Exam II - Lecture I Flashcards
What are the 5 cardinal signs of inflammation?
Redness - rubor
Swelling - tumor
Heat - calor
Pain - dolor
Loss of function - Functio laesa
What is the most important thing in innate immunity?
Intact tissue
Innate immunity consists of what?
Serum complement
Neutrophil
Monocyte-macrophage
What is the line b/t acute inflammation and chronic inflammation?
When monocytes-macrophages get involved, then it goes to chronic and usually involves acquired immunity
Acquired immunity has what cells?
Lymphocytes
What leads to a systemic infection?
Lymphocytes cannot handle the infection
Probing depth is a _________ finding.
Pocket depth is a _________ finding.
Clinical
Histological
Tell me some factors of the histopathology of periodontal disease.
Increased epithelial turnover rate
Increased # of blood vessels
Destruction of collagen fiber network
Tell me histologic symptoms of an initial lesion of periodontitis. 6 symptoms.
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
Tell me clinical symptoms of an initial lesion of periodontitis.
Appears clinically healthy
No pocketing
No radiographic evidence of bone loss
Tell me 5 histologic symptoms of an early lesion of periodontitis.
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
Tell me 4 clinical symptoms of an early lesion of periodontitis.
1- Gingivitis (acute)
2- Changes In gingival color, contour, consistency, and BOP
3- No pocketing
4- No bone loss
Tell me 6 histologic symptoms of an established lesion of periodontitis.
- 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 +/-
Tell me 4 clinical symptoms of an established lesion of periodontitis.
- Gingivitis (Chronic form)
- Changes in gingival color, contour, consistency, and BOP
- No pocketing
- No bone loss
Tell me 8 histologic symptoms of an advanced lesion of periodontitis.
- 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
Tell me 4 clinical symptoms of an advanced lesion of periodontitis.
- Periodontitis
- Changes in gingival color, contour, consistency, and BOP
- Periodontal pocket formation
- Alveolar bone loss as shown on radiographs
Periodontitis in children is evidenced by the presence of ___________, not plasma cells.
Lymphocytes
Periodontitis in adults is characterized by presence of _________.
Plasma cells
FAs, FMLP, and LPS attract what?
PMNs
What is the current model of periodontitis?
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
Those that get aggressive periodontitis are said to be _____-________.
HYPER-Responsive
Those that are said to have no response to a bacterial challenge are called _____-________.
HYPO-Responsive
Tell me the critical pathway model of pathogenesis.
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
What attacks plaque?
Mast cells
Acute phase proteins
Complement
PMNs
Antibodies (Adaptive)
What do mast cells have in them?
Granules
Mast cells release ________ which cause vasodilation.
Histamine
*Also Fc fragments and IgE
T/F - Mast cells have granules.
TRUE
The etiology of gingivitis, periodontitis, and caries is what?
PLAQUE BIOFILM
T/F - Gingivitis is due to the host response.
TRUE
T/F - >90% of Americans have periodontal disease (Gingivitis). ~50% of Americans have periodontitis.
TRUE
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*
What activates and causes anaphylaxis?
MAST CELLS
What do mast cells release? 6 things
Histamine (Vasoactive amines)
Eosinophil chemotactic factor
Platelet activating factor
Enzymes
Leukotrienes C, D, E
Prostaglandin PGD2, thromboxane
T/F - Anaphylaxis can happen from latex and/or rubber gloves.
TRUE
T/F - According to Winkler, C3a binds on the surface of the mast cell.
TRUE
What is histamine SRSA?
Slow reacting substance A
What releases interleukins?
ONLY WBCs
Vasodilation does what to blood flow?
SLOWS IT DOWN
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
What happens in response to tissue injury?
Release of chemical mediators that increase permeability of adj small blood vessels
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
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
Make a card at 57 minutes (Slide 27)
CARD
Histamine has what effects?
Dilation of increase of permeability of small blood vessels : constriction of bronchi
Chemotactic factors have what effects?
Eosinophil and PMN chemotaxis
T/F - Interleukins 3,4,5,6 have many effects.
TRUE
Mast cells release what chemicals that cause effects? 6 things
Histamine
Chemotactic factors
Interleukins 3,4,5,6
TNF-alpha
Leukotrienes
Prostaglandins
TNF-alpha has what effects?
Recruitment of granulocytes to area of inflammation - inducement of fever
Leukotrienes have what effects?
Dilation of small blood vessels
Constriction of bronchi
Chemotaxis of leukocytes
Prostaglandins have what effects?
Increase in vascular permeability
Regulation of immune responses
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
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
What are 2 well established risk factors for cardiovascular disease?
Tobacco smoking
High LDL
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
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
Understand complement
Seriously.
T/F - PMNs have granules.
TRUE
A non stimulated PMN is what?
Round
A stimulated PMN is what shape?
Takes a bipolar shape
-It’s a shapeshifter
T/F - PMN comes from a myeloid stem cell.
TRUE
What does never let mean eat burritos mean?
Most common WBCs in the blood
Neutrophils
Lymphocytes
Macrophages
Eosinophils
Basophils
Tell me about neutrophils.
Lobed nucleus
Granules
Most of the circulating leukocytes
Phagocytosis of bacteria
If an infection is present, what happens to PMNs?
Large increase in PMNs
Tell me about eosinophils?
Granules
Few in tissues
Inflammatory
Tell me about basophils.
Lobed nucleus
Granules
Tissues
Release histamine
Tell me about monocytes.
- Macrophages
- Dendritic cells
Single nucleus
All tissues and linings
Phagocytosis and presenting of cells
What is the half life of a PMN?
- 5 to 90 days*
- Die in spleen or killed by infection
Name three things PMNs do.
Phagocytosis
Release of enzymes
Release of chemical mediators
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)
What is in the phagolysosome?
Proteolytic enzymes
When these phagocytosize things, they degrade and cause local tissue damage
Cellular adherence molecules (ICAM-1,2 and ELAM) do what?
Tell PMNs to stop at that site
IL-8 does what?
Modifies the endothelium
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
What granules are in PMNs?
Primary - (azurophilic)
Secondary - (specific)
Tertiary
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
What two important receptors are on the surface of PMNs?
Fc fragment receptor
C3b receptor
Primary/azurophilic granules. Tell me.
Myeloperoxidase
Bactericidal/permeability-increasing protein (BPI)
Defensins
Elastase - SERINE PROTEASE
Cathepsin G - SERINE PROTEASE
Specific granules (secondary granules). Tell me.
Alkaline phosphatase
Lysozyme
NADPH oxidase
Collagenase
Lactoferrin
Cathelicidin
Tertiary granules. Tell me.
Cathepsin
Gelatinase
What are some oxygen dependent microbiocidal mechanisms?
NADPH oxidase complex
Myeloperoxidase
Superoxide dismutase
What are some O2 independent microbicidal mechanisms?
Serine Proteases
Acid hydrolases
Metalloproteinases
Lysozyme
Bactericidalensins
T/F - Fibroblasts release a lot of collagenase which causes self-tissue damage by cutting tissue into 1/3 and 2/3 fragments.
TRUE
Tell me about elastase.
SERINE PROTEASE
Highly active non-specific protease
Collagenase/Gelatinase does what?
Breakdown collagen
- Released as proenzyme
- Gets to environment and is cleaved into the active enzyme
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
What can HOCL do?
Oxidatively inactivate 3 major tissue anti-proteases
Can oxidatively activate collagenase and gelatinase - these are released as proenzymes
T/F - Nonoxidative PMN enzymes bind metal.
TRUE
*Most common way to deal with stuff
What is a PMN respiratory burst?
PMNs can glow
-Chemoluminescent
Reactive species from bleach and H2O2
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
What 5 things are associated with PMN immunology?
Quantitative/Qualitative
Chemotaxis/Chemokinesis
Phagocytosis
Killing
Respiratory burst
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
What are 2 types of healthy gingiva?
Pristine
-Little to no inflammatory infiltrate
Clinically healthy state
-Inflitrate is present, but this is normal
T/F - The apical termination of the JE is at the CEJ in gingivitis.
TRUE
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
Histologically, gingivitis. Talk about it.
PMNs
T lymphocytes w/ lesser number of plasma cells
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
