Immunology Flashcards
– Plaque-induced
– Inflammation (edema/bleeding upon probing)
– No destruction of PDL and bone
– No apical migration of epithelial attachment
Epithelial attachment = Junctional epithelium
Gingivitis
–Plaque-induced –Inflammation (edema/bleeding upon probing) –Destruction of bone –Apical migration of epithelial attachment –Not all cases of gingivitis progress to periodontitis
Periodontitis
- Plaque-induced similar to gingivitis.
- Host-related (susceptible host).
- Each site is individualized or a specific
environment. - A % of affected population experiences
severe destruction. - The progression of the disease is
probably
Periodontitis
______ model (1940-1960’s) of periodontitis
– 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.)
- gingival col
Progressive
________ model (1980-2000’s) of periodontitis
– 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.)
Random burst
________ model of periodontitis
(1980-2000’s)
– 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
Asynchronous multiple burst
What are the least common teeth lost to periodontitis?
Mand canine and 1st PM
What is the most commonly lost tooth to perio disease?
Max 2nd molars
2nd: 1st max molar
What are the 5 signs of inflammation?
- Rubor (redness)
- Calor (heat)
- Dolor (pain)
- Tumor (swelling)
- Functio Laesa (loss of function)
Inflammation is a ____ phenomenon
vascular
do blood vessels dilate or constrict due to inflammation?
Dilate
What are the first cells to defense in inflammation?
PMNs
Monocytes/macrophages
(phagocytosis)
What are the mediators of 2ndary defense?
B and T cells
Plasma cells produce antibodies
– Activated B-cells become Plasma cells
– Plasma cells produce immunoglobulins
B lymphocytes
– developed in the thymus
– several functions (antigen presentation)
– help B-cells divide; can destroy virally infected cells;
can down-regulate immune response
T lymphocytes
(TH0/TH1/TH2)
• help B cells to divide
• control leukocyte development
• activate innate cell lining
• CD 4 - MHC class II molecules – T helper cells
- MHC class I molecules
– T cytotoxic
• destroy virally infected target cells
• CD 8
phagocytosis; produce lysosomal enzymes
PMNs:
phagocytosis; process antigens;
cytokine secretion
Macrophages:
• Plasma cells: produce antibodies
B-Lymphocytes
: first responder; largest in size
IgM
: second responder; most abundant; crosses
placenta
IgG
salivary IgA; a dimer
IgA:
: on Mast cells, allergic reactions
IgE
part of both innate and adaptive
immunity systems. (A biochemical cascade that
helps clear pathogens by lysis, opsonization,
binding, and clearance of immune complexes).
Complement:
– now T-regulatory cells,
down-regulate T and B cells (CD8 ,CD25expression); prevent autoimmune disease
T suppressor cells
- mononuclear cells that kill cells
sensitized with antibody (via Fc receptors) (CD28cells which were signaled by CD8 cells)
K (Killer) cells
- kill virally infected
and transformed target cells that have not been
previously sensitized (CD56 cells)
NK (Natural Killer) cells
- activation in connective tissue
►will become macrophages*
Monocytes (5%)
(> 70%)* - 48 hours lifespan in
blood with migration to sites for phagocytosis
Neutrophils
(2-5%) - cause damage by
exocytosis (eg: histamine release)
Eosinophils
- contain mediators of inflammation
(histamine, prostaglandins, leukotrienes and
cytokines)-involved in allergic reactions
Mast cells
(< 0.5%) - are in some ways
functionally similar to mast cells
Basophils
• Definition: soluble, locally active polypeptides;
regulate cell growth, differentiation, function;
produced by cells of the immune system
Cytokines
: (cytokine) Pro-inflammatory: stimulates osteoclasts,
fibroblasts, macrophages
- most important proinflammatory mediator of periodontits
IL-1
:(cytokine) Pro-inflammatory: stimulates T and B cells
IL-6
: (cytokine) Pro-inflammatory: attracts and activates
PMNs
IL-8
: (cytokine) Pro-inflammatory: activates osteoclasts
TNF
\: (cytokine) Vasodilation Pyrogenic Releases mediator from mast cells Cell-mediated cytotoxicity
PGE2
What 2 growth factors are needed to stimulate fibroblasts?
PDGF
FGF
What growth factor stimulates epithelial cells and fibroblasts?
TGF
What growth factor stimulates epithelial cells?
EGF
Can you accurately predict which gingivitis cases will progress to periodontitis?
No
Clinically \_\_\_\_\_ Gingiva** • 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)
Healthy
• 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
Initial Lesion
Clinical Features of \_\_\_\_\_ Lesion • Increased GCF flow • Sulcus increases from 0→3 mm by formation of a pseudopocket • Alveolar bone is normal on the radiograph
Initial
• 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**
Early Lesion
The family includes 28 metal-dependent endopeptidases (proteases) with activity
against most, if not all, extracellular matrix macromolecules. (used for normal tissue remodeling)
Sub-Classes
- Interstitial Collagenases** - Gelatinases
- Stromelysins - Secreted RXKR (Arg-X-Lys-Arg)
- Membrane type - Metalloelastase
Matrix Metalloproteinases
MMPs
How much collagen loss is expected in early lesion?
up to 70%
Clinical Features of ___ Lesion
- Edema of gingiva
- Increased GCF flow
- Loss of gingival stippling
- Erythema of gingival margin
- No migration of JE attachment
- Alveolar bone is normal-no bone loss
- Reversible
Early lesion
The ____ Lesion
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 (causes BOP)
-More proliferation of JE
-More elongation of epithelial rete pegs into
connective tissue
3. Bystander Damage
4. Two-edged “sword” of immune system
Established lesion
Which lesion of gingivitis has micro ulcerations of sulcular epithelium?
Established lesions
Which lesion of gingivitis is a b cell to plasma cell lesion?
Established lesion
Which lesion of gingivitis involves t cells and horizontal migration of JE?
Early lesion
Clinical Features of \_\_\_\_\_ lesion 1. Edema 2. Erythema 3. Bleeding on probing (BOP) 4. Gingival changes: • color, contour, consistency 5. No bone loss
Established lesion
\_\_\_\_\_ 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
Advanced lesion
Clinical Features of\_\_\_\_\_\_\_ 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
Advanced
How much volume/density needs to be lost of bone before detection on radiograph?
50%
_____ is the primary etiology
for both gingivitis and periodontitis
Plaque
