Chapter 4 Flashcards

1
Q

what is gingivitis

A
  • mildest form of PD
  • inflammation of the gingival tissues
  • no clinical attachment loss
  • to alveolar and supporting bone loss
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2
Q

what is periodontitis

A
  • clinical attachment loss: detachment of gingival connective tissue (collagen fibers) attachment apical migration of the junctional epithelium
  • alveolar and supporting bone loss
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3
Q

what is periodontal disease activity

A
  • ongoing loss of clinical connective tissue attachment and bone loss; detection of attachment loss
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4
Q

what is the inflammatory and immune response

A
  • host defines cells: PMNs (neutrophils), macrophages.. microorganisms overtake - infection/tissue damage occur
  • balance between host defines and destruction
  • important to detect; difficult - active vs inactive
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5
Q

what are the 3 models of disease activity

A
  1. continuous model theory
  2. random burst theory
  3. asynchronous multiple burst theory
    * no one theory is correct; all contribute to understanding and its cumulative effect*
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6
Q

what is the continuous model theory

A
  • slow, constant eventual tooth loss (‘everyone will lose their teeth anyway’)
  • lack of evidence
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7
Q

what is the random burst theory

A
  • episodic (comes and goes), site specific
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8
Q

what is the asynchronous multiple burst theory

A
  • limited time period, then remission
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9
Q

what must first exist in the periodontium before periodontitis

A
  • gingivitis
  • must be present, not completely understood why some forms of gingivitis progress while other don’t (genetics? host response?)
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10
Q

what happens to the bacteria when periodontal disease exists

A
  • change in host-bacteria equilibrium
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11
Q

3 conditions must exist for progression of perio:

A
  1. bacteria: critical mass - more bad than good
  2. conducive environment: favourable to bacterial growth and destruction, long standing, sub-g
  3. host response: bacteria continue to invade, contributing to the disease, destruction of own tissues in response
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12
Q

summary of bacterial invasions

A
  1. poor oral hygiene with/without contributing environmental, systemic and acquired factors
  2. accumulation of dental biofilms and other antigens at the gingival margin and in the gingival crevice; bacteria release antigenic substances through the crevice into the connective tissue
  3. host’s inflammatory and immune systems activated
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13
Q

what are the 2 common anaerobic subgingival bacteria

A
  1. PP

2. AA

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14
Q

how does the host respond to bacteria

A
  • protective
  • destructive (if overwhelmed): hard and soft tissue
  • bacteria initiate disease process
  • enzymes and by products of host cells (a lot of breakdown of perio tissues)
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15
Q

what gets released when bacteria cells die

A
  • endotoxins
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16
Q

what are leukotoxins

A
  • destroys PMNs
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17
Q

what are matrix metalloproteinases (MMPs)

A
  • family of 25 members, enzymes breaking down tissue
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18
Q

what is collagenases

A
  • breaks down collagen
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19
Q

what is proteases

A
  • breaks down protein, collagen fibers, connective tissue ground substances
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20
Q

what do endotoxins do

A
  • amplify the inflammatory process
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21
Q

what are the 3 areas of host-bacteria interaction

A
  1. supragingival
  2. gingival crevice/sulcus
  3. gingival connective tissue
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22
Q

what is the first attempt of the oral defence mechanism

A
  • prevent movement into subgingival

- saliva, gingival crevicular fluid and oral epithelium

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23
Q

how does saliva help protect from bacteria

A
  • antibacterial products

- antibodies - immunoglobulins to fight bacteria

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24
Q

how does gingival crevicular fluid help protect from bacteria

A
  • cleanses the sulcus
  • delivers more antimicrobial
  • interacts first with bacteria
25
Q

how does oral epithelium help with protecting from bacteria

A
  • keratin - helps to prevent entrance
  • close attachment of cells
  • shedding/turnover of cells
26
Q

what happens if bacteria is not stopped at the supra gingival level

A
  • inflammatory/immune response is further stimulated to eliminate the irritant and prevent the spread of infection
27
Q

what is the inflammatory/immune response

A
  • non specific reaction to bacteria
  • prevent spread of invading bacteria
  • works together with the immune system
  • objective of activation of the host inflammatory/immune system
  • eliminate or slow down the invader (bacteria)
  • limit further tissue destruction
  • beginning of healing phase
  • antigens enter tissue (some bacteria, PG and AA, endotoxins and wastes)
28
Q

what are the 3 steps of the inflammatory/immune response?

A
  1. elimination of bacteria
  2. limit further tissue destruction
  3. begin healing
    * handout is good for this!*
29
Q

what does the acute inflammatory response involve

A
  • PMNs, macrophages, mast cells, gingival crevicular fluid
30
Q

if the acute inflammatory response is ineffective, what happens

A
  • chronic inflammatory response occurs

- healing, but will cause damage to tissues

31
Q

why is the inflammatory response a double edged sword

A
  • good because phagocytosis
  • bad because it causes damage to tissues by releasing lysosomes, which destroys periodontal tissues (when bacteria die, they release toxins and enzymes which will destroy tissues)
32
Q

what do PMNs and neutrophils to

A
  • white blood cell involved in phagocytosis or engulfing bacteria
33
Q

what do macrophages do

A
  • phagocyte in connective tissues
34
Q

what do mast cells do

A
  • cell found in connective tissue that contains granules and releases substances such as heparin and histamine
35
Q

what does the serum complement do

A
  • serum proteins that work with (complement) antibody activity to eliminate pathogens; stimulate inflammation
36
Q

what does gingival crevicular fluid do

A
  • fluid found in small amounts in gingival crevice; important in cleansing substances from crevice and has antimicrobial properties
37
Q

what is clinical healthy gingiva

A
  • microscopically mild inflammatory reaction
  • PMNs in junctional epithelium move into gingival crevice
  • PMNs are WBC from lamina propria, not the epithelium
  • PMNs form a protective way between bacteria and epithelium
38
Q

review of the inflammatory process

A
  • oral biofilms at gingival margin
  • inflammation starts
  • gingival tissues react to bacteria in biofilm
  • acute inflammation
  • first inflammatory response is vascular (vasodilation)
39
Q

when are inflamed gingiva first visible

A
  • 3-4 days of undisturbed biofilm
40
Q

what is being transported to the lamina propria through blood vessels during vasodilation

A
  • PMNs (neutrophils)
  • histamine: increased permeability of blood vessels, mast cells create histamine which will allow the blood cells to open up
  • prostaglandins (fatty acids): found in cell membranes, vasodilation, pain and bone loss
41
Q

what do we see in the first response to the inflammatory process

A
  • vasodilation
  • increased gingival crevicular fluid (thicker, stringy-er than normal)
  • gingival bleeding due to edema (swelling)
42
Q

what is the neutrophil

A
  • a PMN
  • first line of defence; enters the gingival sulcus and junctional epithelium by going from the blood, through connective tissues, to the JE and into the sulcus or pocket
  • phagocytic cell (type of lysosome)
43
Q

what can cause impaired PMN functions

A
  • diabetes

- other diseases - decrease chemotaxis ability of PMN

44
Q

what is a macrophage

A
  • a phagocytic cell (remains in connective tissue for months)
  • produces and secretes cytokines: proteins, regulates activity of other cells, interleukin-1 (IL-1), TNF
  • overall, a macrophage is a phagocyte that ingests foreign material such as periodontal bacteria
45
Q

what does damage to the host tissue cause for macrophages

A
  • IL-1 - increases histamine
  • increases PMN and macrophages
  • increases number of osteoclasts
  • more host destruction
46
Q

what are cytokines

A
  • regulatory proteins such as IL1 and TNF
  • chemical messengers
  • affect cells that release them or other cells (PMN’s, macrophage PE2, osteoclast…)
  • many different functions (interleukins, chemokins/chemotaxis)
47
Q

what are opsonins

A
  • antibodies bind to surface of bacteria
  • coat the bacteria
  • easily identified by PMNs/macrophages
  • engulfed and swallowed by phagocytes
48
Q

what is the complement system

A
  • group of plasma proteins

- destroy antigens (foreign material) through chemotaxis

49
Q

what are the 2 chemotactic factors that attract PMNs

A
  1. classical pathway: activated when antibodies (proteins) bind to antigens (bacteria)
  2. alternative pathway: activated by endotoxins
50
Q

what are the 2 types of immune response

A
  1. humoral (B cell response

2. cellular (T cell response)

51
Q

what are lymphocytes

A
  • found in WBCs
  • also predominate in lamina propria
  • patrol the host
  • identify foreign pathogens
52
Q

what are the 3 types of lymphocytes

A
  1. B cells - mediators of humeral immunity
  2. T cell - mediators of cellular immunity
  3. natural killer cells
53
Q

what is humoral immunity and when is it triggered

A
  • triggered during bacterial infections (ie perio) when inflammatory response is inadequate
  • B lymphocytes are transformed into plasma cells
  • plasma cells make antibodies which bind to the antigens (bacteria)
  • immunoglobulins (family of antibodies); IgG (primary antibody produced by plasma cells)
54
Q

how does humoral immunity work

A
  • antibodies bind to the antigens
  • antigens are destroyed by macrophages
  • antibodies to different periodontal bacteria are found in gingival crevicular fluid
55
Q

how many B cells are found in the lamina propria in cases of periodontitis (percentage)

A
  • B cells are found in the lamina propria at sites with periodontitis can be as high as 90%
56
Q

what is cellular immunity

A
  • T cells migrate from blood into gingival tissues and lymph nodes
57
Q

what are the 2 types of lymph nodes

A
  1. T helper cells (CD4 receptor): secrete cytotoxins; activate phagocytosis, activate B cells
  2. T cytotoxins cells (CD8 receptor): cytotoxic T lymphocytes (CLTs) secrete molecules that destroy the cells that is bound to it
58
Q

what is the role of the CD8 T cells

A
  • to monitor all of the cells of the body
  • destroys/kills foreign antigens
  • CTLs help to keep virus-infected or malignant cells in check
59
Q

overall, what are the 5 key elements in immune response

A
  • B-lymphocytes
  • antibodies
  • macrophages
  • cytokines
  • T-lymphocytes (T-killer and T-helper)