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33 Cards in this Set
- Front
- Back
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What type of component in the immune system sort of stradles between innate and adaptive?
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macrophage
take about 1 week of time for adaptive immunity to really kick in to place. Macrophage will activate B and T cell. |
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1. Autoimmunity?
2. Immunodeficiency? |
1. breakdown of self tolerance
2. defects in the immune system |
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What is platelet rich plasma? What's the advantage of PRP vs. natural clot?
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Source of GFs that support bone and soft tissue healing.
Blood clot: initiates soft tissue healing and bone regeneration, since the clot forms + healing process starts. Natural clot: 95% rbs, 4% plt, 1% wbc PRP: 95% plts, 4% rbs, 1% wbc. Here you reverse the percentage of rbcs from natural clot so its better for the clot. |
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Describe PRP technology
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-can extract platelet from plasma in human serum samples.
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What are platelets?
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-end product of megakaryocytes
-no nucleus for replication Has PDGF, TGF-Beta, Epidermal GF, VEGF, fibronectin, and vitronectin. -These are all very beneficial |
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Use of PRP? What makes it so safe?
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-Tissue grafts
-Wound sealing and healing -Acceleration of bone graft healing and maturation of graft -Its completely autogenous you avoid risk of transmissable disease such as HIV, and Hep B,C, D. |
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After spinning serum what's in the bottom?
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RBCs. Platelet core plasm is right above that and with this, you can make a membrane although it doesn't last long.
-Good for soft tissue, not as great for bone. |
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What do all cells of the immune system come from?
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Comes from a progenitor cell. Really depends on the particular environment where cell is being developed
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What's the main immune cell in periodontitis?
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Neutrophils mostly.
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PMNs/Neutrophils
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-make up 50-70% of circulating leukocytes
-critical to host defense against injury + infection -as lesion becomes more chornic, PMNs decrease. They don't disappear, they just don't drive the action. -Phagocytosis is enhanced by complement receptors; plays role in local tissue damage. -1st to localize into sites of infection |
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Eosinophils
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-orange color, stain pink
-Major response to parasitic infection |
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Basophils
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-retains hematoxylin, blue dye
-His, Heparin, slow reaction substance of anaphylaxis |
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Monocytes/Macrophages
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-direct role in cell mediated immunity also
-large, long living, highly phagocytic -most abundant in later stages -Have receptors for Fc portion of IgG -Leads to stimulation of T and B lymphocytes. key producers of inflammatory mediators: cytokines, prostaglandins in response to both host + bacterial components. |
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B cells vs plasma cells
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Plasma cells - B cells that move into the tissue. Antibody factories
B cells - programmed to produce antigen specific antibody |
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Nk cells
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capable of killing tumor cells as well as virally infected cells, cancerous cells.
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What are opsonins?
Inflammatory mediators? Anaphylatoxins? |
C3b, IC3b, C4b. Coats the cell and makes it more likely to be engulfed by the macrophage.
Inflammatory mediators: C5a, C3a release of anaphylatoxins (his) - causes dilation blod vessels, increasing permeability, and influx of serum factors. |
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What is a MAC?
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Membrane attack complex - lysis of bacteria occurs through this.
-Chemoattractants are generated from complement split products, which causes migration and influx of PMNs and macrophages. |
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C5a does what?
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Attracts neutrophils and leukocytes to migrate.
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Clotting cascade?
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Triggered by intrinsic or extrsinc converge into Factor Xa. This converts prothrombin into thrombin, which then triggers fibrinogen into fibrin. This forms the clot
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Kinin system?
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Bradykinin acts to increase vascular dilation an permeability, stim smooth muscle contraction, activate leukocyte chemotaxis. Good for initial start.
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Cytokines
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Intracellular messengers between white blood cells. aka interleukins.
-every cell in body have some receptor for cytokines. -fcn in autocrine or paracrine fashion. |
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Pleiotropic?
Redunant? Synergistic? Antagonistic? |
Single cytokind can cause many different effects on target cell
-many cytokines can elicit same response -2 cytokins on target cell are more than additive -one cytokine is capable of blocking effect of another cytokins |
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Functions of cytokines?
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1. activation
2. proliferation / inhibition of proliferation 3. Apoptosis 4. Differentiation 5. Chemotaxis |
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Acute phase proteins?
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-Class of proteins that are made in liver in response to inflammation.
-in response to injury, local inflammatory cells (neutrophils, macrophages, etc.) interact with this. Major one: C-reactive protein. Connetcs overall health to periodontal disease. |
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Lipid mediators
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Derived from arachidonic acid in cell membranes when its damaged. Enzymes in serum and ECM that will act on the acid and metabolize it into prostaglandins.
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Two pathways that the arachidonic acid can take?
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-Cyclooxygenase pathway: gets you vasodilation, PGE, pain, PGD, PGF, etc. prostaglandins.
-Lipoxygenase pathway: gets you leukotrienes, potent chemo attractants for neutrophils. Corticosteroids will inhibit phospholipases. NSAIDs inhibit the cyclooxygenase pathway - dont want to use this long term due to GI problems. COX1 in GI system is expressed all the time; if we inhibit it, you see side effects. |
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Prostaglandin E2
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One of hte most potent stimulators for bone resorption.
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What lipid mediators shut down inflammation?
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If there's too much of the enzyme, they start to work on each other. You get lipoxins. Lipoxin A4 - works to shut down the inflammatory cascade from a lipid stand point.
-Resolvants - help resolve inflmmation. Naturally occuring so promoting formation of this will reduce our dependence on drugs. This hasnt been doen yet though. |
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COX 2 inhibitors
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Super aspirins - designed to work as effectively as NASAIDs but without side effects of ulcers and GI bleeding.
-Celebrex, Vioxx. |
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Symptoms of type 1 hypersensitivity
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mild rash to anaphylaxis
-mast cells, His, rapid effect, IgE receptor on mast cell. Large amt of His released. |
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Type 2 hypersensitivity
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deals with complement, classical pathway.
-longer to develop, few min to hours. Ab-Ag interactions. |
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Type 3 hypersensitivity
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Arthus reaction - hrs to day. Immune complexes
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Type 4 hypersensitivity
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Delayed type through T cells. Takes few days to develop since you're dealing with acquired immune response.
-Macrophages are primary effector cell. |
