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47 Cards in this Set
- Front
- Back
Why is oxygen toxic?
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Direct: oxidize proteins
Indirect: H202 and free radicals |
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Redox potential
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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 |
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conditions that lead to low redox potential
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loss of vascular supply
Acid production Tissue necrosis |
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non spore forming bacteria virulence factor
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invasion of host tissue
growth and injury to host tissue destruction of tissue resistant to host mechanism |
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non spore forming anaerobes other than those involved in periodontal pathogens
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Bacteriodes
Propionbacterium acnes Mobiliuncus Bifidobacterium Lactobacillus |
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Bacteriodes
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Gram negative, rod
Infections below the abdomen: colon and vagina Bacteriodies thetaiomicron MOST abundant in the gut |
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Bacteriodes fragiles
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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) |
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Propionbacterium acnes
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Gram positive rod
root surface caries, dental plaque propionic acid |
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Mobiliuncus
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Gram positive rod
curved bacterial vagiones |
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Bifidobacterium
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normal flora
>90% of intestinal flora in breast fed infants |
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Lactobacilus
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normal flora : mouth, GI, vagina
in vagina produce hydrogen peroxide |
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Periodontitis
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Chronic (adult)
Aggressive (early onset) Manifestation of systemic disease necrotising |
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Pathogenesis
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Host factor
Genetics Local factors Bacteria Systemic conditions SMOKING |
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Bacteria associated with periodontal disease
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-Aggregatibacter actinomycetemcomitans
-Porphymonas -Tanerrala forsythia |
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AA
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gram negative rod
facultative anaerobe related to Haemophilus Virulence - Leukotoxin - immunosuppresive - endotoxin Colonize buccal mucosa Bacteriemia : DOC: cephalosporin |
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Porphymonas
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Gram negative
bile sensitive pigmented Virulence factor - endotoxin, protease, fimbrial protein, collagenase |
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Tannerral forsythia
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gram negative
non-pigmented Virulence -BspA protein(release bone resorbing cytokines) |
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BACTERIA ASSOCIATED WITH PERIODONTIAL DISEASE
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Fusobacterium
Prevotella Eikenella Campylobacter Capnocytophaga Treponema |
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Fusobacterium
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Gram negative rod
Vincent organism one or both end pointed |
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Prevotella
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gram negative rod
bile sensitive 15% produce beta lactamase |
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Prevotella melaninogenica
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black pigment
gingival crevice/saliva infections ABOVE diaphragm Oral surgery mixed anaerobes PULMONARY ABSCESS |
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Campylobacter rectus
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Gram negative
Virulence: flagella, slime, cytotoxin SUBGINGIVAL DENTAL PLAQUE OF CHRONIC PERIODONTITIS PATIENTS |
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Capnocytophaga
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Gram negative
filamentous |
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Eubacterium
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Gram positive rods
plaque and calculus COMPROMISE 50% OF ANAEROBES OF PERIODONTAL POCKETS |
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Actinomyces
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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 |
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Gram + and - cocci
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Peptostreptococcus/Streptococcus: gram positive, clinical infections, normal flora of mouth
Veillonella gram negative, oxidase negative, colon and oral cavity |
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Treponema denticola
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anaerobe
differ from pallidum by >10% production of cytotoxic proteases and peptidases |
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Oral leukocytes in health
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small vessels express adhesion molecules (E selectin)
mostly neutrophils 530,000 |
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Oral leukocytes in inflammation
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enhanced expression of adhesion molecules, emigration of neutrophils, inflammatory infiltrate
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experimental gingivits- inital lesion
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2-4 days
increase of PMN from junctional epithelium migrating to gingival crevice (PROTECTIVE) small number of macrophage and lymphocytes MAJORITY = T cells |
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Early lesion
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4-7 days
form rete pegs increase in lymphocytic infiltrate initially T cells predominate (then B cells) Th1 increase in PMN reduction in collagen |
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Established lesion
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intense PMN infilrtaion
pocket epithelium destructive changes B cells transform into plasma cells (IgG) |
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Advanced lesion
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bone destruction
apical extension of junctional epithelium plasma cells predominate in CT infiltrate PMN predominate in pocket and junctional epithelium |
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Antibodies
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IgG and IgA
IgG:activate complement IgA: neutralize bacterial proteases |
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T Lymphocytes in chronic periodontitis
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Cd4 T cells
Th2 cytokines predominate (IL6,IL10, IL13) |
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PMN Dysfunction
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Neutropenia: Congenital, cyclic, myelosuppression
Leukocyte adhesion deficiency Lazy leukocyte syndrome Chediak Higashi Chronic granulmatous disease Diabetes mellitus Downs syndrome |
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Phagocytic cell function
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Adherence
Chemotaxis Ingestion Killing: Degranulation and respiratory burst |
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Adherence
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Rolling adhesion: selectins
Tight binding: Integrins Diapedesis: Pecam, CD31 Migration: IL8 |
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Chemotaxis
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Bacterial products (fMET peptides)
Host products (C3A, C5A, LTB4) |
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Phagocytosis
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opsonization
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PMN granules
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primary (azurophilic) active form
secondary (sepcific) inactive form (receptors that can be incorporated into the plasma membrane) Gelatinas |
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Early onset aggressiveq
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INCREASED number of PMN
reduced chemotaxis, chemotaxis receptors, killing function |
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Chronic adult
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increased PMN, increased activty and levels of PMN in GCF
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IL beta and TNF alpha
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pro-inflammatory
bone resorptive stimulate fibroblast proliferation stimulate fibroblast production of prostaglandin E2, matrix metalloproteinases |
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IL1 and TNF alpha
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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 |
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Diabetes mellitus
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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 |
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advanced glycation end products
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stimulate inflammatory cells leading to increased production of IL1 and TNF
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