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65 Cards in this Set

  • Front
  • Back
Normal Microbial Flora
-10% of cells in body are of human origin
-90% are commensal microbial flora
-diferent anatomical sites areassociated with their own characteristic flora
Commensal Flora
-microbes that have evolved to adhere to and grow in a particular loation
-once established they are the resident flora at that site
Transient Flora
-microbes ill equipped to exploit the area they come into contact with body
-easily removed from body
Oral Ecology
-portal of entry for food
-acces to transient flora
-diverse and rich commensal flora with distinct ecological sites (saliva, teeth, tongue etc)
Pathogens in Oral Cavit
-Strep Pyogenes
-Strep Pneumonia
-Candida Albicans
Oral flora dominated by what kind of bacteria?
-alpha hemolytic strep
Bacteria metabolic relationship to oxygen
- Anaerboic: may survive in oxygen but don't grow because they might be killed in the oxygen while dividing
- Facultative: it has the facility to be able to switch between aerobic and anaerobic (e.coli some of the enteric bacteria can do either)
- Aerotolerant anaerobic (like the alpha hemolytic strep can tolerate)
- Microaerophilic- like the oxygen amt just right sensitive to atmospheric but need a little bit of oxygen to grow
- Capnophilic- relationship to CO2 need elevated carbon dioxide
Infant- Predentate Oral Flora
-alpha hemolytidc Strep (attached to epithelial surfaces)
-strep Salivarius
-influence of breast feeding
Eruption of teeth
-mineralized non-sloughin surfaces
-pellicle as salivary source
-mutans strep, strep orali and strep sanguis (all obligate hard surface colonizers and antagonistic/competitive)
-gingival crevice
oral infections may afect the course and pathogenesis of a number of systemic diseases such as....
-diabetes
-CV disease
-premature birth
-respiratory disease
Significance of Oral disease
-spread of infection from oral cavity as result of transient bacteremia
-injury from circulating oral microbial toxins
-inflammation caused by bacterial component-virulence determinants
-subgingival dental plaque as reservoirs of gram negative bacteria, resulting in inflammatory mediators
What is the best sample source for determining what the bacteria are in oral cavity?
depends on what area you are interested in because it is a complex environment
What determines differences in areas of bacteria?
-pH, surfaces, temp differences, metabolic differences, ionic differences etc
Which will attach faster the salivary components or the bacteria?
-The salivary components. This forms the pellicle which the bacteria then can attach to.
How much saliva do we produce per day?
1-2L
Amylase
-this digests starch and all bacteria cannot digest starch but when it is digested it turns to sugar which bacteria can use
-therefore having amylase in saliva may help bacteria
Salivary Glands
-Submandibular gland. (mixed) Wharton's duct
-Sublingual gland. (mucous)
-submand/sublingual = 70% of saliva
-Parotid gland. (serous) Stensons duct. 30% of whole saliva
-Minor glands contribute 1-2% of whole saliva
Which gland mixes best and gets around oral cavity best?
The parotid because it is more watery because of serous content and less mucous.
Whole saliva
-a mixture of secretions from all of the glands
Lysozyme
-muramidase
-hydrolyzes the peptidoglycan (cell wall polymer of N-acetlyl muramic acid and N-acetyl glucosamine)
-results in bacterial lysis
Lactoferrin
-glycoprotein capable of high affinity binding of iron
-deprives bacteria of iron as essential nutrient
-regulate the valence of iron preventing its particpation in generation of oxygen free radicals
Secretory peroxidases
-catalyzes interaction between hydrogen peroxide and selected halides such as SCN- (thiocyanate)
-generates highly reactive oxidized species.
Saliva has alot of thiocynate which when around hydrogen peroxide (formed by bacteria) and the salivary peroxidase it forms OSCN-(hypothiocyanate). This oxidizes sulfhydryls of bacterial enzymes necessary for their metabolism
results in reversible inhibition of bacterial metabolism
- some bacteria are capable of restoring enzymatic activity and bacterial metbolism (i.e. resistant to the peroxidase action)
Salivary agglutins
-variety of glycoproteins rich in carbs that are cabpable of clumping bacteria together.
-also sticky for other salivary molecules including secretory IgA possible permitting synergism between these two species
Antimicrobial peptides
-small weight peptides that are alpha helical in structure and perturb the bacterial membrane.
-defensins of neutrophils and histatins of saliva are these
-may be alternatives to traditional antibiotics
Innate soluble factors of mucosal immunity
1. lysozyme
2. lactoferrin
3. Secretory peroxidases
4. Agglutinins
5. Antimicrobial peptides
Aquired factors of mucosal immunity
-Secretory IgA
Scretory IgA
-principal immunoglobulin of mucosal secretions of normally healthy people
-Secretory IgM in people with selective IgA deficiency
Secretory IgA
-local factor
-polymeric
->ratio of IA2:IgA1
-earlier maturation
-distinct antigen repertoires
Greater ration of IGA2 in secretory IgA
-pathogens produce proteases that are specific for IgA1.
-IgA2 is resistant to these proteases giving the secretory IgA an advantage at mucosal surfaces
Sites of synthesis (serum vs. secretory IgA
-serum IgA synthesized and secreted by plasma cells (B-cell) in the spleen and lymp nodes. Antibody circulates in the blood.
-secretory IgA is synthesized by plasma cells in the lamina propria at mucosal surfaces. NOT DERIVED from blood.
Polymeric nature of Secretory IgA
-generally dimeric and larger
-J chain synthesized by plasma cell
small protien. initiates the association of Ig Subunits
disulfide bridged
- IgA subunits joined before secretion from the plasma cell
Secretory component
-80Kd protein synthesized by epithelial cells at mucosal surfaces
-plasma cells secrete dimeric/multimeric IgA in the lamina propria proximal to the basal surfaces of these epithelial cells
-membrane associated secretory component (100Kd) serves as a receptor (PIgR) for these IgA -transported through cell by pinocytosis
-secreted on distal surface by proteolytic cleavage of the membrane anchoring sequence of secretory component.
pIgR
-poly immunoglobulin receptor
-this is on membrane of epithelial cell and becomes part of membrane of the vessicle the secretory IgA is transported in and eventually a piece of it will stay with the secreted IgA.
Secretory component function
-requires J chain for association
-is disulfide bridged when secreted
-protects against acid hydrolysis and proteolysis
-permits SIgA to function in varied and adverse environments
Earlier maturation of secretory IgA
-reaches adult levels at 13 months of age
-Serum IgA doesn't reach adult levels until puberty
-we need the secretory IgA earlier in life!
Secretory IgA has distinc antigen repertoire
-recognizes antigens common to mucosal surfaces not generally evoked by systemic immunization
-serum IgA is stimulated by parenteral (systemic) immunization
Routes for stimulation of SIgA
-local antigen presentation can stimulate antigen commitment of IgA synthesizeing B-cells (like in salivary glands)
-antigen ingestion (oral polio vaccine) results in expression of antibodies at remote mucosal surfaces (saliva, tears, milk, urogenital tract)
-common mucosal immune system: MALT (mucosal associated lymphoid tissue)
-sites of specialized antigen processing (Peyes patches -GALT, NALT- upper respiratory tract)
Cellular components of mucosal imune system
-intraepithelial lymphocytes
-laminal propria lymphocytes
-Mucosal lymphoid follicles (M cells)
Intraepithelial lymphocytes
-CD8+ T cells
-limited range of specificities
Lamina propria lymphocytes
-large number of activated B cells and plasma cells- IgA producing (60-70% of toal produced)
-T cells- CD4+
-macrophages, eosinophils, mast cells
Mucosal lymphoid follicles (M cells)
-eyes patches, appendix, tonsils etc
-B cells (50-70%), T cells (CD4+) 10-30%
- M cells : pinocytotic lack microvilli, not APC
Innate Cellular Imunity
-rapid response without induction or maturation
-neutrophils, monocytes, mast cells and histiocytes sense pathogenic structures
-responses include phagocytosis, proinflammatory cytokines, co-stimulatory molecules- Ag presentation
-innate-adaptive interface
Inflammation
-margination, rolling, attachement, diapedesis, chemotaxis & phagocytosis
Systemic innate defense factors
Epithelial cells
-mechanical barrier
-initial response
-bioactive molecules
Vasoactive Molecules
-nitric oxide
-histamine
-bioactive lipids
endothelial cells & platelets
complement
macromolecules (lysozyme, transferrin etc)
phagocytic cells
Pathogen associated molecular patterns (PAMP)
-LPS
-peptidogylcan
-lipoteichoic acid
-lipoproteins
-bacterial CpG DNA
Pattern recognition receptors (PRR)
-fMLP receptors
-toll-like receptors (TLR)
-selected over the course of evolution
-insects, plants and mammals
Pattern recognition receptors
-TLR4 recognizes LPS (gram negative)
-TLR2 recognizes gram positive
-TLR9 bacterial DNA
Phagocytosis
-opsonization of target (antibody complement)
-receptors on phagocyte
-toll like receptors
-phagosome membrane
-granule fusion
Granules
-have membrane around them because they are a membrane contained vesicle
-can have proteins in the membrane that are unique to that membrane
-two different kind of granules some with them in the matrix and some only with it in the membrane
-lactoferrin and myeloperoxidase are two types of granules in PMNs
Bactericidal mechanisms of PMN oxygen dependent:
NADPH oxidase
1. superoxide generation
2. myeloperoxidase (primary lysosomal granule)
-H2O2 dependent generation of HOCL
3. hydroxyl radical generation
Bactericidal mechanisms of PMN oxygen independent:
. specific granule components: lactoferrin, lysozyme
2. defensins
3. cationoic peptides/proteases
Membrane Interactive Peptides
-defensins
-lactoferrin
-complement components
-Membrane attack complex (MAC)
-opsonins (C3b/iC3b)
lactoferrin antimicrobial activity bacteriostatic
-iron deprivation due to high affinity for iron
-inhibition of metabolism through interaction with membrane
lactoferrin antimicrobial activity bacteriocidal
-generation of toxic radicals through iron transition
-lactoferricin- alpha helical membrane interactive domain (peptide fragment of lactoferrin)
Myeloperoxidase
-primary granules of neutrophil
-released into phagosome
-H2O2 + Cl- ---> HOCL (bleach)
-bactericidal (not reversible)
Lactoperoxidase
-cannot use Cl-
-salivary peroxidase
-H2O2 + SCN - (saliva) ---> Enz-S-SCN + OH-
-reversible inhibition of bacterial enzymes
PMN Dysfunctions
-leukocyte adhesion deficiencies
-severe congenital neutropenia (kostmans disease)
-idiopathic chronic neutropenia
-cyclic neutropenia- mutation in ELA2
-chronic benign neutropenia
-chemotactic dfects
-chronic granulomatous disease
-granule dysfunctions- MPO deficiency, Chediak-Higashi syndrome, specfic granule dificiency
-papillon- Lefevre- cathepsin C deficiency
Leukocyte adhesion deficiencies
-severe periodontal disease associated with the failure of the PMN to reach sites of infection.
-not direct evidence of protective function of PMN
LAD type 1- CD18 defect
LAD type 2- CHO fucosylation
Neutropenias
- when you have <500 PMN/mm^3
-normal is about 4,000
variety of causes
-best evidence of protective role for neutrophils
Chemotactic dfects
-localized juvenile perio, diabetes etc
-different forms of perio
-receptors and mediators
Neutrophil respiratory burst
-neutrophil metabolism is independent of O2
-consumes large amount of O2 when stimulated
-O2 is converted to super oxide anion and hydrogen peroxide
-products resonsible for oxidative killing
Chronic Granulomatous disease
-defect in NADPH oxidase results in inability to mount a respiratory burst
Granule dysfunctions
-(Chdediak Higashi syndrome- giant lysosumes due to granule fusion dysfunctions
-specific granule deficiencies including lactoferrin, defensins, elastase etc.
Roles of Neutrophils in Perio
Protective
-phagocytosis and killing
Destructive
Releasing granular enzymes (elastase etc)
releasing toxic oxygen species (O2-, H2O2 etc)
releasing inflammotory mediators (TNF-alpha, IL-1)
PMN modulation by inflammatory mediators
-priming is mechanism where dormant neutrophils acquire a state of preactivation that enables an enhanced response to be genreated once the cells are activated
-priming agents are LPS and cytokines