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Periodontics > Immunology > Flashcards

Immunology Flashcards

1
Q

Gingivitis
(4)

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

Epithelial attachment =

A

Junctional epithelium

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3
Q

Periodontitis
(4)

A

–Plaque-induced
–Inflammation (edema/bleeding upon
probing)
–Destruction of bone
–Apical migration of epithelial
attachment

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4
Q

–Not all cases of gingivitis
progress to —

A

periodontitis

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5
Q

In other words, periodontitis is:
1. —induced similar to gingivitis.
2. —-related (susceptible host).
3. Each site is
4. A % of affected population experiences
5. The progression of the disease is
probably (?)———–

A

Plaque
Host
individualized or a specific
environment.
severe destruction.

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6
Q

Continuous model (1900-1950’s)

A

– Continuous throughout life at same rate of
loss (i.e. Everyone gets perio disease.)
* Progressive model (1940-1960’s)

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7
Q

Progressive model (1940-1960’s)
(4)

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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8
Q

Random burst model (1980-2000’s)
(5)

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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9
Q

Asynchronous multiple burst model
(1980-2000’s)
–
– Prolonged period of —; remission
– Cumulative extent of — varies
among sites
– Some sites don’t develop —
– (—=not occurring at same time)
– Bursts due to —

A

Several sites have one or more bursts of
activity during one period of life
inactivity
destruction
attachment loss
asynchronous
Risk Factors

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10
Q

Signs of Inflammation
(5)

A
  • Rubor (redness)
  • Calor (heat)
  • Dolor (pain)
  • Tumor (swelling)
  • Functio Laesa (loss of function)
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11
Q

Inflammation is a — phenomenon

A

vascular

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12
Q

Inflammation:
(2)

A

– Leukocyte migration
– Vasculitis

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13
Q

Vasculitis
(3)

A

Vasculitis
* Dilation
* Venous stasis (congestion)
* Increased Permeability
– Transudate
– Exudate

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14
Q

Adaptive and Innate Immunity
1st defense

A

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

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15
Q

Adaptive and Innate Immunity
2nd defense

A

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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16
Q

B lymphocytes
(2)

A

– Activated B-cells become Plasma cells
– Plasma cells produce immunoglobulins

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17
Q

T lymphocytes
(3)

A

– 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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18
Q

T cells can differentiate into 2 major
forms:
(2)

A

CD4
CD8

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19
Q

CD 4 - MHC class II molecules
– T helper cells (TH0/TH1/TH2)
(3)

A
  • help B cells to divide
  • control leukocyte development
  • activate innate cell lining
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20
Q

CD 8 - MHC class I molecules
– T cytotoxic
(1)

A
  • destroy virally infected target cells
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21
Q

PMNs:

A

phagocytosis; produce lysosomal enzymes

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22
Q

Macrophages:

A

phagocytosis; process antigens;
cytokine secretion

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23
Q

B-Lymphocytes
* Plasma cells:

A

produce antibodies

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24
Q

T-Lymphocytes
* T-helper (CD4):
* T-suppressor (CD8 & CD25):
* NK cell (natural killer-T cell) (CD56):
* T-cytotoxic cell (CD8):
* K (killer-T cell) (CD28):

A

helps B-cells divide
down-regulates T and B cells
kills virally-infected cells
destroys infected cells
kills infected cells

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25
Q

Humoral immunity
a. Antibodies
* IgM :
* IgG :
* IgA:
* IgD :
* IgE :

A

first responder; largest in size
second responder; most abundant; crosses
placenta
salivary IgA; a dimer
co-expressed with IgM (role?)
on Mast cells, allergic reactions

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26
Q

Complement:

A

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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27
Q

Fab=
Fc =

A

spec. antigen
binding
Constant
portion

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28
Q
  • T suppressor cells –
A

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

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29
Q
  • K (Killer) cells -
A

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

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30
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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31
Q
  • Monocytes (5%)
A
  • activation in connective tissue
    ►will become macrophages*
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32
Q
  • Neutrophils (> 70%)*
A
  • 48 hours lifespan in
    blood with migration to sites for phagocytosis
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33
Q
  • Eosinophils (2-5%)
A
  • cause damage by
    exocytosis (eg: histamine release)
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34
Q
  • Mast cells -
A

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

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35
Q
  • Basophils (< 0.5%)
A
  • are in some ways
    functionally similar to mast cells
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36
Q

Cytokines
* Definition:
produced by

A

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

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37
Q

Specific cytokines may have different
biologic properties dependent on:
(4)

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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38
Q

IL-1

A

Pro-inflammatory: stimulates osteoclasts,
fibroblasts, macrophages

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39
Q

IL-6

A

Pro-inflammatory: stimulates T and B cells

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40
Q

IL-8

A

Pro-inflammatory: attracts and activates
PMNs

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41
Q

PGE2
(4)

A

Vasodilation
Pyrogenic
Releases mediator from mast cells
Cell-mediated cytotoxicity

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42
Q

TNF

A

Pro-inflammatory: activates osteoclasts

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43
Q

TGF

A

Stimulates epithelial cells and fibroblasts

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44
Q

PDGF

A

Stimulates fibroblasts

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45
Q

FGF

A

Stimulates fibroblasts

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46
Q

EGF

A

Stimulates epithelial cells

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47
Q

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

A
48
Q

One can only identify risk
factors such as:
(3)
The answer is in the host’s

A
  • Habits: Smoking
  • Systemic disorders: HIV and Diabetes
  • Patients with risk factors are more
    likely to have attachment loss!!!

immune system/genetics

49
Q

Clinically Healthy Gingiva**
* Some (2) are present in
connective tissue
* A few neutrophils are migrating
through the —
* No — destruction
* Intact —
* — is present
* Appears clinically healthy
(Color, Contour, Consistency)

A

neutrophils and macrophages
JE
collagen
epithelial barrier
Gingival crevicular fluid

50
Q

Mechanical (plaque retention factors)
(5)

A

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

51
Q

Inflammatory Response Modifiers
* Systemic
(8)

A

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

52
Q

Inflammatory Response Modifiers
* Genetic
(9)

A

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

53
Q

Initial Lesion
* Develops in — days
* Cells of — inflammation present
* Increased — flow
* Start of — formation

A

2 to 4
acute
GCF
pseudopocket

54
Q

Remember:
Acute =
Chronic =
Increase in chronicity ►►►

A

PMNs
Lymphocytes
Plasma cells

55
Q

The Initial Lesion
Plaque is deposited on the tooth

A

Bacterial byproducts are released into
the periodontal tissues (virulence
factors)

56
Q

Virulence factors
* 2 types

A

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

57
Q

Stimulation of the host defense systems
(2)

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)
58
Q

Degradation of the host tissues
* Enzymes
(4)

A

– Collagenase
– Trypsin-like enzymes
– Keratinase
– Phospholipase A

59
Q

Bacterial-Host Interaction*
(Aa, Fn, Pg)
Increased release of Interleukin-1

A

PMNs and Macrophages

60
Q

(Aa, Cr, Ec)
Increased release of Interleukin-6

A

Macrophages, epithelial cells and fibroblasts

61
Q

(Aa, Ec, Fn, Cr)
Increased release of Interleukin-8

A

PMNs, epithelial cells and fibroblasts

62
Q

(Aa, Fn)
Increased release of TNF

A

PMNs and Macrophages

63
Q

(Cr, Aa, Pi, Pg)
Increased release of PGE

A

Monocytes

64
Q

Poor plaque control

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

65
Q

Plaque accumulation
(3)

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

66
Q

Clinical Features of Initial
Lesion
(3)

A
  • Increased GCF flow
  • Sulcus increases from 0→3 mm by
    formation of a pseudopocket
  • Alveolar bone is normal on the
    radiograph
67
Q

Selectins

A

“slow” the
PMNs and
cause
them to
“roll”.

68
Q

Cytokines

A

activate
ICAM
receptors
on
endothelial
cells for
PMN
attachment

69
Q

Early Lesion
(4)

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**
70
Q

How is collagen lost
(3)

A

Microbial Factors(LPS and Antigens)
Stimulate not only
release of Cytokines
But also activation
and release of
MMPs
But also activation
and release of
MMPs

71
Q

The MMP family includes

A

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

72
Q

Sub-Classes (MMPs)
(6)

A
  • Interstitial Collagenases**
  • Gelatinases
  • Stromelysins
  • Secreted RXKR (Arg-X-Lys-Arg)
  • Membrane type
  • Metalloelastase
73
Q

Early Lesion Histopathology
1. Collagen loss up to

A

70%*

74
Q

What causes collagen destruction?

A

PMN’s products, Cytokines, MMPs are
included, so a combination of bacterial
products and host’s defense system cause
the destruction.

75
Q

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

A

gingiva
sulcus
Fibroblasts
Rete pegs

76
Q

Early lesion
(4)

A

More inflammatory infiltrate
Proliferation of JE rete pegs
T-cell lesion
Loss of collagen in the connective
tissue, but no bone loss

77
Q

Clinical Features of Early Lesion
1. — of gingiva
2. Increased —
3. Loss of gingival —
4. — of gingival margin
5. No migration of —
6. Alveolar bone is
7. Reversible?

A

Edema
GCF flow
stippling
Erythema
JE attachment
normal-no bone loss
Yes

78
Q

Host Defenses
1. Inhibit Dramatic Plaque Growth thus it
2. Prevents infection becoming dramatically
worse, but a
3. Stand-off exists, since plaque unable to
be eliminated and there is a

A
  1. Shift to a B-Cell/Plasma Cell lesion
79
Q

The Established Lesion
(4)

A
  1. Acute inflammation persists
  2. PMN “wall”: host tries to contain the infection
  3. Bystander Damage
  4. Two-edged “sword” of immune system
80
Q

The Established Lesion
1. Acute inflammation persists
(2)

A

-After 2-3 weeks early lesion shifts to
established lesion (a stable lesion)
-Chronic inflammation dominates
* Activated B-lymphocytes → Plasma cells**

81
Q

The Established Lesion
2. PMN “wall”: host tries to contain the infection
(3)

A

-Micro-ulcerations of pocket epithelium
-More proliferation of JE
-More elongation of epithelial rete pegs into
connective tissue

82
Q

The Established Lesion-Disease
Activity
1. Two processes
2. Shift to activated B-cell►
3. Highly —
4. Immature —

A

– Damage
* Bacterial
* Immunological
– Repair

plasma cell
lesion

vascular
connective tissue

83
Q

Effect on the Ground Substance
1. Bacterial Enzymes produce:
(2)

A

a. Proteases
b. Hyaluronidase

84
Q
  1. Fibroblasts, Macrophages, PMN’s
    produce:
    (2)
A

a. Gelatinase
b. Stromelysin

85
Q

Loss of Collagen
1. Decreased rate of —
2. Increased rate of —

A

synthesis
breakdown

86
Q

Connective Tissue Repair
1. Attempts to minimize —
2. Fibroblasts are —
3. Recruitment of —
4. — ”The shut-off mechanism”

A

tissue damage
cytokine-regulated
new cells
Tissue Inhibitors of Metalloproteinases (TIMP)

87
Q
  1. Fibroblasts are cytokine-regulated
    (1)
A
  • Synthesis of extracellular matrix
88
Q
  1. Recruitment of new cells
    (2)
A
  • Cytokine regulated (TGF-beta, PDGF)
  • Chemotactic collagen and elastin fragments
89
Q

Histopathology of the established lesion
(9)

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
90
Q

The Established Lesion
* Clinical Features
(5)

A
  1. Edema
  2. Erythema
  3. Bleeding on probing (BOP)
  4. Gingival changes:
    * color, contour, consistency
  5. No bone loss
91
Q

The established lesion is the final stage of

A

“pure” gingivitis

92
Q

This lesion can remain stable for weeks,
months, or even years until/if it

A

progresses to
periodontitis

93
Q

The mechanisms that cause the change from
gingivitis to periodontitis are not well
understood:

A

Host factors?
* Difficult to predict which patients will develop
periodontitis –but one can identify the risks
groups (smokers, diabetics, etc.)

94
Q

Features of periodontal breakdown
(4)

A
  1. Pocket formation
  2. Asynchronous Multiple Burst Model (?)
  3. Bystander damage
  4. Host balance of damage/repair is upset
95
Q
  1. Pocket formation
    (3)
A

a. PDL destruction
b. Apical migration of JE
c. Bone resorption

96
Q
  1. Asynchronous Multiple Burst Model (?)
    (2)
A

a. Short bursts of disease activity
b. Long periods of quiescence

97
Q

Pocket formation results from

A

apical migration of JE
Loss of fiber attachment
- cementum
- PDL
Loss of bone

98
Q
  1. Alveolar bone resorption
    a. Activation of —
    b.— produced (active site)
    c. — enzymes released
    d. — released
    e. — produced
    f. — produced (inflammatory
    mediators and involved in allergic reactions)
A

osteoclasts
Ruffled border
Hydrolytic
Cytokines )* IL-1, IL-11, TNF
Prostaglandins * PGE 2
Leukotrienes

99
Q

Advanced lesion:
Mechanisms of bone
loss
Microbial factors:
Activates inflammatory cells
to release (2)
Activates PMNs to release —
Activates Osteoclasts to
release — for
bone (MMP-13)
— loss

A

LPS
IL-1 and PGE2
Collagenase (MMP-8)
Collagenase
Collagen

100
Q

Histopathology of the Advanced
Lesion
1. PMNs
2. — 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—
8. Quiescence & exacerbation

A

B-cells, plasma
pocket formation
– Attachment loss

101
Q

Clinical Features of Advanced
Lesion
1. — formation
2. Pocket epithelium —
3. Radiographic …
4. Bleeding on —
5. Changes in gingival (3)
6. Attachment Loss
7. Mobility

A

Periodontal pocket
ulceration
bone loss
– 50% of volume/density needs to be lost before
detection on radiograph
probing
color, contour, consistency

102
Q

Immune cells Overview
* Initial lesion
(2)

A

– PMNs, macrophages

103
Q
  • Early lesion
    (3)
A

– PMNs, macrophages, T-lymphocytes

104
Q
  • Established lesion
    (5)
A

– PMNs, macrophages, T-lymphocytes, B-lymphocytes,
plasma cells

105
Q
  • Advanced lesion
    (5)
A

– PMNs, macrophages, T-lymphocytes, B-lymphocytes,
plasma cells

106
Q

Treatment
* Gingivitis
– Reversible
* Method

A

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

107
Q

Treatment
* Periodontitis
– Irreversible
– There is no cure for periodontitis, only control
* Method

A

– Suppression of microflora
* Scaling and root planing
– (SRP + Antibiotics (?))
– Reeval
* Surgery
* Maintenance
– Modulation of host
* Low Dose Doxycycline- collagenase inhibitor

108
Q

Is plaque necessary to initiate
gingivitis and/or periodontitis?

A

yes

109
Q

Does everybody that has poor
plaque control eventually develop
gingivitis?

A

yes

110
Q

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

A

no

111
Q

— is the primary etiology
for both gingivitis and periodontitis

A

Plaque
No plaque (bacteria) =No disease!

112
Q

Plaque is necessary and sufficient
to initiate —

A

gingivitis

113
Q

Plaque is necessary but not
sufficient to initiate —

A

periodontitis

114
Q

Old concept = everybody develops gingivitis
and eventually will progress to periodontitis
New concept =

A

everybody develops
gingivitis but only
susceptible patients will develop
periodontitis

115
Q

Definition of primary etiology

A

Primary etiology of periodontal
disease is bacterial plaque
in a susceptible host
Plaque Dysbiosis

116
Q

Therefore, patient’s — is
extremely important in the pathogenesis
of periodontal disease

A

immunology

117
Q

Immune system = provides a — process but
also may account for most of the tissue injury observed
in

A

defensive
gingivitis and periodontitis

Periodontics (13 decks)

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