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
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
3
Q
what is periodontal disease activity
A
- ongoing loss of clinical connective tissue attachment and bone loss; detection of attachment loss
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
5
Q
what are the 3 models of disease activity
A
- continuous model theory
- random burst theory
- asynchronous multiple burst theory
* no one theory is correct; all contribute to understanding and its cumulative effect*
6
Q
what is the continuous model theory
A
- slow, constant eventual tooth loss (‘everyone will lose their teeth anyway’)
- lack of evidence
7
Q
what is the random burst theory
A
- episodic (comes and goes), site specific
8
Q
what is the asynchronous multiple burst theory
A
- limited time period, then remission
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?)
10
Q
what happens to the bacteria when periodontal disease exists
A
- change in host-bacteria equilibrium
11
Q
3 conditions must exist for progression of perio:
A
- bacteria: critical mass - more bad than good
- conducive environment: favourable to bacterial growth and destruction, long standing, sub-g
- host response: bacteria continue to invade, contributing to the disease, destruction of own tissues in response
12
Q
summary of bacterial invasions
A
- poor oral hygiene with/without contributing environmental, systemic and acquired factors
- 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
- host’s inflammatory and immune systems activated
13
Q
what are the 2 common anaerobic subgingival bacteria
A
- PP
2. AA
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)
15
Q
what gets released when bacteria cells die
A
- endotoxins
16
Q
what are leukotoxins
A
- destroys PMNs
17
Q
what are matrix metalloproteinases (MMPs)
A
- family of 25 members, enzymes breaking down tissue
18
Q
what is collagenases
A
- breaks down collagen
19
Q
what is proteases
A
- breaks down protein, collagen fibers, connective tissue ground substances
20
Q
what do endotoxins do
A
- amplify the inflammatory process
21
Q
what are the 3 areas of host-bacteria interaction
A
- supragingival
- gingival crevice/sulcus
- gingival connective tissue
22
Q
what is the first attempt of the oral defence mechanism
A
- prevent movement into subgingival
- saliva, gingival crevicular fluid and oral epithelium
23
Q
how does saliva help protect from bacteria
A
- antibacterial products
- antibodies - immunoglobulins to fight bacteria
24
Q
how does gingival crevicular fluid help protect from bacteria
A
- cleanses the sulcus
- delivers more antimicrobial
- interacts first with bacteria
25
how does oral epithelium help with protecting from bacteria
- keratin - helps to prevent entrance
- close attachment of cells
- shedding/turnover of cells
26
what happens if bacteria is not stopped at the supra gingival level
- inflammatory/immune response is further stimulated to eliminate the irritant and prevent the spread of infection
27
what is the inflammatory/immune response
- 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
what are the 3 steps of the inflammatory/immune response?
1. elimination of bacteria
2. limit further tissue destruction
3. begin healing
* handout is good for this!*
29
what does the acute inflammatory response involve
- PMNs, macrophages, mast cells, gingival crevicular fluid
30
if the acute inflammatory response is ineffective, what happens
- chronic inflammatory response occurs
| - healing, but will cause damage to tissues
31
why is the inflammatory response a double edged sword
- 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
what do PMNs and neutrophils to
- white blood cell involved in phagocytosis or engulfing bacteria
33
what do macrophages do
- phagocyte in connective tissues
34
what do mast cells do
- cell found in connective tissue that contains granules and releases substances such as heparin and histamine
35
what does the serum complement do
- serum proteins that work with (complement) antibody activity to eliminate pathogens; stimulate inflammation
36
what does gingival crevicular fluid do
- fluid found in small amounts in gingival crevice; important in cleansing substances from crevice and has antimicrobial properties
37
what is clinical healthy gingiva
- 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
review of the inflammatory process
- oral biofilms at gingival margin
- inflammation starts
- gingival tissues react to bacteria in biofilm
- acute inflammation
- first inflammatory response is vascular (vasodilation)
39
when are inflamed gingiva first visible
- 3-4 days of undisturbed biofilm
40
what is being transported to the lamina propria through blood vessels during vasodilation
- 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
what do we see in the first response to the inflammatory process
- vasodilation
- increased gingival crevicular fluid (thicker, stringy-er than normal)
- gingival bleeding due to edema (swelling)
42
what is the neutrophil
- 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
what can cause impaired PMN functions
- diabetes
| - other diseases - decrease chemotaxis ability of PMN
44
what is a macrophage
- 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
what does damage to the host tissue cause for macrophages
- IL-1 - increases histamine
- increases PMN and macrophages
- increases number of osteoclasts
- more host destruction
46
what are cytokines
- 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
what are opsonins
- antibodies bind to surface of bacteria
- coat the bacteria
- easily identified by PMNs/macrophages
- engulfed and swallowed by phagocytes
48
what is the complement system
- group of plasma proteins
| - destroy antigens (foreign material) through chemotaxis
49
what are the 2 chemotactic factors that attract PMNs
1. classical pathway: activated when antibodies (proteins) bind to antigens (bacteria)
2. alternative pathway: activated by endotoxins
50
what are the 2 types of immune response
1. humoral (B cell response
| 2. cellular (T cell response)
51
what are lymphocytes
- found in WBCs
- also predominate in lamina propria
- patrol the host
- identify foreign pathogens
52
what are the 3 types of lymphocytes
1. B cells - mediators of humeral immunity
2. T cell - mediators of cellular immunity
3. natural killer cells
53
what is humoral immunity and when is it triggered
- 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
how does humoral immunity work
- antibodies bind to the antigens
- antigens are destroyed by macrophages
- antibodies to different periodontal bacteria are found in gingival crevicular fluid
55
how many B cells are found in the lamina propria in cases of periodontitis (percentage)
- B cells are found in the lamina propria at sites with periodontitis can be as high as 90%
56
what is cellular immunity
- T cells migrate from blood into gingival tissues and lymph nodes
57
what are the 2 types of lymph nodes
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
what is the role of the CD8 T cells
- 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
overall, what are the 5 key elements in immune response
- B-lymphocytes
- antibodies
- macrophages
- cytokines
- T-lymphocytes (T-killer and T-helper)
Periodontics
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