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Perio - Exam 2 > Exam II - Lecture I > Flashcards

Exam II - Lecture I Flashcards

1
Q

What are the 5 cardinal signs of inflammation?

A

Redness - rubor

Swelling - tumor

Heat - calor

Pain - dolor

Loss of function - Functio laesa

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2
Q

What is the most important thing in innate immunity?

A

Intact tissue

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3
Q

Innate immunity consists of what?

A

Serum complement

Neutrophil

Monocyte-macrophage

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4
Q

What is the line b/t acute inflammation and chronic inflammation?

A

When monocytes-macrophages get involved, then it goes to chronic and usually involves acquired immunity

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5
Q

Acquired immunity has what cells?

A

Lymphocytes

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6
Q

What leads to a systemic infection?

A

Lymphocytes cannot handle the infection

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7
Q

Probing depth is a _________ finding.

Pocket depth is a _________ finding.

A

Clinical

Histological

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8
Q

Tell me some factors of the histopathology of periodontal disease.

A

Increased epithelial turnover rate

Increased # of blood vessels

Destruction of collagen fiber network

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9
Q

Tell me histologic symptoms of an initial lesion of periodontitis. 6 symptoms.

A

1- Classic vasculitits of vessels subjacent to the JE

2- Exudate

3- Increased migration of leukocytes into the JE and sulcus

4- Presence of serum proteins, esp fibrin

5- Alteration of the most coronal portion of the JE

6- Loss of perivascular collagen

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10
Q

Tell me clinical symptoms of an initial lesion of periodontitis.

A

Appears clinically healthy

No pocketing

No radiographic evidence of bone loss

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11
Q

Tell me 5 histologic symptoms of an early lesion of periodontitis.

A

1- Accentuation of features of the initial lesion

2- Accumulation of lymphoid cells subjacent to JE

3- Cytopathic alterations of fibroblasts

4- Further loss of collagen fiber network of the marginal gingiva

5- Beginning proliferation of basal cells of JE

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12
Q

Tell me 4 clinical symptoms of an early lesion of periodontitis.

A

1- Gingivitis (acute)

2- Changes In gingival color, contour, consistency, and BOP

3- No pocketing

4- No bone loss

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13
Q

Tell me 6 histologic symptoms of an established lesion of periodontitis.

A
  • Persistence of the symptoms of the acute inflammation
  • Predominance of plasma cells w/o appreciable bone loss
  • Presence of immunoglobulins extravascularly in the CT an dJE
  • Continuing loss of CT noted in early lesion
  • Proliferation, apical migration, and lateral extension of JE
  • Early pocket formation +/-
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14
Q

Tell me 4 clinical symptoms of an established lesion of periodontitis.

A
  • Gingivitis (Chronic form)
  • Changes in gingival color, contour, consistency, and BOP
  • No pocketing
  • No bone loss
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15
Q

Tell me 8 histologic symptoms of an advanced lesion of periodontitis.

A
  • All features of established lesion
  • Extension into alveolar bone and PDL w/ significant bone loss
  • Continuous loss of collagen
  • Altered plasma cells
  • Formation of pockets
  • Periods of quiescence and exacerbation
  • Conversion of distant bone marrow into fibrous CT
  • Widespread manifestations of inflammation
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16
Q

Tell me 4 clinical symptoms of an advanced lesion of periodontitis.

A
  • Periodontitis
  • Changes in gingival color, contour, consistency, and BOP
  • Periodontal pocket formation
  • Alveolar bone loss as shown on radiographs
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17
Q

Periodontitis in children is evidenced by the presence of ___________, not plasma cells.

A

Lymphocytes

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18
Q

Periodontitis in adults is characterized by presence of _________.

A

Plasma cells

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19
Q

FAs, FMLP, and LPS attract what?

A

PMNs

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20
Q

What is the current model of periodontitis?

A

Microbial challenge ->Host Immune-inflammatory response -> CT and bone metabolism -> Clinical signs of disease initiation and progression

*Genetic risk, environmental, and acquired risk factors lead into this as well

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21
Q

Those that get aggressive periodontitis are said to be _____-________.

A

HYPER-Responsive

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22
Q

Those that are said to have no response to a bacterial challenge are called _____-________.

A

HYPO-Responsive

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23
Q

Tell me the critical pathway model of pathogenesis.

A

Pathogenic flora->immune response (Complement, mast cells, antibodies, neutrophil clearance)

IF clearance does not occur, then what?
-Bacterial penetration
—Either a systemic exposure, or
—Monocyte, lymphocyte axis
—-Initial periodontitis has begun
-Leads to cytokines, inflammation and tissue destruction, pocketing and bone loss
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24
Q

What attacks plaque?

A

Mast cells

Acute phase proteins

Complement

PMNs

Antibodies (Adaptive)

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25
What do mast cells have in them?
Granules
26
Mast cells release ________ which cause vasodilation.
Histamine *Also Fc fragments and IgE
27
T/F - Mast cells have granules.
TRUE
28
The etiology of gingivitis, periodontitis, and caries is what?
PLAQUE BIOFILM
29
T/F - Gingivitis is due to the host response.
TRUE
30
T/F - >90% of Americans have periodontal disease (Gingivitis). ~50% of Americans have periodontitis.
TRUE
31
What WBC is one of the 1st responders to an infection?
MAST Cell - Granules - No phagocytosis - Comes from myeloid stem cell line * -Common receptor is the Fc fragment receptor of IgE*
32
What activates and causes anaphylaxis?
MAST CELLS
33
What do mast cells release? 6 things
Histamine (Vasoactive amines) Eosinophil chemotactic factor Platelet activating factor Enzymes Leukotrienes C, D, E Prostaglandin PGD2, thromboxane
34
T/F - Anaphylaxis can happen from latex and/or rubber gloves.
TRUE
35
T/F - According to Winkler, C3a binds on the surface of the mast cell.
TRUE
36
What is histamine SRSA?
Slow reacting substance A
37
What releases interleukins?
ONLY WBCs
38
Vasodilation does what to blood flow?
SLOWS IT DOWN
39
In order to get WBCs to the site, what must happen?
Vasodilation of vessel to slow blood flow Permeability of vessel must increase to get the WBCs thru the endothelium
40
What happens in response to tissue injury?
Release of chemical mediators that increase permeability of adj small blood vessels
41
What happens when blood vessels are dilated and increased permeability to plasma?
Tissues swell due to plasma leakage Elevated temp from increased blood flow Redness Pain from increased fluid in tissues and direct effect of chemicals on sensory nerve endings
42
What happens when circulating WBC adhere to walls of altered blood vessels?
WBC chemotaxis thru vessel walls and to area of injury This induces phagocytosis of foreign material and tissue debris and initiation of Ab production
43
Make a card at 57 minutes (Slide 27)
CARD
44
Histamine has what effects?
Dilation of increase of permeability of small blood vessels : constriction of bronchi
45
Chemotactic factors have what effects?
Eosinophil and PMN chemotaxis
46
T/F - Interleukins 3,4,5,6 have many effects.
TRUE
47
Mast cells release what chemicals that cause effects? 6 things
Histamine Chemotactic factors Interleukins 3,4,5,6 TNF-alpha Leukotrienes Prostaglandins
48
TNF-alpha has what effects?
Recruitment of granulocytes to area of inflammation - inducement of fever
49
Leukotrienes have what effects?
Dilation of small blood vessels Constriction of bronchi Chemotaxis of leukocytes
50
Prostaglandins have what effects?
Increase in vascular permeability Regulation of immune responses
51
What are acute phase proteins?
Proteins whose plasma concentrations increase or decreases Increase - Positive acute-phase proteins Decrease - Negative acute-phase proteins - this is in response to inflammation
52
What plasma proteins are increased due to microbial infection? 6 of them.
C-reactive protein Fibrinogen Complement Mannose-binding protein Metal-binding proteins (These 5 are associated with increased risk of heart disease) Alpha1-antitrypsin, alpha1-anticymotrypsin
53
What are 2 well established risk factors for cardiovascular disease?
Tobacco smoking High LDL
54
Recent evidence has identified __________ __________ as an important risk factor for MI, like a 2-5 fold increased risk
C-reactive protein **This is a better indicator of risk over tobacco smoking or high LDL
55
Where is complement synthesized? (In what organs?)
Liver -Risk of bone infection if a liver problem is also present Small intestine Macrophages Other mononuclear cells
56
Understand complement
Seriously.
57
T/F - PMNs have granules.
TRUE
58
A non stimulated PMN is what?
Round
59
A stimulated PMN is what shape?
Takes a bipolar shape -It’s a shapeshifter
60
T/F - PMN comes from a myeloid stem cell.
TRUE
61
What does never let mean eat burritos mean?
Most common WBCs in the blood Neutrophils Lymphocytes Macrophages Eosinophils Basophils
62
Tell me about neutrophils.
Lobed nucleus Granules Most of the circulating leukocytes Phagocytosis of bacteria
63
If an infection is present, what happens to PMNs?
Large increase in PMNs
64
Tell me about eosinophils?
Granules Few in tissues Inflammatory
65
Tell me about basophils.
Lobed nucleus Granules Tissues Release histamine
66
Tell me about monocytes. - Macrophages - Dendritic cells
Single nucleus All tissues and linings Phagocytosis and presenting of cells
67
What is the half life of a PMN?
* 5 to 90 days* | - Die in spleen or killed by infection
68
Name three things PMNs do.
Phagocytosis Release of enzymes Release of chemical mediators
69
Tell me the movement of PMNs.
Leaves circulation to get to site of action by squeezing through endothelium - Sticks to endothelium (selectins, adhesins) - Squeeze thru endothelium (diapedesis) - Chemotaxis (inflammatory mediators) - Phagocytosis - Death (apoptosis)
70
What is in the phagolysosome?
Proteolytic enzymes When these phagocytosize things, they degrade and cause local tissue damage
71
Cellular adherence molecules (ICAM-1,2 and ELAM) do what?
Tell PMNs to stop at that site
72
IL-8 does what?
Modifies the endothelium
73
Tell me the difference b/t chemokinesis and chemotaxis.
Chemokinesis - Live cells will move when stimulated -*Except for KERATINOCYTES —They are full of keratin and dead Chemotaxis - Directed movement of WBCs toward a chemotactic gradient
74
What granules are in PMNs?
Primary - (azurophilic) Secondary - (specific) Tertiary
75
What are the 5 general steps of phagocytosis?
Bacterium is bound Brought into phagosome Phagosome and lysosome combine for the phagolysosome Bacteria degraded Bacterial debris is exocytosed
76
What two important receptors are on the surface of PMNs?
Fc fragment receptor C3b receptor
77
Primary/azurophilic granules. Tell me.
Myeloperoxidase Bactericidal/permeability-increasing protein (BPI) Defensins Elastase - SERINE PROTEASE Cathepsin G - SERINE PROTEASE
78
Specific granules (secondary granules). Tell me.
Alkaline phosphatase Lysozyme NADPH oxidase Collagenase Lactoferrin Cathelicidin
79
Tertiary granules. Tell me.
Cathepsin Gelatinase
80
What are some oxygen dependent microbiocidal mechanisms?
NADPH oxidase complex Myeloperoxidase Superoxide dismutase
81
What are some O2 independent microbicidal mechanisms?
Serine Proteases Acid hydrolases Metalloproteinases Lysozyme Bactericidalensins
82
T/F - Fibroblasts release a lot of collagenase which causes self-tissue damage by cutting tissue into 1/3 and 2/3 fragments.
TRUE
83
Tell me about elastase.
SERINE PROTEASE Highly active non-specific protease
84
Collagenase/Gelatinase does what?
Breakdown collagen * Released as proenzyme - Gets to environment and is cleaved into the active enzyme
85
What are 3 reasons that neutrophil proteases are NOT thought to be significantly involved in tissue damage?
Tissue bathed in plasma anti-proteases Metalloproteases are released in a latent inactive form Anti-oxidants exert strong anti-inflammatory effects in neutrophil-dependent tissue damage model systems *TIMPs - Tissue inhibitors metalloproteases
86
What can HOCL do?
Oxidatively inactivate 3 major tissue anti-proteases Can oxidatively activate collagenase and gelatinase - these are released as proenzymes
87
T/F - Nonoxidative PMN enzymes bind metal.
TRUE *Most common way to deal with stuff
88
What is a PMN respiratory burst?
PMNs can glow -Chemoluminescent Reactive species from bleach and H2O2
89
T/F - There is a quantitative and qualitative aspect to PMN immunology.
TRUE Must be sufficient number of them, and must be properly functioning in immunity
90
What 5 things are associated with PMN immunology?
Quantitative/Qualitative Chemotaxis/Chemokinesis Phagocytosis Killing Respiratory burst
91
What are 4 host risk factors associated with modifiers of disease expression genetic/induced neutrophil defects - decreased killing, dysregulation?
Leukocyte adhesion deficiency (LAD) Papillon LeFevre Syndrome Diabetes Smoking
92
What are 2 types of healthy gingiva?
Pristine -Little to no inflammatory infiltrate Clinically healthy state -Inflitrate is present, but this is normal
93
T/F - The apical termination of the JE is at the CEJ in gingivitis.
TRUE
94
What happens in gingivitis?
Sulcus has deepened and changed into pocket epithelium Gingival CT near the PE is heavily infiltrated with inflammatory cells -PMNs, T-lymphocytes, few plasma cells PE into inflamed CT No apical migration of the JE or resorption of alveolar bone has occurred
95
Histologically, gingivitis. Talk about it.
PMNs T lymphocytes w/ lesser number of plasma cells
96
Histologically, periodontitis. Tell me.
JE has converted to an ulcerate PE that is located on the root surface apical to the crest of the alveolar bone ICGT underlying the PE has been replace with a heavy inflammation

Perio - Exam 2 (8 decks)

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