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247 Periodontics > Chapter 14 & 15 > Flashcards

Chapter 14 & 15 Flashcards

1
Q

What is innate immunity?

A
  • Inborn
  • First line of defense against invading organisms
  • Present and ready immediately
  • No memory
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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
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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
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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

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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
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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
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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
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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
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9
Q

What are the functions of immunoglobulins?

A
  • Neutralize bacteria or bacterial toxins
  • Coat bacteria to facilitate phagocytosis
  • Activate the complement system
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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

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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
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12
Q

What are cytokines?

A

General name for protein secreted by cells which affects the behavior of nearby cells

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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
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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
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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
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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
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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
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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)
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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

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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
Q

What is an example of an acquired factor and how does it affect the host immune response?

A

Diabetes mellitus
Decrease in PMN function
Decrease in PDL fibroblast and osteoblast growth
Increase in IL-1, TNF-a, PGE

26
Q

What is catabasis?

A

Resolution of inflammation and return to non-inflammatory state is regulated return to homeostasis

27
Q

What is resolution of inflammation regulated by?

A

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
Q

What initiates most of the alveolar bone destruction in periodontitis?

A

Prostaglandins

29
Q

When does extensive collagen destruction occur in periodontal tissues?

A

In the presence of matrix metalloproteinase levels

30
Q

What is the function of Periostat?

A
  • Inhibits the activity of matrix metalloproteinases
  • Used as an adjunct to periodontal administration
31
Q

What occurs in the initial lesion in days 2-4?

A
  • 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
Q

What happens in the early lesion at 4-7 days?

A
  • 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
Q

What occurs in established lesion/established gingivitis at about 21 days?

A
  • 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
Q

What happens in the advanced lesion- Periodontitis?

A
  • 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
Q

What are the factors that influence host failure to control bacterial challenge?

A
  • Abnormal PMN function
  • Persistance and virulence of bacteria
  • Acquired and environmental factors: smoking, stress
  • Systemic factors: diabetic control, genetics
36
Q

What are osteoclasts?

A

Multinucleated cells that resorb existing bone matrix

37
Q

What are osteoblasts?

A

Synthesize collagen and other bone proteins, involved in mineralization of bone matrix

38
Q

Why does remodeling occur?

A

During growth, to maintain shape and structure, in response to new stresses, in a repeating cycle throughout life

39
Q

What are the phases of remodeling?

A
  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
Q

How does regulation occur?

A

Giverned by intricate signaling mechanism btw blasts and clasts

41
Q

What does RANKL mean?

A

* Receptor Activator of Nuclear factor-kB
* Cell-membrane-bound protein that regulates osteoclast maturation and activation
* RANKL stimulates osteoclasts to resorb alveolar bone

42
Q

What is OPG?

A

Osteoprotegerin
Secreted by osteoblasts, protects bone from excessive resorption by binding to RANKL

43
Q

What happens when RANKL and OPG levels are in balance?

A

Homeostasis
Stable bone levels

44
Q

What occurs when OPG levels are decreased?

A

Osteoclastic resorption of alveolar bone (occurs in inflammation of periodontium)

45
Q

What inhibits bone resorption?

A
  • Inhibitory cytokines- anti-inflammtory mediators
  • OPG inhibits osteoclastic differentiation
46
Q

When does bone resorption occur?

A
  • OPG-to-RANKL levels are out of balance
  • RANKL stimulate osteoclasts
  • Osteoclasts cause bone resorption
47
Q

When does bone formation occur?

A
  • RANKL/OPG levels are in balance
  • OPG blocks RANKL, thus inhibiting activation of osteoclasts
  • Osteoblasts maintain bone levels
48
Q

Describe periodontitis and RANKL-mediated bone resorption

A
  • 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 (19 decks)

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