Oral Immunology A6: Microbiology Of Dental Caries

Front 1

1) What are germ free animals called?
2) Are caries transmissible?
3) Do antibiotics increase or decrease the incidence of caries?

Back 1

1) Gnotobiotic
2) Yes
3) Decrease

Front 2

1) What is plaque?
2) How many bacteria are in plaque?
3) How many bacterial species are in plaque?
4) Besides bacteria, what else is found in plaque?
5) Describe the order of: enamel, plaque, pellicle

Back 2

1) Biofilm composed of bacteria in matrix of glucan and fructan polysaccharides
2) 10^10 bacteria
3) 700 bacterial species
4) Epithelial cells, leukocytes,
5) Enamel -> pellicle -> plaque

Front 3

What are the four main components of plaque?

Back 3

1) Bacteria
2) Matrix: glucans and fructans
3) Lipids
4) Inorganic ions

Front 4

1) Where does lipids in plaque come from?
2) What do these lipids have an affinity for?

Back 4

1) Phospholipids of gram - organisms
2) Calcium and phosphate ions

Front 5

What are the inorganic ions in plaque and what do they help form?

Back 5

Calcium, magnesium, carbonate, phosphate. Calculus formation.

Front 6

1) **What is the primary colonizer of the tooth surface?**
2) What is the predominant organism involved in caries formation?
3) What is a significant bacteria that is not predominant in caries formation?

Back 6

1) Strep sanguis
2) Strep mutans
3) Strep sobrinus

Front 7

1) What organisms form the biofilm?
2) What drives biofilm formation?
3) What are the secondary colonizers and when do they appear?
4) What are tertiary colonizers and when do they appear?

Back 7

1) Pioneer salivary pellicle colonizers Gram-positive cocci Strep Sanguis and rods.
2) Homo and heterotypic associations
3) Gram - cocci and rods (1-3 days)
4) Gram - filaments, fusobacteria, spirochetes (1 week)

Front 8

Give an example of bacterial proteases.

Back 8

S. sanguis proteases destroy salivary proteins for food, pave way for more cariogenic bacteria like S. mutans

Front 9

What are corn cob arrangements? Where are they found in particular?

Back 9

Cocci attaching and growing on the surface of filamentous microorganisms - particularly on the outer surface of the tooth

Front 10

Strep mutans:

1) Viridans group?
2) **What serotypes are human pathogens?
3) Why is it one of the primary organisms associated with caries?
4) What paves the way for S. mutans?
5) When does it appear in the mouth?
6) What does its number correlate with?
7) **What does its percentage in plaque correlate with?**

Back 10

1) Alpha hemolytic
2) C, E, F
3) It's a homolactic fermenter
4) Strep sanguis
5) When the tooth erupts
6) Colonization of mother
7) **Sucrose consumption**

Front 11

1) **What is among the most cariogenic carbohydrates?
2) What are some other, less cariogenic carbs?
3) What are weakly non-cariogenic?
4) How does xylitol work to prevent caries?

Back 11

1) **Sucrose
2) Glucose, fructose
3) Sorbitol, aspartame, mannitol
4) Disrupts S. mutans metabolism, anti-cariogenic

Front 12

1) What are the two types of **homopolymers**? **Which one is more important? Why?**
2) What are they formed from?

Back 12

1) **Glucans, fructans**. Glucans more imp. due to **solubility**, allows nutrients to penetrate biofilm without the bacteria being swept away.
2) Transfer of glucosyl/fructosyl groups from sucrose to pre-existing glucan/fructan polymers.

Front 13

1) What is a major virulence trait of cariogenic organisms?
2) What does it mediate?
3) How does it work?

Back 13

1) Glucans
2) Adhesion to tooth
3) Clumps Strep mutans, enhances plaque mass, changes diffusion property of plaque matrix to trap lactic acid (no access to salivary pH buffers)

Front 14

What are the two main virulence factors of Strep mutans?

Back 14

1) Glucan binding protein
2) Homolactate fermentation

Front 15

1) What species produce lactic acid?
2) Why are bacteria continually capable of producing lactic acid?

Back 15

1) **S mutans and Lactobacilli
2) Stores of IPS (intracellular polysaccharide granules)

Front 16

1) When are intracellular polysaccharide storage product made?
2) What are they similar to?
3) When are they metabolized and what's associated with its metabolism?

Back 16

1) During periods of carb excess
2) **Glycogen, iodophilic
3) **Fasting periods - extended production of acid, lower pH, demineralization

Front 17

1) What is the structure of hydroxyapatite?
2) When is mineralization:demineralization at equilibrium?
3) What does lactic acid break hydroxyapatite down into?

Back 17

1) Ca10(PO4)6OH2
2) Ca2+, PO4-3 ions at saturation, pH 6.8
3) Calcium, phosphate ions

Front 18

1) What is the mechanism of the action of fluoride?
2) What does fluoride promote?
3) What does fluoride inhibit and how?

Back 18

1) OH-apatite + F- = F-apatite, less soluble
2) Remineralization
3) Bacterial enolase by reducing PEP production, blocking glycolytic pathway and pyruvate production for bacteria

Front 19

What three things do all cariogenic bacteria do?

Back 19

1) Make glucans
2) Bind glucans
3) Make lactic acid

Front 20

Lactobacilli:

1) Gram? Shape?
2) Where is it found?
3) What does it produce and what is it involved in?

Back 20

1) Gram + rod
2) Normal flora of mouth, GI tract, vagina
3) Lactic acid, caries progression

Front 21

What do organisms use for sucrose independent adhesion? What do these things bind?

Back 21

**Type 1 pili**. Bind things like PrP

Front 22

1) What are actinomyces viscosus and naeslundii?
2) What do they bind to?
3) What do they produce?

Back 22

1) Early colonizers
2) PrP - proline rich proteins that coat tooth surface (not in saliva or fluid phase)
3) Organic acids

Front 23

1) What are a major fraction of salivary proteins?
2) What does it maintain?
3) What is a significant portion of the salivary pellicle?
4) What are the 2 genes that encode it?
5) **What does PRH2 encode**?
6) **What are some variants associated with?**

Back 23

1) PrP
2) Calcium and phosphate saturation of saliva
3) PrP
4) PRH-1, PRH-2
5) **PRP-1 and PRP-2**
6) Susceptibility to caries

Front 24

1) Where is lactoferrin found? How does it work? What is highly susceptible?
2) What do lysozymes do? How do they work?
3) What are mucins and what do they do?

Back 24

1) Tears, mucus, breast milk. Bactericidal. Strep mutans highly susceptible.

2) Hydrolyze Beta1-4 bond NAG NAM (peptidoglycan). Antibacterial.

3) NIA - non-immunoglobin agglutinin, facilitate bacterial clearance

Front 25

What are three defects in innate immunity and what results?

Back 25

1) Sjogrens - autoimmune disorder, salivary/lacrimal glands affected, induced xerostomia

2) Salivary hypofunction/dysfunction

3) Xerostomia - lack of fluid-phase factors, NIA. Lack of buffering capacity, antimicrobials

Front 26

**What are the oral immunoglobins?**

Back 26

**IgA, IgM**

Front 27

1) Is sIgA present in saliva at birth?
2) When do IgA and IgM appear?
3) **Do predentate infants have sIgA
4) **When is sIgA to oral strep detected in saliva?
5) **What is sIgA directed against?
6) Are antibodies to S. mutans detected?

Back 27

1) No
2) **Shortly after birth**
3) **Yes
4) As early as 6 weeks**
5) **Mucosal colonizers ie Strep salivarius**
6) NO

Front 28

In dentate children:

1) Antibodies to what organisms are detected?
2) Within how many years are sIgA levels the same as the adult?
3) Adult whole saliva contains how much IgA?

Back 28

1) Colonizers S. sanguis and S. mutans in 1 yr old children
2) 10
3) 30-160 mg/mL IgA

Front 29

1) **What is the most common immunodeficiency involving caries?
2) What is the status of the B cells?
3) What is found in 1/3 patients?
4) Symptoms?
5) What are they missing?
6) Do they possess salivary IgM antibodies to S. mutans? What happens if they don't have it?

Back 29

1) **IgA deficiency
2) B cells normal
3) Anti-IgA
4) Asymptomatic - some rhinitis, sinusitis, Giardisis
5) IgG2 subclass
6) Some - if missing, lack of IgM = increased caries

Front 30

What are 4 candidates for caries vaccine?

Back 30

1) Glucosyltransferases
2) Adhesins
3) Glucan-binding proteins
4) Surface antigens

Front 31

1) **What do you use for active immunization and what is a risk?**
2) **What do conjugate vaccines combine**?
3) **What do conjugate vaccines do?**

Back 31

1) Whole organisms - **Rheumatic fever**
2) Immunogens and bacterial components (GTF, AGI/II), GTF + cholera toxin subunit)
3) Increase immunogenic response