Oral Immuno& Micro (Test 1) Flashcards
Oral immunity includes many innate processes like Saliva what helps with what?
1) Constant H2O flush
2) Dissolves food
3) Buffers (for acids)
4) Contains anti-bacterial molecules
5) Provides protective oral coating
Oral immunity includes many innate processes like Thick, continually recycling epithelium it contains what?
1 ) Tough keratin layer with high lipid content
2) Tight junctions
3) Impermeable
Oral immunity includes many innate processes like Gingival junctional epithelium –. different = “leaky” contains what?
1) Non-keratinized w/ low lipid content
2) loose junctions
3) Allows plasma fluid & inflammatory cells access to mouth
Note: Competitive normal flora is also included for the innate processes.
The gingiva helps provide what?
Provides numerous protective components for oral immunity
The keratinocytes of the junctional epithelium are poorly differentiated and make little ____ ?
Little KERATIN, little HYDROPHOBIC granular materials and are loosely linked to each other
What does the keratinocytes of the junctional epithelium that are loosely linked, allow capillary plasma exudade & migrating PMNs to do what?
To readily pass into the gingival crevice area = LEAKY
Junctional epithelial cells display HLA class II and therefor can present what?
Present extracellular ANTIGENIC PEPTIDES, thereby activating Th cells
Junctional epithelial cells if stimulated by certain microbial products can release what?
The Chemokine IL-8 and numerous other cytokines & chemokines that can activate and stimulare local cappillaries, mast cells, and are chemotactic for PMNs.
Outside of the teeth, all surfaces in the mouth are ___________?
- continuously shedding
- Microorganisms that colonize are quickly swallowed with the shed epi.
Most of the gingiva is tough, highly keratinized and mostly impermeable. The EXCEPTION is what?
The Junctional epi closely surrounding the tooth, where bacterial numbers can get very high. (This epi area is non-keratinized, non-hydrophobic, ‘leaky’ surface.
What are layers of the attached Gingiva?
1) Keratin layer- blocks invasion tough surface
2) Granular layer- releases lipid DECREASE H2O permeability
3) Prickle layer- tight junctions blocks invasion
4) Germinativum layer- Stimulation = sloughing
What makes up the salivary fluid?
- Buffers (maintain pH-anti-caries effect)
- dilutes
- anti-microbials ( lysozyme, antimicrobial peptides, etc)
- Large amounts of Ig A and little Ig G
What makes up sulcular (crevicular) fluid & cells ?
Fluid: (Ig G), Hemin, Complement (very low in Saliva)
Cells: PMNs (90%) fight invasion, Monocytes, Lymphocytes- Mianly IgG B-cells = 10%
What are PMNs?
The life cycle of the PMN provides huge numbers of short-lived, rapid-attack, phagocytic cells that are commonly used in oral defense.
Note: They have tons of receptors
Where are PMNs produced and what is their function?
Produced in the bone marrow and they function as the MAJOR PHAGOCYTIC cell in the body
What fraction of WBCs are PMNs and how long do they live?
2/3 and they are VERY SHORT LIVED.
in blood their half-life is only 6 hours & in Tissues it is extended to 1-2 days
Where are PMNs found?
They are constantly leaving the capillaries and entering into inflamed tissue, gut, mouth, etc.
**They are drawn into sites of inflammation, where they travel along a chemotacic trail to infection site.
How do PMNs attach to foreign microorganisms and their products?
-What happens to the microorganisms?
They will use various cell-surface receptors (FcR, C3b-R) to attach
-Microorganisms are then ENGULFED (PHAGOCYTOSIS) and destroyed in the phagolysosome
What are the functions of the specific ligand binding?
1) Recruitment
2) Attachment
3) Activation
What happens in the Tissues with PMNs?
1) Margination
2) Emigration
3) Chemotaxis
4) Phagocytosis-Endocytosis
5) Local release- Exocytosis
6) Death –> DNA & Myeloperoxidase = Viscous GREEN PUS
Why does the body keep 5-20 x the # of blood & tissue PMNs in a bone marrow “jail” (storage center)?
PMNs can be released if the body needs a quick boost in PMNs at some infection/inflammation site
What happens to the PMNs once they enter the blood stream?
They “go with the flow” until they reach a site of inflammation.
What do the PMNs grab onto at inflammation sites?
At inflammation sites the capillary endothelial cells express adhesion molecules (CAM)s
How do the PMNs get to the problem sites?
They crawl between the endothelial cells and “CLIMB” thru the tissues. At the site the use SURFACE RECEPTORS (e.g., FcR, C3b-R, etc) to bind and engulf opsonized pathogens
