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ICS1 > Midterm I : Sugar Metablism + Intro Cariology > Flashcards

Midterm I : Sugar Metablism + Intro Cariology Flashcards

1
Q
  1. what percentage of us people have had caries by age 35?

2. what percentage of seniors /over 65 have caries in permanent teeth

A
  1. 95%

2. 94%

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2
Q

what are protective factors for caries

A
  • salivary flow
  • proteins, antibacterial components and agents
  • fluoride, calcium and phosphate
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3
Q

what are pathologic factors for caries

A

reduced salivary function, mutans streptococci and lactobacilli, and diet with high frequency of carbs

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4
Q

describe the type of bacteria of streptococcus mutans

A
  • gram positive (thick cell wall) cocci with strepto-cell arrangement
  • cocci means spherical, strepto means in chains
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5
Q

what are vertical and horizontal transmissions

A

vertical is parent to child (mother to baby) and horizontal is within same generation, not parent to progeny

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6
Q

what types of transmission of streptococcus mutans is there

A

both vertical AND horizontal

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7
Q

describe the process of dental plaque formation

whats another word for dental plaque

A

plaque =biofilm
process:
-colonization: bacterial cells adhere to salivary pellicle which lies directly on the tooth and contains proteins. gp-340 in the pellicle binds to streptococcus mutans most commonly.
-there is a formation of microcolonies expressing extracellular polymers (glucan chains) which allows for adherence/accumulation of bacteria cemented by polysaccharides onto the salivary pellicle

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8
Q

what sugar does s mucans ferment

A

a RANGE of sugars, making lactic acid.

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9
Q

At what pH does enamel start to degrade?

A

5.5 and below= degredation!

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10
Q

how many ATP does glycolysis produce

A

4 gross, net production is TWO!

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11
Q

where does glycolysis occur? when is it used for energy production?

A

occurs in the cytoplasm of ALL cells. prokaryotes and eukaryotes!
-cells that have limited access to oxygen or dont have mitochondria rely on glycolysis/fermentation for their energy production!

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12
Q

what is step 1 of glycolysis (enzyme, product and reactant)

A

hexokinase enzyme converts glucose to glucose-6-phosphate (uses 1 ATP)

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13
Q

(enzyme, product and reactant) what is step 2 of glycolysis

A

phosphoglucose isomerase converts glucose-6-phosphate to fructose 6-biphosphate
-uses 1 atp

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14
Q

(enzyme, product and reactant) what is step 3 of glycolysis

A

phosphofructokinase converts fructose 6-phosphate to fructose 1,6 biphosphate , uses 1 atp

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15
Q

what is step 4 of glycolysis

A

last energy consuming step!!!
aldolase converts fructose 1,6 biphosphate to glyceraldehyde 3-phosphate. but triose phosphate isomerase converts it into dihydroxyacetone phosphate and back (reversible). only glyceraldehyde 3 phosphate can go on to next steps which drives it that way i think

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16
Q

what is step 5 of glycolysis

A

first step in energy producing stage.

glyceraldehyde 3 phosphate dehydrogenase converts glyceraldehyde 3 phosphate to 1,3-biphosphoglycerate (makes 1 NADH)

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17
Q

what is step 6 of glycolysis

A

second energy producing step

phosphoglycerate kinase converts 1,3 biphosphoglycerate into 3-phosphoglycerate. makes 1 atp!

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18
Q

what is step 7 of glycolysis

A

phosphoglycerate mutase converts 3-phosphoglycerate to 2-phosphoglycerate

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19
Q

what is step 8 of glycolysis

A

enolase converts 2-phosphoglycerate into phosphoenolypyruvate and water

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20
Q

what is the last step of glycolysis

A

9th step total, 5th energy producing step..

pyruvate kinase converts phosphoenol pyruvate into pyruvate, makes 1 atp

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21
Q

what are the 3 fates of pyruvate

A
  • could be turned into lactate (fermentation) this process makes NAD+ allowing glycolysis occur again
  • could be turned into acetyl coA and carbon dioxide, acetylcoa goes for further oxidation
  • could be converted into acetaldehyde and co2, then ethanol (this makes NAD+)
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22
Q

where does fermentation occur, how many atp is generated

A

cytosol, usually under anaerobic conditions. 2 generated from glycolysis

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23
Q

what are obligate anaerobes

A

can only survive in anaerobic conditions, cant survive with oxygen around. use fermentation for enery

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24
Q

how does fermentation valuable for energy production

A

it makes NAD+, cells have LIMITED NAD+ , it comes from vitamin niacin b3.
-because glyceraldehyde 3-phosphate reduced NAD+ to NADH in glycolysis, we now need more NAD+ to go again.

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25
Q

what enzyme is involved in lactic acid fermentation

A

lactate dehydrogenase (pyruvate->lactate)

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26
Q

what is the warburg effect and why does it occur

A

cancer sells selectibvely do aerobic glycolysis because:

  • produces lactic acid/acidification of environment facors tumor invasiveness and inhibits local immune response
  • cancer cells grow faster than blood vessels that nourish them, so cancer cells experience hypoxia.. aerobic glycolysis reduces need of oxygen.
  • high levels of biosynthetic intermediates (NAD+, nucleotides , etc) supports rapid growth.
27
Q

what is 2-deoxy-o-glucose

A

modulator, target is hexokinase. hexokinase is first enzyme in glycolysis. so it binds it and glycolysis doesnt occur. tumor cells die

28
Q

what does cambra stand for/what is it

A

caries management by risk assessment

  • uses caries risk assessment (CRA) to measure risk of future caries disease
  • followed by diagnosis and prognosis
  • determines specific treatments based on unique risk of individual patient
29
Q

what are the 3 general areas where caries occurs

A

pits and fissures
smooth surface
root surface

30
Q

what percentage of carious lesions in 5-17 yr olds is pit and fissures and where are they typically found

A

84%

-usually found on maxillary lingual pits and buccal mandibular pits

31
Q

what is a white spot lesion

A

earliest sign of subsurface demineralization. the surface IS intact, and can be remineralized. surface still prevents bacterial penetration.
incipient lesion

32
Q

what is a brown spot lesion

A

previously white spot lesion that has become more porous (some demineralization is happening) and exogenous stain has entered into the lesion. this lesion can also be remineralized, become smooth and shiny. but remains stained.

33
Q

what are: prevalence, incidence, and trends

A

prevalence: number of individuals with the disease at a specific point in time
incidence: number of people in a population who experience new disease during a specific period of time
trends: changes or differences in prevalence of incidence of disease with respect to time

34
Q

what are DMFT and DMFS

A

decayed missing filled teeth/surfaces

DMFT: 0-28, doesnt include 3rd molars, unerupted, congenitally missing, supernumerary teeth, teeth removed for other than caries reasons,

DMFS: (0-128) posterior teeth each have 5 surfaces, anterior teeth have 4 surfaces (doesnt include 3rd molars either)

35
Q

what are the limitations to the DMF index?

A
  • values dont relate to number of teeth at risk
  • gives equal weight to missing, untreated, decayed or well restored teeth.
  • doesnt account for teeth lost for reasons other than decay (perio disease)
  • data isnt useful in estimating individual treatment needs
  • doesnt account for sealed teeth (sealants didnt exist)
  • DOESNT CONSIDER PRECAVITATED LESIONS!!!
36
Q

what is a case control study

A

weakest type of research (vs cohort and randomized controlled clinical trials)

  • it involves identifying subjects with a clinical condition (cases) and subjects free from the condition (controls), and investigating if the two groups have similar or different exposures to risk indicators or factors associated with the disease
  • – visit slide 24 for more weakest->strongest!!
37
Q

what is a cohort study

A

in between case control and randomized controlled clinical trial in terms of strength of evidence

  • involves identifying two groups (cohorts) of patients, one which did receive exposure of interest, and one which didn’t, and then following these cohorts forward for the outcome of interest.
  • – visit slide 24 for more weakest->strongest!!
38
Q

what is a randomized controlled clinical trial

A

stronger evidence than both case control and cohort studies’

  • study randomly assigns participants of a defined population to receive one or two or more interventions. one of the interventions acts as standard of comparison or control. the control may be the standard of practice, a placebo or no intervention. Another intervention is/are the treatments under investigation. these groups are followed over time for outcome of interest.
  • – visit slide 24 for more weakest->strongest!!
39
Q

what is the evidence hierarchy (top to bottom)

A
  • systematic reviews (BEST)
  • randomized controlled trials (REALLY GOOD- these top two are strong to support recommendations)
  • cohort studies
  • case reports
  • narrative reviews/expert opinions/editorials
  • animal and laboratory studies
40
Q

what are systematic reviews, what are some sources for it

A

scientific investigations that use rigorous methods to review original research.

  • synthesize results from multiple trials addressing the same question
  • statistically combines data
  • distills large quantities of data into clinically useful info
cochrane collaboration (international), database of abstracts and reviews of effectiveness (UK), national institute of clinical excellence (UK), agency for healthcare research and quality (US)
https://ebd.ada.org
41
Q

what impacts the demin/remin cycle

A

(demineralization/remineralization) - saliva, pellicle, diet, structure of mineral

42
Q

what is the specific plaque hypothesis

A

only a limited species of bacteria in plaque can cause disease. Mutans streptococci and lactobacilli are main culprits

43
Q

what is the nonspecific plaque hypothesis

A

states that plaque is considered the etiologic agent of dental disease. There is no bacteriological difference acknowledged to exist between plaque from diseased and nondiseased sites

44
Q

what is the ecological plaque hypothesis

what is EXTENDED ecological plaque hypoth.

A

pathogens may be present at sound tooth sites, but in too low numbers to cause disease
-disease will result when there is a shift in the homeostatic balance of the resident microflora due to a change in pH conditions which favors growth of pathogens.
-its the pH not the sugar which causes pathologic shifts in biofilm
EXTENDED:
– in presence of low pH, non-Mutans streptococci (MS) and Actinomyces (normally non-pathogenic) can adapt to produce acid
— the destabilization of homeostatic biofilm. causes a shift to a more acidogenic biofilm
—- MS and lactobacilli can predominate at a lower pH

45
Q

how do MS and LB bacteria change when pulsed with glucose and lowered pH

A

they prevail and result in a larger percentage of bacteria (study done)

46
Q

what is the relationship between bacteria in the mouth and the heart

A

a study found that the positive rate of S mutans in cardiovascular specimens from patients who dental plaque was also positive for s mutans was 78% , significantly higher than any other tested species when same analysis was done.
– specific oral bacterial species like s mutans and A actinomyectemcomitans are related to bacteria in the blood, can be factors for cardiovascular diseases

47
Q

what role does saliva play (factors)

A
  • produces salivary pellicle
  • proteins (statherins, PRPs, histatins, and cystatins)
  • antimicrobial (IgA, lysozyme, lactoferrin, peroxase)
  • clears bacteria and carbs
  • buffers acids
  • contains calcium/phosphate/fluoride
  • lubricates oral mucosa
  • mediates taste acuity
  • enzymes
48
Q

what is the difference between xerostomia and salivary gland hypofunction

A

xerostemia is how a patient feels (subjective)

salivary gland hypofunction (SGH) is objectively measured using a flow rate measurement. (rested and stimulated rates)

49
Q

what can cause xerostomia

A

medications, cancer treatment (radiation/chemo), sjogrens syndrome or other autoimmune CT diseases, diseases like HIV or diabetes, metabolic disturbances, stress and depression, physiological blockage of salivary gland ducts, dehydration

(amphetamines, antimicrobials, analgesics/narcotics, antipsychotics, anti-inflammatories, asthma drugs, nsaids, ace inhibitors, anticonvulsants, calcium channel blockers, anti anxiety drugs, gastric acid drugs, antidepressants, smoking cessation drugs, antihistamines)

50
Q

what aspect of saliva should be analyzed /salivary assessment

A

assessment: resting flow rate, resting pH, stimulated flow rate(>1ml/min is WNL), stimulated pH

important things also include:

  • resting consistency/hydration
  • buffer test
51
Q

what are complex vs simple carbohydrates

A

carbohydrates (CHO) btw

  • complex (starches)
  • simple (sucrose, glucose, fructose)
52
Q

if surface layer is intact but you see dark spot in dentin, what does it mean

A

staining, not caries/cavity. if this is left untreated, it will cavitate and bacteria can then get into the dentin- surgical restoration required at that point

53
Q

describe the demin/remin process

A

enamel crystal (carbonated apatite) ->combines with acid-> partly dissolved crystal –> combined with calcium/phosphate/fluoride will remineralize–> recreate crystal nucleus

ca10(PO4)5(F)2= fluoroapatite like coating on crystals leads to crystal nucleus , can be formed when we add calcium/phosphate/fluoride at the right time

SLIDE 70

54
Q

how does ion exchange strengthen the tooth

A

replacing carbonate (CO3 2-) with phosphate (PO4 3-) in hydroxyapatite makes it stronger.

55
Q

what are the zones of an early lesion

A

surface zone, body, dark zone, and translucent zone (In order) – slide 75

56
Q

what is the stephan curve

A

curve shows pH throughout the day as we eat acidic foods , and rise as our saliva buffers.

57
Q

what are the protective factors for caries

A

SAFER —- Saliva & sealants, Antibacterials, Fluoride/calcium/phosphate, Effective lifestyle habits , Risk based reassessment

SAFER acronym to remember it

58
Q

what are the risk factors forcaries

A

BAD – Bad bacteria, Absence of saliva, Destruction of lifestyle habits

59
Q

what are the disease indicators for caries

A

WREC (total wreckage)

-White spots, Restorations < 3 yrs, Enamel lesions, Cavities/dentin

60
Q

what categories will you see in axium for risk assessment

A

disease indicators, risk factors, protective factors, bacteria/saliva test results

61
Q

how can you tell if there is a low flow rate?

A

thick stringy saliva or very frothy saliva

62
Q

what is pilocarpine hydrochloride used for

A
  • stimulates saliva production!

i. e. salagen 5 mg, one tablet 3 times a day - lowest dose tolerated (have to consult physician)

63
Q

what is cariscreen

A

‘caries susceptibility test’
measures bacterial load. real time (15 seconds) inexpensive test for identifying high /low risk people.
-ATP bioluminescence, acidogenic bacterial load detected. correlates to caries risk levels

reaction: ATP + luciferin+ O2 with luciferase and MG —–> light is a product

ICS1 (23 decks)

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