Midterm Flashcards
What are the four main stages of periodontal disease-pathogenesis?
- Colonization
- Invasion
- Tissue Destruction
- Healing
What are the histological findings in the following four categories: 1)Normal 2)Early Gingivitis 3)Chronic Gingivitis 4)Adult Periodontitis
- Few bacteria at orifice, Tight intercellular junctions and JE at CEJ, supracrestal attachment intact,
- Complex flora fills gingival pocket, widened intercellular spaces containing leukocytes, JE at CEJ, loss of gingival connective tissue attachment and connective tissue is infiltrated mainly by lymphocytes
- Complex flora fills gingival pocket and calculus may be present, greater leukocytic infiltration of JE but JE still at CEJ, loss of gingival connective tissue attachment and connective tissue is infiltrated mainly by plasma cells
- Subgingival flora contains specific pathogens and calculus goes to bottom of pocket, the JE is now apical to CEJ and is converted to pocket epithelium, loss of gingival connective tissue attachment and plasma cells are predominant in CT, loss of attachment of periodontal ligament, cementum and bone and cementum resorption
When the body responds to bacteria, it creates an immune response with accompanied plaque accumulation and initiation of gingivitis, and which 4 cells are mostly involved?
- Mast Cells (bone marrow, multipotent sc, myeloid sc, mast cell progenitor). Microbe to C3a (complement peptide) to mast cell histocyte, to TNF to IL
- Acute Phase Proteins
- PMNs
- Antibodies
What are the 4 effects of the event with blood vessel dilation and increased permeability to plasma, which may clot?
1. Tissues swell due to plasma leakage 2. Elevated temp from increased blood flow in dialated vessels 3. Redness 4. Pain from increased fluid in tissues and direct effect of chemicals on sensory nerve endings
What is the effect of the event with circulating WBC adhering to walls of altered blood vessels?
WBC chemotaxis through vessel walls and to area of injury induce phagocytosis of foreign material and tissue debris and initiate Ab production
What is the effect of the event of a tissue injury?
Release of chemical mediators that increase permeability of adjacent small blood vessels
What are the six chemical mediators that mast cells release during inflammation?
- Histamine - Dilation and increase of permeability of small blood vessels: constriction of bronchi
- Chemotactic factors - Eosinophil and PMN chemotaxis
- Interleukins 3,4,5,6 - Many interactions
- TNF Alpha - Recruitment of granulocytes to area of inflammation; inducement of fever
- Leukotrienes - Dilation of small blood vessels; constriction of bronchi; chemotaxis of leukocytes
- Prostaglandins - Increase in vascular permeability; regulation of immune responses
What are the six plasma proteins increased due to a microbial infection?
- C-reactive Protein* (for inflammation, and is also an increased factor for myocardial infarction, 2-5 fold increase)
2.Fibrinogen*
3.Complement* - Mannose-binding protein *
5.Metal-binding proteins * - alpha1- antitrypsin, - anticymotrypsin
(all of these are associated with an increased risk of heart disease, except the bottom one)
What are two well-established risk factors for cardiovascular disease?
- Tobacoo smoking
2. High LDL
What is the complement immune system?
It is part of the Innate immune system, it consists of over 11 proteins and glycoproteins, it is activated by Ag-Ab interaction, it is around 10% of proteins in normal sera, it is not affected by immunization, synthesized in liver and small intestine, and it can help control the microbe and help with acute inflammation resolution. It is the first line of defense for innate immunity, then neutrophils, then monocytes, then lymphocytes with acquired immunity. But C3a and C5a are complement peptides which trigger the release of mast cell mediators and bring on inflammation
What is the Membrane Attach Complex (MAC) of the complement system?
The membrane attack complex (MAC) is a structure typically formed on the surface of pathogenic bacterial cells as a result of the activation of the host’s alternative pathway, classical pathway, or lectin pathway of the complement system, and it is one of the effector proteins of the immune system. The membrane-attack complex (MAC) forms transmembrane channels. These channels disrupt the phospholipid bilayer of target cells, leading to cell lysis and death.
How does Opsonization and PMN Phagocytosis work and which complement peptide is involved?
C3 and C3b are involved and opsonizing means marking it for destruction and ingestion by a phagocyte.
What are some of the characteristics of neutrophils?
They also come from the myeloid stem cell, just like all of the other leukocytes, they also have a lobed nucleus, granules, they phagocytize and digest engulfed materials, few in tissues except during inflammation, their short half-life helps limit damage to the host during inflammation.
How does margination, chemotaxis, and phagocytizing work with neutrophils? Which factors are involved?
The neutrophil is rolling around and the bacteria activates complement immune system, which goes to resident leukocyte and along with C3a or C5a signals with P-selectin and E-selectin and IL8 and TNF-alpha, then you have increased rolling with the selectins, and then you have chemokine signaling, then you have LFA’s expressed with integrins, then you have the CD31 zipper, then it leaves the venule and with chemotaxis goes to the bacterium
Neutrophils need chemoattractants to know what to do and where to go, what are the different sources and what attractants do those sources use to get neutrophils?
Macrophages and monocytes - Leukotriene and IL8
Many cells - Platelet activating factor
Serum/plasma - C5a
Bacteria - f-Met peptides
Mast cells - neutrophil chemotactic factor
Endothelium - IL8
B cells - IL1
