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PERIO I > immunology > Flashcards

immunology Flashcards

1
Q
  • I. Gingivitis
A

– Plaque-induced
– Inflammation (edema/bleeding upon probing)
– No destruction of PDL and bone
– No apical migration of epithelial attachment

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2
Q
  • II. Periodontitis
A

–Plaque-induced
–Inflammation (edema/bleeding upon probing)
–Destruction of bone
–Apical migration of epithelial attachment
–Not all cases of gingivitis progress to periodontitis

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3
Q

In other words, periodontitis is:

A
  1. Plaque-induced similar to gingivitis.
  2. Host-related (susceptible host).
  3. Each site is individualized or a specific environment.
  4. A % of affected population experiences severe destruction.
  5. The progression of the disease is probably (?)———–
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4
Q

Models of disease progression

A
  • Continuous model (1900-1950’s)
  • Progressive model (1940-1960’s)
  • Random burst model (1980-2000’s)
    • Asynchronous multiple burst model
      (1980-2000’s)
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5
Q
  • Continuous model (1900-1950’s)
A

– Continuous throughout life at same rate of
loss (i.e. Everyone gets perio disease.)

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6
Q
  • Progressive model (1940-1960’s)
A

– Progressive loss over time of some sites
– No destruction in others
– Time of onset and extent vary among sites
– (i.e. Periodontal disease affects mainly posterior teeth.)

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7
Q

Random burst model (1980-2000’s)

A

– Activity occurs at random at any site
– Some sites show no activity
– Some sites have one or more bursts of activity
– Cumulative extent of destruction varies among sites
– (i.e. Periodontitis is different in various sites in the same individual and it is difficult to predict attachment loss.)

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8
Q

who doesnt show BOP?

A

smoking due to nic vasoconstriction

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9
Q
  • Asynchronous multiple burst model
    (1980-2000’s)
A

– Several sites have one or more bursts of activity during one period of life
– Prolonged period of inactivity; remission
– Cumulative extent of destruction varies among sites
– Some sites don’t develop attachment loss
– (asynchronous=not occurring at same time)
– Bursts due to Risk Factors

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10
Q

how long to form established gingivitis?

A

3 wks

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11
Q

Signs of Inflammation

A
  • Rubor (redness)
  • Calor (heat)
  • Dolor (pain)
  • Tumor (swelling)
  • Functio Laesa (loss of function)
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12
Q

Inflammatory Response

A
  • Inflammation is a vascular phenomenon
  • Inflammation:
    – Leukocyte migration
    – Vasculitis: Dilation, Venous stasis (congestion), and Increased Permeability
    – Transudate
    – Exudate
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13
Q

innate immunity

A

1st defense
a. Innate (non-adaptive, genetic) (kills by
phagocytosis)
– PMNs
– Monocytes/Macrophages

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14
Q

adaptive immunity

A

2nd defense
b. Adaptive (production of immunoglobulins by
antibodies)
– highly specific
– B and T cells involved
– Plasma cells produce specific antibodies to
individual antigens

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15
Q

B cells and T cells**

A

c. B lymphocytes
– Activated B-cells become Plasma cells
– Plasma cells produce immunoglobulins
d. T lymphocytes
– developed in the thymus
– several functions (antigen presentation)
– help B-cells divide; can destroy virally infected cells;
can down-regulate immune response

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16
Q

t cells can dif into:

A

CD4 and CD8

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17
Q

CD 4

A
  • CD 4 - MHC class II molecules
    – T helper cells (TH0/TH1/TH2)
  • help B cells to divide
  • control leukocyte development
  • activate innate cell lining
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18
Q
  • CD 8
A
  • CD 8 - MHC class I molecules
    – T cytotoxic
  • destroy virally infected target cells
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19
Q

. PMNs:

A

phagocytosis; produce lysosomal enzymes

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20
Q

Macrophages:

A

phagocytosis; process antigens; cytokine secretion

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21
Q

B-Lymphocytes

A
  • Plasma cells: produce antibodies
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22
Q

T-Lymphocytes classes/functions

A
  • T-helper (CD4):helps B-cells divide
  • T-suppressor (CD8 & CD25): down-regulates T and B cells
  • NK cell (natural killer-T cell) (CD56): kills virally-infected cells
  • T-cytotoxic cell (CD8): destroys infected cells
  • K (killer-T cell) (CD28): kills infected cells
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23
Q

Humoral immunity components

A

a. Antibodies
* IgM : first responder; largest in size
* IgG : second responder; most abundant; crosses
placenta
* IgA: salivary IgA; a dimer
* IgD : co-expressed with IgM (role?)
* IgE : on Mast cells, allergic reactions
b. Complement: part of both innate and adaptive
immunity systems. (A biochemical cascade that helps clear pathogens by lysis, opsonization, binding, and clearance of immune complexes).

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24
Q

Immunoglobulins**

A
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25
Q

4 proven risk factors of perio dx

A

plaque
smoking
DM
immunosuppresion

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26
Q

T suppressor cells

A

ow T-regulatory cells,
down-regulate T and B cells (CD8 ,CD25expression); prevent autoimmune dx

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27
Q

K (Killer) cells

A

K (Killer) cells - mononuclear cells that kill cells sensitized with antibody (via Fc receptors) (CD28cells which were signaled by CD8 cells)

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28
Q

NK (Natural Killer) cells

A

kill virally infected and transformed target cells that have not been previously sensitized (CD56 cells)

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29
Q

is dx progression consistent throughout mouth?

A

no, may be variable

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30
Q

Monocytes (%)

A

(5%) - activation in connective tissue
►will become macrophages*

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31
Q

Neutrophils (%)

A

Neutrophils (> 70%)* - 48 hours lifespan in
blood with migration to sites for phagocytosis

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32
Q

Eosinophils (%)

A

Eosinophils (2-5%) - cause damage by
exocytosis (eg: histamine release)

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33
Q

Mast cells

A

Mast cells - contain mediators of inflammation
(histamine, prostaglandins, leukotrienes and
cytokines)-involved in allergic reactions

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34
Q

Basophils (< %) -

A

Basophils (< 0.5%) - are in some ways
functionally similar to mast cells

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35
Q

Cytokines Definition:

A

soluble, locally active polypeptides; regulate cell growth, differentiation, function;
Produced by cells of immune system

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36
Q
  • Specific cytokines may have different
    biologic properties dependent on:
A

– Their concentration
– The cells that produce them
– The cells being attracted and acted upon
– Presence and extent of extracellular matrix

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37
Q

Important Cytokines

A

IL-6,IL-8,IL-1, TNF, PGE2

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38
Q

IL-1

A

Pro-inflammatory: stimulates osteoclasts, fibroblasts, macrophages
MOST IMPORTANT IN PERIO, can be tested for its presence

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39
Q

IL-6

A

IL-6 Pro-inflammatory: stimulates T and B cells

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40
Q

IL-8

A

Pro-inflammatory: attracts and activates
PMNs

41
Q

TNF

A

TNF Pro-inflammatory: activates osteoclasts

42
Q

PGE2 functions

A

Vasodilation
Pyrogenic
mast cells degranulation
Cell-mediated cytotoxicity

43
Q

which cell is IgE on?

A

mast cells

44
Q

TGF

A

TGF Stimulates epithelial cells and fibroblasts

45
Q

PDGF

A

PDGF Stimulates fibroblasts

46
Q

EGF

A

EGF Stimulates epithelial cells

47
Q

FGF

A

FGF Stimulates fibroblasts

48
Q

keystone pathogen of perio dx

A

p. gingivalis, can reprogram cell to evade host immune cells

49
Q

Histologic/Immunologic Phases of Periodontal Disease

A
50
Q

Clinically Healthy Gingiva**
* cells present in connective tissue
* cells migrating through the JE
* collagen destruction?
* epithelial barrier?
* Gingival crevicular fluid?
* Appears?

A
  • Some neutrophils and macrophages are present in
    connective tissue
  • A few neutrophils are migrating through the JE
  • No collagen destruction
  • Intact epithelial barrier
  • Gingival crevicular fluid is present
  • Appears clinically healthy (Color, Contour, Consistency)
51
Q

Inflammatory Response Modifiers

A
  • Mechanical (plaque retention factors)
  • Systemic
  • Genetic
52
Q

Inflammatory Response Modifiers
* Mechanical (plaque retention factors)

A

a. Calculus
b. Caries
c. Restorations: defective margins, subgingival margins, overcontoured margins
d. Prosthesis
e. Tooth Anatomical Factors
* i.e. Palatogingival Grooves, Furcations

53
Q

Inflammatory Response Modifiers
* Systemic

A

– Uncontrolled/controlled diabetes**
– PMN defects
– Hematological
– Hormonal: Puberty, Pregnancy**
– Immune disturbances
– HIV/AIDS
– Medications*
– Nutrition deficiencies

54
Q

Inflammatory Response Modifiers
* Genetic

A

– Agranulocytosis
– Neutropenias
– Lazy Leukocyte
– Leukocyte adhesion deficiency (LAD)
– Down’s syndrome
– Papillon-Lefevre
– Hypophosphatasia
– Chediak-Higashi
– Ehlers-Danlos syndrome

55
Q

Initial Lesion
* Develops in?
* Cells present
* GCF flow
* Start of what formation

A
  • Develops in 2 to 4 days
  • Cells of acute inflammation present
  • Increased GCF flow
  • Start of pseudopocket formation
    – Remember:
    Acute = PMNs
    Chronic = Lymphocytes
    Increase in chronicity ►►►Plasma cells
56
Q

The Initial Lesion plaque

A

Plaque is deposited on the tooth
Bacterial byproducts are released into the periodontal tissues (virulence factors)

57
Q

Can we then accurately predict which patients with gingivitis are going to develop periodontitis?

A

Today: NO (?)
One can only identify risk factors such as:
- Habits: Smoking
- Systemic disorders: HIV and Diabetes
- Patients with risk factors are more likely to have attachment loss!!!
- The answer is in the host’s immune system/genetics

58
Q

Virulence factors types

A

– Stimulation of the host defense systems
– Degradation of the host tissues

59
Q

– Stimulation of the host defense systems

A
  • Stimulates cells to release cytokines (ie: IL-1, TNF and PGE) and chemoattractant factors (IL-8)
  • Attracts inflammatory cells (example of LPS causing chemotaxis of PMNs)
60
Q

– Degradation of the host tissues

A
  • Done with Enzymes
    – Collagenase
    – Trypsin-like enzymes
    – Keratinase
    – Phospholipase A
61
Q

Poor plaque control result

A

Bacterial byproducts are released into the periodontal tissues (virulence factors)
Stimulation of epithelial cells and fibroblasts to release IL-8 into the CT which attracts and activates PMNs

PMNs are present in the connective tissue

PMN’s are attracted to and near JE and sulcular epithelium

62
Q

Plaque accumulation result (after poor control)

A

Bacterial byproducts are released into the periodontal tissues (virulence factors)
Stimulation of inflammatory cells to release cytokines into the CT

PMN’s attracted near and to the JE and sulcular epithelium

63
Q

Attraction inflammatory cells

A
64
Q

p gingivalis main VF

A

collagenase

65
Q

Aa main VF

A

leukotoxin

66
Q

do all bac make same VF

A

no

67
Q

Clinical Features of Initial Lesion
* I GCF flow
* Sulcus depth
* Alveolar bone on radio

A
  • Increased GCF flow
  • Sulcus increases from 0→3 mm by formation of a pseudopocket
  • Alveolar bone is normal on the radiograph
68
Q

PMN Diapedesis
which cytokines?
molecules playing a role?

A

e

69
Q

Selectins

A

Selectins“slow” the PMNs and cause them to “roll”.
Cytokines activate ICAM receptors on endothelial cells for PMN attachment

70
Q

Early Lesion
* time
*result of?
GCF flow? pocket?
* Cells that appear/dominate?
* loss of/ what enzyme actives?

A
  • 4-7 days
  • Acute inflammation persists (initial lesion►►), increased GCF, pseudopocket formation
  • Cells of chronic inflammation appear and then dominate
  • (chronic→shift to T lymph. from PMNs) Collagen loss continues**
    MMPs Activation begins**
71
Q

How is collagen lost diagrammed
microbial factors?
cytokines involved?
enzyme?

A

IL-1 and 6

72
Q

Matrix Metalloproteinases
(MMPs)

A

The MMP family includes 28 metal-dependent endopeptidases (proteases) with activity against most, if not all, extracellular matrix macromolecules. (used for normal tissue remodeling)

73
Q

Early Lesion Histopathology
1. Collagen loss up to%*
2. cause?

A
  1. Collagen loss up to 70%*
  2. What causes collagen destruction?
    PMN’s products, Cytokines, MMPs are included, so a combination of bacterial products and host’s defense system cause the destruction.
74
Q

Early Lesion Histopatholgy
2. PMNs accumulation in?
3. PMNs accumulation in?
4. Cells of _______ inflammation accumulate
and predominate– called?
5. Fibroblasts?
6. Rete pegs ?

A

Early Lesion Histopatholgy
2. PMNs accumulation in gingiva
3. PMNs accumulation in sulcus
4. Cells of chronic inflammation accumulate and predominate– T-cell lesion
5. Fibroblasts show cell damage
6. Rete pegs proliferation of JE into CT

75
Q

early lesion diagram

A
76
Q

Clinical Features of Early Lesion
1. Edema of what tissue?
2. GCF flow?
3. Loss of what on gingiva?
4. Erythema of what part of gingiva?
5. migration of JE attachment?
6. Alveolar bone lost?
7. Reversible?

A

Clinical Features of Early Lesion
1. Edema of gingiva
2. Increased GCF flow
3. Loss of gingival stippling
4. Erythema of gingival margin
5. No migration of JE attachment
6. Alveolar bone is normal-no bone loss
7. Reversible

77
Q

Host Defenses of the established lesion

A
  1. Inhibit Dramatic Plaque Growth thus it Prevents infection from becoming dramatically worse, but a Stand-off exists, since plaque is unable to be eliminated and there is a Shift to a B-Cell/Plasma Cell lesion
78
Q

The Established Lesion
inflamm
time frame
what cell activates?
PMN wall?

A
  1. Acute inflammation persists
    -After 2-3 weeks early lesion shifts to established lesion (a stable lesion)
    -Chronic inflammation dominates
    * Activated B-lymphocytes → Plasma cells
  2. PMN “wall”: host tries to contain the infection
    **-Micro-ulcerations of pocket epithelium= BOP **
    -More proliferation of JE
    -More elongation of epithelial rete pegs into connective tissue
  3. Bystander Damage
  4. Two-edged “sword” of immune system**
79
Q

The Established Lesion-Disease Activity
processes occurring?
dominate cell?
vascular?
conn tissue app?

A
  1. Two processes
    – Damage: Bacterial and Immunological
    – Repair
  2. Shift to activated B-cell►plasma cell lesion
  3. Highly vascular
  4. Immature connective tissue with new collagen forming
80
Q

Effect on the Ground Substance in established lesion

A
  1. Bacterial Enzymes produce:
    a. Proteases
    b. Hyaluronidase
  2. Fibroblasts, Macrophages, PMN’s produce:
    a. Gelatinase
    b. Stromelysin

both create destruction, majority caused by host cells

81
Q

loss of collagen in established lesion, affected rates?

A
  1. Decreased rate of synthesis
  2. Increased rate of breakdown
82
Q

The Established Lesion
* Connective Tissue Repair
1. Attempts to minimize?
2. Fibroblasts are _______-regulated
* Synthesis of?
3. Recruitment of ?
* regulated by?
* Chemotactic?
4. ”The shut-off mechanism”?

A
  1. Attempts to minimize tissue damage
  2. Fibroblasts are cytokine-regulated
    * Synthesis of extracellular matrix
  3. Recruitment of new cells
    * Cytokine regulated (TGF-beta, PDGF)
    * Chemotactic collagen and elastin fragments
  4. Tissue Inhibitors of Metalloproteinases (TIMP)-”The shut-off mechanism”
83
Q

Established lesion diagram

A
84
Q

The Established Lesion
* Histopathology of the established lesion
1. Cellular damage of?
2. change to Collagen loss?
3. Micro-ulcerations of?
4. Persistence of?
5. Marked numbers of what cell in pocket?
6. Degradation of?
7. infiltrate?
8. JE proliferation and extension?
9. Elongation of ?

A
  1. Cellular damage of fibroblasts, epithelium
  2. Collagen loss increases
  3. Micro-ulcerations of pocket epithelium
  4. Persistence of acute inflammation
  5. Marked numbers of PMN’s in pocket
  6. Degradation of extracellular matrix
  7. Dense T-cell, B-cell, Plasma cell infiltrate
  8. JE proliferation and extension into CT
  9. Elongation of rete peg ridges
85
Q

The Established Lesion
* Clinical Features
1. Edema?
2. Erythema?
3. Bleeding?
4. Gingival changes?
5. bone loss?

A

The Established Lesion
* Clinical Features
1. Edema
2. Erythema
3. Bleeding on probing (BOP)
4. Gingival changes:
* color, contour, consistency
5. No bone loss

86
Q

Stages of gingivitis diagrammed
time frame
dominate cell
collagen loss
sulcular epi
clinical findings

A

e

87
Q

establioshed lesion progression

A
  • The established lesion is the final stage of
    “pure” gingivitis
  • This lesion can remain stable for weeks,
    months, or even years until/if it progresses to
    periodontitis
  • The mechanisms that cause the change from
    gingivitis to periodontitis are not well
    understood: Host factors?
  • Difficult to predict which patients will develop
    periodontitis –but one can identify the risks
    groups (smokers, diabetics, etc.)
88
Q

The Advanced Lesion
* Features of periodontal breakdown
1. Pocket?
a. PDL?
b. JE?
c. Bone?
2. Model of progression (?)
3. Bystander damage
4. Host balance of ?

A

The Advanced Lesion
* Features of periodontal breakdown
1. Pocket formation
a. PDL destruction
b. Apical migration of JE
c. Bone resorption
2. Asynchronous Multiple Burst Model (?)
a. Short bursts of disease activity
b. Long periods of quiescence
3. Bystander damage
4. Host balance of damage/repair is upset

89
Q

The Advanced Lesion
5. Alveolar bone resorption
a. Activation of?
b. Ruffled border produced (active site)
c. enzymes released?
d. Cytokines?
e. Prostaglandins?
f. Leukotrienes?

A

a. Activation of osteoclasts
b. Ruffled border produced (active site)
c. Hydrolytic enzymes released
d. Cytokines released: IL-1, IL-11, TNF
e. Prostaglandins produced: PGE 2
f. Leukotrienes produced (inflammatory mediators and involved in allergic reactions)

90
Q

Advanced lesion: Mechanisms of bone loss diagrammed

A
91
Q

Histopathology of the Advanced Lesion
1. cells present
3. infiltrate?
4. Extension of lesion into?
5. Loss of collagen?
6. altered plasma cells?
7. pocket formation?
8. phases?

A

Histopathology of the Advanced
Lesion
1. PMNs
2. B-cells, plasma cells dominate
3. Inflammatory infiltrate
4. Extension of lesion into PDL and bone
5. Loss of collagen continues
6. Cytopathologically altered plasma cells
7. Progressive pocket formation
– Attachment loss
8. Quiescence & exacerbation

92
Q

Clinical Features of Advanced
Lesion
1. Periodontal pocket?
2. ulceration where?
3. Radiographic bone loss?
4. Bleeding?
5. Changes in gingival?
6. Attachment Loss?
7. Mobility?

A

Clinical Features of Advanced
Lesion
1. Periodontal pocket formation
2. Pocket epithelium ulceration
3. Radiographic bone loss
– 50% of volume/density needs to be lost before
detection on radiograph
4. Bleeding on probing
5. Changes in gingival color, contour, consistency
6. Attachment Loss
7. Mobility

93
Q

Immune cells Overview
* Initial lesion
* Early lesion
* Established lesion
* Advanced lesion

A
  • Initial lesion
    – PMNs, macrophages
  • Early lesion
    – PMNs, macrophages, T-lymphocytes
  • Established lesion
    – PMNs, macrophages, T-lymphocytes, B-lymphocytes,
    plasma cells
  • Advanced lesion
    – PMNs, macrophages, T-lymphocytes, B-lymphocytes,
    plasma cells
94
Q

Treatment
* Gingivitis

A

Treatment
* Gingivitis
– Reversible
* Method
– Suppression of microflora for plaque-induced
gingivitis
* Scaling
* Polishing
* Patient’s daily removal of plaque

95
Q

Treatment
* Periodontitis

A

– Irreversible
– There is no cure for periodontitis, only control
* Method
– Suppression of microflora
* Scaling and root planing
– (SRP + Antibiotics (?))
– Reeval
* Surgery
* Maintenance
– Modulation of host
* Low Dose Doxycycline- collagenase inhibitor

96
Q

Does everybody that has gingivitis because of poor long-term plaque control eventually develop periodontitis?

A

no

97
Q

Primary etiology of periodontal
disease is

A

bacterial plaque in a susceptible host
Plaque Dysbiosis

98
Q

everybody develops gingivitis but only __________ patients will develop
periodontitis

A

only susceptible patients will develop
periodontitis

PERIO I (13 decks)

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