Den 7110

Front 1

Why is oxygen toxic?

Back 1

Direct: oxidize proteins
Indirect: H202 and free radicals

Front 2

Redox potential

Back 2

E+ : more likely to accept electrons
E -: more likely to donate electrons
positive reduction potential: oxidize form higher affinity for electrons
negative: reduced potential has lower affinity for electrons

Front 3

conditions that lead to low redox potential

Back 3

loss of vascular supply
Acid production
Tissue necrosis

Front 4

non spore forming bacteria virulence factor

Back 4

invasion of host tissue
growth and injury to host tissue destruction of tissue
resistant to host mechanism

Front 5

non spore forming anaerobes other than those involved in periodontal pathogens

Back 5

Bacteriodes
Propionbacterium acnes
Mobiliuncus
Bifidobacterium
Lactobacillus

Front 6

Bacteriodes

Back 6

Gram negative, rod
Infections below the abdomen: colon and vagina
Bacteriodies thetaiomicron MOST abundant in the gut

Front 7

Bacteriodes fragiles

Back 7

virulence factor
- capsule
- endotoxin: lack Lipid A (low toxicity)
- collagenase, IgA protease
- beta lactamase (penicillin resistant)
- in abdominal cavity
can cause brain abscesses, gyencologic, skin/soft tissue, bacteremia (peritonitis)

Front 8

Propionbacterium acnes

Back 8

Gram positive rod
root surface caries, dental plaque
propionic acid

Front 9

Mobiliuncus

Back 9

Gram positive rod
curved
bacterial vagiones

Front 10

Bifidobacterium

Back 10

normal flora
>90% of intestinal flora in breast fed infants

Front 11

Lactobacilus

Back 11

normal flora : mouth, GI, vagina
in vagina produce hydrogen peroxide

Front 12

Periodontitis

Back 12

Chronic (adult)
Aggressive (early onset)
Manifestation of systemic disease
necrotising

Front 13

Pathogenesis

Back 13

Host factor
Genetics
Local factors
Bacteria
Systemic conditions
SMOKING

Front 14

Bacteria associated with periodontal disease

Back 14

-Aggregatibacter actinomycetemcomitans
-Porphymonas
-Tanerrala forsythia

Front 15

AA

Back 15

gram negative rod
facultative anaerobe
related to Haemophilus
Virulence
- Leukotoxin
- immunosuppresive
- endotoxin
Colonize buccal mucosa
Bacteriemia : DOC: cephalosporin

Front 16

Porphymonas

Back 16

Gram negative
bile sensitive
pigmented
Virulence factor
- endotoxin, protease, fimbrial protein, collagenase

Front 17

Tannerral forsythia

Back 17

gram negative
non-pigmented
Virulence
-BspA protein(release bone resorbing cytokines)

Front 18

BACTERIA ASSOCIATED WITH PERIODONTIAL DISEASE

Back 18

Fusobacterium
Prevotella
Eikenella
Campylobacter
Capnocytophaga
Treponema

Front 19

Fusobacterium

Back 19

Gram negative rod
Vincent organism
one or both end pointed

Front 20

Prevotella

Back 20

gram negative rod
bile sensitive
15% produce beta lactamase

Front 21

Prevotella melaninogenica

Back 21

black pigment
gingival crevice/saliva
infections ABOVE diaphragm
Oral surgery
mixed anaerobes
PULMONARY ABSCESS

Front 22

Campylobacter rectus

Back 22

Gram negative
Virulence: flagella, slime, cytotoxin
SUBGINGIVAL DENTAL PLAQUE OF CHRONIC PERIODONTITIS PATIENTS

Front 23

Capnocytophaga

Back 23

Gram negative
filamentous

Front 24

Eubacterium

Back 24

Gram positive rods
plaque and calculus
COMPROMISE 50% OF ANAEROBES OF PERIODONTAL POCKETS

Front 25

Actinomyces

Back 25

Gram positive rod
A. naeslundii - root surface caries
A. odontolyticus - enamel deminearlization, progression of small caries lesion
A israelii: opportunist, cervicofacial actinomycosis (lumpy jaw) - pyogenic abscesses, sinus formation, sulfur granules

Front 26

Gram + and - cocci

Back 26

Peptostreptococcus/Streptococcus: gram positive, clinical infections, normal flora of mouth

Veillonella
gram negative, oxidase negative, colon and oral cavity

Front 27

Treponema denticola

Back 27

anaerobe
differ from pallidum by >10%
production of cytotoxic proteases and peptidases

Front 28

Oral leukocytes in health

Back 28

small vessels express adhesion molecules (E selectin)
mostly neutrophils
530,000

Front 29

Oral leukocytes in inflammation

Back 29

enhanced expression of adhesion molecules, emigration of neutrophils, inflammatory infiltrate

Front 30

experimental gingivits- inital lesion

Back 30

2-4 days
increase of PMN from junctional epithelium migrating to gingival crevice (PROTECTIVE)
small number of macrophage and lymphocytes
MAJORITY = T cells

Front 31

Early lesion

Back 31

4-7 days
form rete pegs
increase in lymphocytic infiltrate
initially T cells predominate (then B cells)
Th1
increase in PMN
reduction in collagen

Front 32

Established lesion

Back 32

intense PMN infilrtaion
pocket epithelium
destructive changes
B cells transform into plasma cells (IgG)

Front 33

Advanced lesion

Back 33

bone destruction
apical extension of junctional epithelium
plasma cells predominate in CT infiltrate
PMN predominate in pocket and junctional epithelium

Front 34

Antibodies

Back 34

IgG and IgA
IgG:activate complement
IgA: neutralize bacterial proteases

Front 35

T Lymphocytes in chronic periodontitis

Back 35

Cd4 T cells
Th2 cytokines predominate (IL6,IL10, IL13)

Front 36

PMN Dysfunction

Back 36

Neutropenia: Congenital, cyclic, myelosuppression
Leukocyte adhesion deficiency
Lazy leukocyte syndrome
Chediak Higashi
Chronic granulmatous disease
Diabetes mellitus
Downs syndrome

Front 37

Phagocytic cell function

Back 37

Adherence
Chemotaxis
Ingestion
Killing: Degranulation and respiratory burst

Front 38

Adherence

Back 38

Rolling adhesion: selectins
Tight binding: Integrins
Diapedesis: Pecam, CD31
Migration: IL8

Front 39

Chemotaxis

Back 39

Bacterial products (fMET peptides)
Host products (C3A, C5A, LTB4)

Front 40

Phagocytosis

Back 40

opsonization

Front 41

PMN granules

Back 41

primary (azurophilic) active form
secondary (sepcific) inactive form (receptors that can be incorporated into the plasma membrane)
Gelatinas

Front 42

Early onset aggressiveq

Back 42

INCREASED number of PMN
reduced chemotaxis, chemotaxis receptors, killing function

Front 43

Chronic adult

Back 43

increased PMN, increased activty and levels of PMN in GCF

Front 44

IL beta and TNF alpha

Back 44

pro-inflammatory
bone resorptive
stimulate fibroblast proliferation
stimulate fibroblast production of prostaglandin E2, matrix metalloproteinases

Front 45

IL1 and TNF alpha

Back 45

produced by: monocytes, gingival fibroblasts, gingival epithelial cells, PMN
In response to bacteria (plaque): LPS binds to CD 14 on phagocytic cells, stimulate release of proinflammatory mediators

Front 46

Diabetes mellitus

Back 46

Type 1: 5x increase, Type2: 3x
increase with age and disease duration
Mechanism: higher glucose levels lead to altered energy metabolism, increased production of proinflammatory cytokines, altered wound healing, accumulation of irreversibly glycated proteins in periodontium and other tissues

Front 47

advanced glycation end products

Back 47

stimulate inflammatory cells leading to increased production of IL1 and TNF