1
Q
What is innate immunity?
A
- Inborn
- First line of defense against invading organisms
- Present and ready immediately
- No memory
2
Q
What is adaptive immunity?
A
- Develops throughout life
- Requires time to react to invading organisms
- Demonstrates immunological memory; reacts more rapidly on subsequent exposure to the same organism
3
Q
What is the prime purpose of the immune system?
A
- Defense of the life of the host
- Recognizes bacteria, viruses, fungi, parasites as “foreign”
- Responds by: 1) sending certain types of cells to infection site 2) producing substances to counteract the invaders
4
Q
What is the consequence of an overzealous immune response?
A
Misdirected or intense immune response can harm the body that it is trying to protect
5
Q
What are the function of PMNs?
A
- Phagocytosis
- First line of defense
- Short-lived
- Attracted to bacteria by chemotaxis
- Release of lysosomes
- Release of cytokines (regulatory proteins) that signal the immune system to send additional phagocytic cells to site of infection
- Bacteria associated with perio disease are effectively phagocytized by PMNs
6
Q
What are the characteristics of macrophages?
A
- Large phagocytes
- “Monocytes” in the blood stream, “macrophages” in the tissue
- Phagocytosis
- Slower to arrive at infection site
- Longer-lived, numerous in chronic inflammation
- Present antigen to T-cells
7
Q
What are the characteristics of B-lymphocytes?
A
- WBC’s differentiate into: plasma B-cells, memory B–cells, B-cells make antibodies
- Produce immunoglobulins
8
Q
What is the function of T-lymphocytes?
A
- Intensify the response of other immune cells like (b-lymphocytes and macrophages) to bacterial invasion
- Produce cytokines (interleukins) that further stimulate immune response
9
Q
What are the functions of immunoglobulins?
A
- Neutralize bacteria or bacterial toxins
- Coat bacteria to facilitate phagocytosis
- Activate the complement system
10
Q
What is the complement system?
A
Complex series of circulating proteins that facilitate phagocytosis or directly kill bacteria by puncturing bacterial cell membranes
Activated by antibodies
11
Q
What are the functions of the complement system?
A
- Destruction of pathogens: Lysis of cell membranes of certain bacteria
- Opsonization- complement coats bacterial surface allowing phagocytes to recognize, engulf and destroy bacteria
- Recruitment of additional phagocytic cells to the ifection site and clearance of immune complexes from circulation
- Immune clearance: removes immune complexes from circulation
12
Q
What are cytokines?
A
General name for protein secreted by cells which affects the behavior of nearby cells
13
Q
How does local tissue damage from phagocytosis occur?
A
- Lysosomal enzymes and microbial products are released from a leukocyte after phagocytosis or when the leukocyte dies
- Release of lysosomal enzymes cause damage to tissue cells in the same way they destroy bacteria
14
Q
What is the inflammatory response in major events?
A
- Triggered by pathogens or injury
- Immediate: Mast cells release chemicals ^ vascular permeability
- In minutes: ^ blood flow brings immune cells to area
- In hours: Lekocytes extravasate, plasma proteins leak out and accumulate in tissue
- Leukocyte phagocutosis of invading pathogens & release infl. mediators: cytokines, prostaglandins, matrix metalloproteinases. Chemokines
15
Q
What is acute inflammation?
A
- Short term, normal process
- Without inflammation, wounds and infections would not heal and would threaten the life of the host
16
Q
What are the 5 classic signed of inflammation?
A
- Heat- local ^ in temp from ^ blood flow
- Redness- due to ^ blood flow
- Swelling- Accumulation of leukocytes and plasma at site
- Pain- excess fluid puts pressure on nerve endings
- Loss of function
17
Q
What occurs during acute inflammation?
A
- PMN phagocytosis occurs first, releasing non-specific toxins
- PMNs release cytokines- acute phase reactant proteins (c-reactive protein/CRP)
- PMNs are short-lived in early stages
- If invaders are eliminated, inflammation stops and tissue homeostasis occurs
- Resolution process: “stop signals” shut down and clear immune cells- prevents acute from progressing to chronic
18
Q
Characteristics of chronic inflammation
A
- Long-lived, out of control inflammatory response resulting in tissue injury (more than several weeks)
- Occurs when acute inflammation doe not eliminate infection
- Pathological
- Loss of symptoms, absent from pain
- Can inflict permanent damage to host tissues (periodontitis)
19
Q
What is the chronic inflammatory process?
A
Macrophage accumulation
Macrophages phagocytize microorganisms
Leukocytes release inflammatory mediators
Duration of months or years
Is abnormal and does not benefit the host
20
Q
What is virulence factor?
A
Mechanisms that enable biofilm bacteria to colonize and damage periodontal tissues
21
Q
What is lipopolysaccharide?
A
An endotoxin present on the outer membrane of gram (-) bacteria that is responsible for initiating inflammation
22
Q
What are factors that affect the host immune response?
A
- Virulence factors
- Genetic factors
- Environmental factors
- Acquired factors
23
Q
What is an example of a genetic factor?
A
Leukocyte adhesion deficiency (LAD)
24
Q
What is an example of an environmental factor and how does it affect the host immune response?
A
- Smoking
- Reduction in ability of PMN phagocytic capabilities
- Decrease in vascularity of tissues
- Affects T- and B-lymphocyte response to pathogens
25
What is an example of an acquired factor and how does it affect the host immune response?
Diabetes mellitus
Decrease in PMN function
Decrease in PDL fibroblast and osteoblast growth
Increase in IL-1, TNF-a, PGE
26
What is catabasis?
Resolution of inflammation and return to non-inflammatory state is regulated return to homeostasis
27
What is resolution of inflammation regulated by?
Pro-resolving lipid mediators:
* Terminate PMN recruitment
* Stimulate macrophages to remove dead cells
* Promote antibacterial activities
* Promote tissue repair and regeneration to achieve homeostasis
28
What initiates most of the alveolar bone destruction in periodontitis?
Prostaglandins
29
When does extensive collagen destruction occur in periodontal tissues?
In the presence of matrix metalloproteinase levels
30
What is the function of Periostat?
* Inhibits the activity of matrix metalloproteinases
* Used as an adjunct to periodontal administration
31
What occurs in the initial lesion in days 2-4?
* Bacteria colonize near the margin
* G (-) bacteria trigger host immune response
* PMNs to site releasing cytokines, local tissue destruction, bacteria phagocytized, complement system
* If pathogens persist--> early gingivitis
32
What happens in the early lesion at 4-7 days?
* Biofilm maturation--> toxins penetrate JE
* PMN migration, release of cytokines, phagocytosis of bacteria
* Migration of macrophages- release cytokines, PGe2, MMPs
* MMPs lead to loss of collagen in CT
* T-lymphocyte migration, produce cytokines
* **Early lesion= T-cell lesion**
* JE proliferates
* **Edema and redness of GM seen clinically**
* **If persistant, progression to established gingivitis**
33
What occurs in established lesion/established gingivitis at about 21 days?
* Biofilm disruption of most coronal portion of JE
* Increase in PMN's, macrophages, lymphocytes
* **Established lesion= plasma cell lesion**
* Deeper epithelian ridges, JE loosens and transforms into pocket epithelium
* All clinical features of gingivitis accentuated
* **In susceptible individuals established gingivitis will progress to periodontitis**
34
What happens in the advanced lesion- Periodontitis?
* Biofilm develops along root surface
* Immune response begins to harm periodontium
* PMNs, macrophages, epithelial cytokines destroy CT and PDL fibers
* Macrophage cytokines, PGE, MMPs destroy CT and alveolar bone
* **Tissue destruction overwhelms repair and becomes the main outcome of the tissue response**
* JE migrates apically creating pocket
* Fibroblasts destroy PDL fibers
* Osteoclasts destroy alveolar bone crest
35
What are the factors that influence host failure to control bacterial challenge?
* Abnormal PMN function
* Persistance and virulence of bacteria
* Acquired and environmental factors: smoking, stress
* Systemic factors: diabetic control, genetics
36
What are osteoclasts?
Multinucleated cells that resorb existing bone matrix
37
What are osteoblasts?
Synthesize collagen and other bone proteins, involved in mineralization of bone matrix
38
Why does remodeling occur?
During growth, to maintain shape and structure, in response to new stresses, in a repeating cycle throughout life
39
What are the phases of remodeling?
1. Resorption- attraction of osteoclasts to the surface
2. Reversal- Clasts detatch, monocytes adhere and attract osteoblasts to eroded area
3. Formation- osteoblasts form matrix to replace resorbed w/ new
4. Resting- lengthy phase maintained until next cycle
40
How does regulation occur?
Giverned by intricate signaling mechanism btw blasts and clasts
41
What does RANKL mean?
*** Receptor Activator of Nuclear factor-kB**
* Cell-membrane-bound protein that regulates osteoclast maturation and activation
* RANKL stimulates osteoclasts to resorb alveolar bone
42
What is OPG?
**Osteoprotegerin**
Secreted by osteoblasts, protects bone from excessive resorption by binding to RANKL
43
What happens when RANKL and OPG levels are in balance?
Homeostasis
Stable bone levels
44
What occurs when OPG levels are decreased?
Osteoclastic resorption of alveolar bone (occurs in inflammation of periodontium)
45
What inhibits bone resorption?
* Inhibitory cytokines- anti-inflammtory mediators
* OPG inhibits osteoclastic differentiation
46
When does bone resorption occur?
* OPG-to-RANKL levels are out of balance
* RANKL stimulate osteoclasts
* Osteoclasts cause bone resorption
47
When does bone formation occur?
* RANKL/OPG levels are in balance
* OPG blocks RANKL, thus inhibiting activation of osteoclasts
* Osteoblasts maintain bone levels
48
Describe periodontitis and RANKL-mediated bone resorption
* Proinflammatory mediators protect the host from microbial attack but also stimulate osteoblasts, fibroblasts, T- and B-lymphocytes to produce RANKL
* RANKL activates osteoclasts- so if left untreates the host inflammatory response leads to irreversible destruction of alveolar bone
247 Periodontics
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