3. complement 4. PMN’s
23
Q
what affect does TNF alpha have?
A
TNF alpha recruits granulocytes to the area of inflammation, induces fever
24
Q
what affect does histamine have?
A
histamine dilate and increases permeability of blood vessels
25
what affect do leukotrines have?
leukotrines dilate small blood vessels, chemotaxis of leukocytes
26
what affect do prostaglandins have?
prostaglandins increase vascular permeability, regulate the immune response
27
what is the difference in hyperresponsive, normal, and hyporesponsive groups to periodontitis?
Hyperresponsive - NUG/ refractory perio Normal - clinincally obvious perio, gingivitis Hyporesponsive - group doesnt get periodontitis
28
what type of immunity is adaptice and specific?
acquired immunity
29
What types of cells are involved in the acquired immunity?
monocytes/ macrophages lymphocytes
30
When monocytes/ macrophages are involved what can occur?
if unresolved or resolved chronic inflammation can occur
31
What can occur if the serum compliment is unable to stop the invasion of bacteria?
acute inflammation recruit PMN's
32
What happens if lymphocytes are able and unable to fight an infection?
able - chronic inflammation unable - systemic infection
33
What type of cell is involved in both the acquired immunity and the innate immunity?
monocytes/macrophages
34
What two types of cells cause acute inflammation?
neutrophils and serum complement
35
what is c-reactive protein? what does is do?
C-reactive protein is an acute phase protein. it is produced by the liver and serves to bind lysophosphatidylcholine (on surface of dying bacteria) to activate the complement system. It has a higher affect on heart attacks than LDL!!
36
What are five types of cells that increase the risk of heart disease?
1. c-reactive protein 2. fibrinogen 3. complement 4. namose binding protein 5. metal binding protein
37
what activates the serum complement?
complement is activated by antigen-antibody interaction
38
What % of normal proteins in blood is the serum complement?
10%
39
Where is the complement made? and by what?
the liver, small intestine made by mononuclear cells
40
What type(s) of complement cause inflammation? What do they do?
C3a and C5a -the release of mast cell mediators = increased permeability of blood vessels and phagocytes can enter tissues
41
What part of complement forms an antibody coat over the bacteria?
C3b - forms antibody coat (opsinization)- helps to internalize the bacteria faster
42
what is the alternative pathway(non-specific) for complement activation/ cleavage?
endotoxins, IgG cleave C3 into C3a and C3b
43
what is the half life of PMN's?
5-90 hours
44
How do PMN's adhere to the endothelium?
via selectins, adhesins- ICAM and ELAM
45
Diapedesis
process of squeezing through endothelium
46
Chemotaxis
directed movement to an increase concentration
47
What affect does NADPH oxidase have? When is it activated?
increase in NADPH oxidase activity on surface of cells and granules helps to phagocytize bacteria. Activated in respiratory burst
48
PMN's are attracted to what?
F-MLP (formyl methionine, leucine, phenylalanine) bacterial cells have this- released as bacteria turn over
49
What are secondary granules?
specific granules -lysosyme, NADPH oxidase, collagenase, lactoferrin
50
What are primary granules?
azurophilic granules -myeloperoxidase, deffensins, elastase, cathepsin
51
explain the process of rolling
PMN's slow down and roll on membrane, grab onto adhesins / ICAM on endothelium and the leave the blood via diapedesis and undergo chemotexis and then phagocytize bacteria.
52
epitopes on bacteria cells bind to?
the FAB region of antibodies
53
macrophages are long lived cells that are involved in what type of immunity?
both innate and acquired immunity
54
are PMN's antigen presenting cells?
No but macrophages, dentritic cells, and plasma cells are
55
the interaction of LPS with macrophages with endotoxins results in the release of what?
1. PGE2 2. TNF alpha 3. IL-1- beta 4. MMP's
56
what molecules of complement are most typically associated with acute inflammation?
C3a and C5a
57
what is true about the IL-1 gene polymorphism?
it can be used as a measure of susceptibility for periodontal disease in some patient populations
58
the initial microbial infection is primarily accomplished by what?
1. antigen-antibody response 2. complement 3. mast cells 4. PMN's
59
c-reactive protein is what type of protein? What part of the immune response is it part of?
-acute phase protein -innate immune response
60
chemokinesis
movement of cells due to chemical or physical stimulation
61
chemotaxis
a specialized type of chemokinesis that is the directed movement of cells towards an increasing chemical gradien
62
the chemotractant that results from the proteolytic breakdown of complement is?
C5a
63
c-reactive protein present in the blood is indicative of what?
inflammation of the whole body
64
what purpose does c-reactive protein serve in the innate immune system?.... it binds to what?
it binds to lysophosphatidylcholine (on surface of dying cells) to activate the complement system
65
what enzyme activates complement?
c3 convertase enzyme
66
where is complement produced? by what?
the liver and small intestine by mononuclear cells
67
how is complement activated in the alternative pathway?
by LPS, endotoxins, aggregated IgG
68
what is a virulence factor that helps bacteria avoid opsonization?
hydrophilic bacteria
69
opsonization is activated by what complement product?
c3b
70
What does the complement particle C3a bind to and do?
C3a binds to the mast cell which releases TNF alpha which causes IL-8 to alter the endothelial surface = vasodilation
71
PMN's express's __________ Endothelium express's \_\_\_\_\_\_\_\_
PMN's- selectins Endothelium- Adhesions/ ICAM
72
complement causes vasodilation through what?
cytokine - IL-8 alters the endothemial surface - caused when C3a binds to a mast cell
73
what is an example of an end cell?
PMN
74
tertiary granules
cathepsin and gelatinase
75
how does the membrane attack complex in complement work?
creates holes in the membrane of bacteria ex- chlorahexadine
76
what are the chemotractants for PMN's from macrophages/ monocytes?
leukotrine B4 IL-8
77
what are the chemotractants for PMN's from serum/ plasma (proteolytic breakdown of complement)?
C5a
78
what are the chemotractants for PMN's from bacteria?
f-met peptides
79
what are the chemotractants for PMN's from mast cells?
neutrophil chemotactic factor
80
what are the chemotractants for PMN's from the endothelium?
endothelial IL-8
81
what are the chemotractants for PMN's from B-cells and macrophages?
IL-1
82
what response is the preferred method of killing for PMN's?
oxidative response via NADPH oxidase
83
what enzymes are involved in the oxidative response of PMN's?
1. NADPH oxidase 2. cytochrome B 3. myeloperoxidase
84
What are the products of the respiratory burst?
1. HOCL (hypochlorous acid) 2. H2O2 (hydrogen peroxide) 3. O2 -
85
what causes the green color of pus in infections?
myeloperoxidase
86
what are proteas inhibitors?
stop enzymes when dumped into connective tissue.
87
what causes frustrated phagocytosis?
HOCL can neutralize the protease inhibitors - mass tissue destruction
88
what is the inside structure of a plasma cell?
rough ER and large golgi apparatus to produce large amounts of antibodies (proteins)
89
what are epitopes? where are they located?
antigenic determinants present on the surface of bacteria
90
how do antibodies bind to bacteria?
antibodies bind with the FAB region to the Epitope.
91
PMN's recognize what region of the antibody?
FC
92
what antibodies are present in the mouth?
IgG and IgA
93
how does IgG get into the mouth?
leaked into mouth by gingival crevicular fluid - but it is broken down easily
94
what antibody can cross into the placenta?
IgG
95
what are the functions of IgG?
opsonization, agglutination, complement fixation
96
what antibody makes up the majority of antibodies in the body?
IgG - 80-85%
97
IgA function?
protect mucous membranes by preventing the attachment of organisms. ex actively secreted by salivary glands - has the J chain to stabolize
98
functions of IgM?
opsonization, agglutination, complement fixation
99
first antibody produced during an immune response?
IgM
100
function of IgD?
facilitates development and maturation of the antibody response. located on the surface of B-cells
101
IgE function?
release granule contents in response to allergic reactions and parasitic infections
102
function of the J-chain in IgA?
interacts with the FC fragments of IgG molecules by disulfide bonds to help stabilize it
103
function of the secretor component of IgA?
provides protection against degradation enzymes in the digestive system
104
is the host in control in a systemic exposure?
no
105
what is the systemic response?
B-cell and interlukins
106
what is the monoclonal response?
antibodies produced to only 1 bacteria like Aa
107
polyclonal response
antibodies produced by B-cells to lots of different antigens
108
is LPS produced from gram (-) or (+) bacteria
gram (-) negative
109
the myeloid stem cell gives rise to what 5 things?
1. PMN's 2. Eosinophils 3. Basophils 4. Mast Cells 5. Monocytes (macrophages)
110
where are mononuclear phagocytes located?
all tissues of the body
111
half life of macrophages?
months- can reenter tissue and then back into circulation
112
2 roles of macrophages?
1. take up microbacteria and neutralize it 2. scavenger role
113
which can be used multiple times, PMN's or Macrophages or both?
only macrophages, PMN's are end cells
114
what is the scavenger role of macrophages?
search for foreign cells and dead cells and phagocytize it
115
LPS stimulated what receptor of macrophages?
CD14 receptor of macrophages
116
the CD14 receptor of macrophages releases _______ which causes extracellular matrix destruction
MMP's
117
fibroblasts can secrete _______ which leads to alveolar bone resorption
PGE2
118
what exposes the peptide fragments of the antigen on the macrophage?
major histocompatibility complex 2 - presents antigenic peptide on the surface
119
LPS stimulated what receptor of macrophages?
CD14 receptor of macrophages
120
the CD14 receptor of macrophages releases _______ which causes alveolar bone resorption
PGE2
121
the CD14 receptor of macrophages releases _______ which causes fibroblasts to activate negatively
IL-1 beta and TNF alpha
122
the CD14 receptor of macrophages releases _______ which causes extracellular matrix destruction
MMP's
123
fibroblasts can secrete _______ which leads to alveolar bone resorption
PGE2
124
what exposes the peptide fragments of the antigen on the macrophage?
major histocompatibility complex 2 - presents antigenic peptide on the surface
125
helper T-cells and MHC 2 present the antigenic fragments to what?
b-cell - to create more b-cells and to create plasma cells
126
what are conditions that lead to monocyte deregulation?
diabetes and smoking
127
what is collagenase and where is it present?
present in fibroblasts and it break down tissues
128
what are MMP's dependent upon?
manganese and magnesium ions (divalent cations)
129
what are TIMPS
tissue inhibitors or metalloproteases - inhibit MMP's
130
how long does connective tissue take to repair?
6 weeks
131
60 year old patient with untreated periodontitis for whole life, how much attachment loss?
60 -20 years (adults dentition) = 40 years thus 4mm of attachment loss ideally
132
what causes macrophages to release lots of collagenases?
IL-1 and endotoxins
133
what is collagenase and where is it present?
present in fibroblasts and it break down tissues
134
purpose of scaling and root cleaning?
remove diseased cementum and restore the junctional epithelium
135
how fast does the epithelium grow?
1mm per day ( 0.5 mm per side of the circle)
136
how long does connective tissue take to repair?
6 weeks
137
the primary cell involved in the non-pathogenic breakdown of collagen in the gingiva is the \_\_\_\_\_\_\_
fibroblast
