Host Defense Against Oral Infections Flashcards

(37 cards)

1
Q

Non Specific Oral defenses

A
  • Saliva flow
  • Mucin/agglutinins-physical removal
  • Lysozome-protease-anion system- lysis
  • Lactoferrin
  • Histatins- Antifungal, some antibacterial
  • Defensins- Antimicrobe, immunomodulatory
  • Chitinase-antifungal
  • Cathelicidin-antimicrobe
  • Neutrophils/macrophages
  • Complement
  • Salivary lactoperoxidase-
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2
Q

Neutrophil

Class, function

A

Granulocyte

Phagocyte

Innate

Most abundunt leukocyte

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3
Q

Lymphocyte

A

Agranulocyte\Adaptive immunity

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4
Q

Monocyte

A

Agranulocyte

Pahgocyte

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5
Q

Eosinophil

A

Granulocyte

Removal of helminths and Ab complexes

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6
Q

Basophil

A

Granulocyte

Allergy

Inflammation

Least abundunt

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7
Q

Soluble mediators of inflammation in oral infections

3 classes and examples

A
  • Antibodies
    • slgA, IgG, IgM
  • Complement
    • C3
  • Cytokines
    • IL-1 IL-6 TNF-alpha
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8
Q

Innate Immune components in Oral health and the barriers they form

A
  • Consists of
    • epithelia, phagocyes, plasma proteins
  • Barriers
    • Anatomic barriers
    • Physiologic barriers
    • Phagocytic barriers
    • Inflammatory barriers
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9
Q

Oral mucosal epithelial cells anatomic barrier function

A
  • Express TLR to recognize PAMPS
    • TLR2 binds lipoteichoic acid on gram POSITIVE bacteria (actinomyces, strep)
    • TLR4 binds lipopolysaccharide (LPS) on gram NEGATIVE (Prevotella)
  • TLR binding signals epithelial cells to make
    • Peptide antibiotics
    • Cytokine
    • Nitric oxide
  • Express receptors for secretory IgA (slgA)
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10
Q

Swallowing

A

Removes bacteria from plaque and mucosa

when blocked gram negative species groq

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11
Q

pH

A
  1. 9 pH in healthy
  2. 25-8 pH in infections

A rise in periodontal pocket pH in gingivitis and periodontal disease favors periodontal pathogen growth

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12
Q

Temperature

A
  • 35035 C normal
  • 39 C in periodontal inflammation
  • Higher temp
    • alter bacterial gene expression
    • immune evasion
    • P gingivalis SOD is up-regulated and can neutralize super oxide anions meant to kill it
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13
Q

Lactoferrin

A

Iron binding

bacteriostatic

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14
Q

Lysozyme

A
  • Found in saliva and in lysosome
  • Breaks down baterial cell wall (peptidoglycan)
  • effective aginst S mutans
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15
Q

Myeloperoxidase System

A

Bactericidal generating halide

hydrogen peroxide in PMN migrates to gum crevice as host inflammatory respoonse

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16
Q

Salivary peroxidase system

A

Bactericidal generating thiocyanate, hydrogen peroxide

17
Q

Antimicrobial Peptides

A

Histatins, defensins

Small cationic

18
Q

Histatins

A

Histidine rich broad spectrum

anti-fungal and bactereial

19
Q

Defensins

A

Broad spectrum

anti- bacterial, fungal, viral

Beta defensins protect oral cavity

20
Q

Leukocytes action in saliva

A

98% PMN

Secrete alpha-defensin

phagocytosis

Increase inflammation

21
Q

Secretory IgA (sIgA) Activity

A

Major antibody in saliva

Inhibits microbial adherence

Agglutinates bacteria

Virus neutralization

22
Q

Describe the phagocytic killing methods that are oxygen independent and dependent

A
  • Oxygen Independent Methods
    • Lysozyme breaks down cell wall
    • Defensin- cationic peptides, antimicrobial
    • Lactoferrin- binds iron
    • Proteolytic and hydrolytic enzymes
  • Oxygen Dependent
    • Respiratory burst intermediates
      • Hydrogen peroxide, superoxide anion, hydoxy radical
      • Myeloperoxidase, hypochlorite, hypohalite
      • Nitric oxide
23
Q

Chronic Granulomatous Disease

Etiology

A
  • Failure of phagocytes to produce Hydrogen peroxide and superoxide
  • Genetic defect in NADPH oxidase
  • Cant kill pathogen
  • Prone to infection
    • pneumonia, lung and lymph node infection, abcesses of skin and liver
24
Q

How to treat chronic granulomatous disease

A
  • Antibiotics
    • high dose, long term, prophylactic
    • Amphotericin B
    • Penicillin
  • IFN-gamma injections to help activate macrophages
25
Principal events of inflammation
* Local phagocytes release of inflammatory * Cytokines: TNF-alpha, IL-1 * Chmokines: MIP MCP * Cytokines * recruit and activate phagocytes * stimulate cell response * Vasodilation inc blood flow * Increased cepillary permeability * Leukocytes migrate to reach site of infection * PMN first * Monocytes and lymphocytes come later * Periodontitis is inflammation based infection
26
Immunoglobulins and antibodies in the oral cavity
Gingival crevice and 1/3 of tooth crown is covered with GCF Gingival Crevicular Fluid contains IgG IgM IgA Salivary Ab is predominantly sIgA Antibody can be locally made paticularly in inflamed gingivae
27
IgG
Monomer Makes up for a lot of AB in serum Crosses placenta Activates complement Major opsonizing AB Found in GCF to protect gum and crown
28
IgM
Pentamer First antibody generated against any antigen Predominant antibody produced by fetus Antibody for carb antigens (ABO groups) GCF contains IgM to protect gum and crown
29
IgA
* 2 forms * In serum as monomer * Secretions as dimer (saliva) sIgA * lines oral mucosa surfaces and protects from infection * interferes with adhesion molecules of pathogen * Opsonize pathogens at mucosal surface to prevent attachment * Confers mucosal immunity * Immune Exclusion-sIgA can differentiate which bacteria can provide a commensal or pathogenic *
30
sIgA
* Mediates humoral mucosal immunity * Structure: polymeric, made locally by plasma cells in mucosal epithelium * IgA is the most abundantlly synthesized antibody * 2 subclasses IgA1 and IgA2 * In plasma IgA1 dominates * in saliva they are equal * IgA1 Ab directed against protein antigens * IgA2 Ab is against polysaccharide antigens * sIgA is part of enamel pellicle and good at agglutinating microbes
31
General Mucosal Immune system
* Mucosal epithelium- physical barrier, first line of defense against invasion * GI & Respiratory mucosa colonized by lymphocytes and APC, respond ton Ags * GI- lymphocytes are w/i epithelial layer, lamina propria and Peryers Patch * each with unique phenotype and function * Intraepithelial lymphocytes are usually CD8 T cells * Ag stimuli at 1 site elicits an antibody response that is restricted to MALT * Immune response to oral AGs differ fundamentally from responses encountered at other sites
32
Oral Mucosa Inflammation and immune protection
* Mucosal surfaces continously flushed by exocrine secretions * DC sample Ags btw epithelial cells * Responds to harmful organisms * regulates influx of immune cells * Prevents inflammatory tissue destruction * Alterations in the normal balance of flora can cause inappropriate immune responses * Commensal bacteria then become surrogate pathogens and stimulate chronic inflammatory response
33
Immune Response in Oral Mucosa GCF
* GCF glushes gingival margin-oral cavity area, a vulnerable area * Plaque at gingival margin results in acute inflammation * Increases the flow of GCFto bring components to site * Healthy: dynamic equilibrium of endogenous oral microbes and host antimicrobial factors *
34
What are caries and periodontal disease a result of
* Ecological imbalance btw resident microbes and host immune response * Dental Caries * Frequently eating fermentable barbs lead to selective advatage to higly acidogenic bacteria (lactobacilli, S. mutans) * Colonize on sugar matrix * Lead to biofilm or plaque
35
Mucosal Ag sampling and presenting
* M cells have specialized microfolds to take up Ag * Bring Ab to Intraepithelial DC * Initiate IgA response, that dominate mucosal surface * sIgA first line of defense * Oral immunization with protein Ags induce tolerance * CD4 T cells important in generation of oral mucosal tolerance *
36
Mucosal epithelial secrete
* Mucins, defensins, trefoil, pellicle, lysozyme and NO * Non-specifically shoeld mucosal from microbial damage
37
Specific Host factors of Mouth
* Intra-epithelial lymphocytes and Langerhans Cells * Cellular barrier to bacteria/ag * CD4 T cells- * Secretion of cytokines * sIgA- * Prevent microbe adhesion and metabolism * IgG, IgA, IgM * Prevent adhesion * Opsonization * Complement activation