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Define microbe
Refers collectively to microscopic organisms:
-Bacteria
-Fungi
-Protozoa
-Viruses
What are surfaces appendages
vesicles, fimbriae, flagella
what is Vesicles
surface appendages of outer membrane (gram -) that contain endotoxin
what is Fimbriae
small proteinaceous projections attached to the external surface of both Gram + and - ; important for adherence and coaggregation
what is flagella
long, fine, wavy filamentous structures used for motility, longer than fimbriae and larger diameter
what is adherence
stick to pellicle
what is coaggregation?
stick to other bacteria
what are the stages of polymicrobial biofilm formation?
stage 1: initial attachment of microbes to pellicle
stage 2: permanent attachment
stage 3: maturation phase I: self-protection matrix formation
stage 4: Maturation phase II: mushroom-shaped microcolonies
stage 5: dispersion: escape from the matrix
stage 1 of polymicrobial biofilm formation
initial attachment of microbes to pellicle
stage 2 of polymicrobial biofilm formation
permanent attachment
stage 3 of polymicrobial biofilm formation
maturation phase I: self-protection matrix formation (think force field) consist of proteins, glycolipids, and bacterial DNA
In stage 3 of polymicrobial biofilm formation what is established?
chronic disease
stage 4 of polymicrobial biofilm formation
Maturation phase II: mushroom-shaped microcolonies
stage 5 of polymicrobial biofilm formation
dispersion: escape (leave) from the matrix
obligate anaerobic bacteria
cannot live in the presence of oxygen
facultative anaerobic
can exist either with or without oxygen
the keystone pathogen hypothesis
Keystone species (p.gingivalis) in biofilm -> Trigger shift to a dysbiotic biofilm community -> Uncontrolled host response initiated -> Damage to periodontal tissues
what is the keystone species?
P.gingivalis: that initiates the change in the biofilm community
in the keystone pathogen hypothesis what triggers the uncrontrolled host reponse that results in damage to periodontal tissue?
the dysbiotic biofilm community
the prime purpose of the immune system is to _______________________ by identifying foreign substances in the boy and developing a defense against them.
defend the life of the individual
what is phagocytosis?
the process by which leukocytes engulf and digest microorganisms
what are the most effectively destroyed by polymorphonuclear (PMN) leukocytes
periodontal pathogens
antibodies are known collectively as
immunoglobulins
what are the 4 functions of complement system?
1. opsonization of pathogens
2. destruction of pathogens
3. recruitment of phagocytes
4. immune clearance
What is the most important action of the complement system?
opsonization
#2 in the function of the complement system is
destruction of pathogens
what are the parts of the destruction system?
- membrane attack complex
- lysis
#3 of the complement system
recruitment of phagocytes, recruit/join
#4 of the compliment system?
immune clearance, housekeeper, removing immune complexes from circulation
- to fight an infection, leukocytes travel through the bloodstream.
- the thin layer of epithelial cells that line the interior surface of the blood vessels is called endothelium
- near the infection site, leukocytes push their way between the endothelial cells and enter the connective tissue.
what is this process called?
transendothelial migration
hemodynamic changes
1. transient (temporary) vasoconstriction = FIrst Then, vasodilation
2. hyperemia: an excess of blood in the vessels in the tissues
3. margination: the movement of WBCs to the periphery of vessel walls
4. payementing: WBCs line the wall of the vessel
5. diapidesis: process by which neutrophils squeeze between endothelial cells in the vessel wall
6. emigration: cells move into tissues from the blood vessels
7. chemotaxis: the movement of cells to the sit of inflammation
8. neutrophils: white blood cells signification to development and progression of disease, most prevalent cell is acute inflammation, most active cell in the periodontal pocket, main function in phagocytosis
first step in hemodynamic changes
transient (temporary) vasoconstriction = FIrst Then, vasodilation
second step in hemodynamic changes
hyperemia: an excess of blood in the vessels in the tissues
third step in hemodynamic changes
margination: the movement of WBCs to the periphery of vessel walls
4th step in hemodynamic changes
payementing: WBCs line the wall of the vessel
5th step in hemodynamic changes
diapidesis: process by which neutrophils squeeze between endothelial cells in the vessel wall
6th step in hemodynamic changes
emigration: cells move into tissues from the blood vessels
7th step in hemodynamic changes
chemotaxis: the movement of cells to the sit of inflammation
8th step in hemodynamic changes
neutrophils: white blood cells signification to development and progression of disease
- most prevalent cell is acute inflammation
- most active cell in the periodontal pocket
- main function in phagocytosis
5 classic signs of acute inflammation
1. heat
2. redness
3. swelling
4. pain
5. loss of function
the classic warning signs seen in acute inflammation usually are ________ in chronic inflammation
absent
in chronic inflmmation: clincially, _______ is often absent
pain
the chronic inflmmatory process: tissue damage....
is the hallmark of chronic inflammation
what initiate most of the alveolar bone destruction in periodontitis?
prostaglandins
In periodontal disease, the immune system fights to defend the body from periodontal pathogens, NOT to.....
NOT to preserve the periodontium or teeth
It is the body's response to the periodontal pathogens that is the cause of...
nearly all the destruction seen in periodontitis
Initial lesion
- bacteria colonize teeth near gingival margin
- gram-negative and their metabolites initiate host response
- JE cells release biochemical mediators to stimulate immune response
- PMNs pass from blood vessels into gingival connective tissue
- as PMNs pass into connective tissue, they relase cytokines
- gingival crevicular fluid increase volume
- Clinically, tissue looks __healthy__
- Host response is successful if most of the bacteria are destroyed
- The body can repair any damage
- If pathogens are not controlled, early __gingivitis____ develops
early lesion
- biofilm maturation continues and bacterial toxins and byproducts penetrate the JE
- cytokines attract more cellular defenders to the site
- increased permeability of blood vessels allows more PMNs to move into connective tissue and form a wall between biofilm and sulcs wall
- PMNs release cytokines that cause localized destruction of connective tissue
- macrophages are recruited to connective tissue and released cytokines and MMPs
- MMPs are responsible for excessive loss of Connective tissue (60-70%)
- sulcular epithelium forms epithelial ridges and JE cells proliferate
- Clinically, __edema___ and __redness____ of gingival marginal tissue is observed
- Initiation of good self-care can mechanically disrupt plaque biofilm for complete return to health
- The body can still repair any damage
- If immune system fails to shut off the response, the lesion progresses to __established______ gingivitis
established lesion
- plaque biofilm extends subgingivally into the sulcus, disrupting attachement of coronal- most portion of JE from the tooth surface.
- more bacteria stimulate more cytokines, resulting in recruitment of more PMNs, macrophages, and lumphocytes
- plasma cella produce large quantities of antibodies to assist in in controlling bacteria
- Immune system sends more immune cells which release more toxic chemicals and more healthy connective tissue is destroyed
- Epithelial ridges extend deeper in connective tissue to try and maintain epithelial integrity
- JE loses attachment to root surface and transforms into pocket epithelium, which is thinner and more permeable
- Clinically, all features of gingivitis are accentuated
- Periodontal instrumentation and patient education for good self-care are vital at this point
- In _some__ individuals, if bacterial infection is not controlled, gingivitis progresses to
___periodontitis__.
advanced lesion
• Plaque biofilm spreads laterally as well as apically along the _root__ __surface___
• Chronic inflammation causes harm to the periodontium
• PMNs, macrophages cause destruction of connective tissue and PDL fibers
• Macrophages produce high concentrations of cytokines, PGE2 and MMPs that destroy __alveolar __bone__
• Gingival pocket progresses to a periodontal pocket
• PGE2 destroys bone by stimulating large numbers of osteoclasts to resorb crestal bone
• Elevated levels of RANKL modulate osteoclast activity which leads to greater bone loss
• Destruction caused by host immune response overwhelms any tissue repair
• Clinically, periodontal pockets are detected, there is bleeding upon probing, bone loss, furcation involvement, and mobility
• These changes are _not_ _reversible_ -the hallmark of periodontitis
in periodontal disease, there is
increased expression of RANKL, from osteoblasts
menopausal gingivostomatitis
is characterized by gingiva that bleeds readily with abnormally pale, dry, and shiny erythematous appearance
osteoPOROSIS
is a reduction in bone mass making the woman more prone to bone fractures
osteoPENIA
is a condition in which there is a lower than average bone density but not necessarily an increase in risk or incidence of bone fracture
what is the most frequent oral lesion
candidiasis
most common means of attachment to enamel surface
attachment to the pellicle
functional occlusal forces
forces produced during the act of chewing food
Parafunctional occlusal forces
results from tooth to tooth contact when not in the act of eating. EX: clenching, bruxism
smookless tobacco results in an ___________ inflammatory response in the tissues
increased
periodontal disease CANNOT....
CANNOT be caused by nutritional deficiencies