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34 Cards in this Set

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Dental Caries
disease of the mineralized tissue of teeth (enamel, dentin, and cementum) caused by fermentation of carbs
4 Factors in the formation of carious lesions:
1. microorganism:
-qualit: known group of bugs that cause caries
-quant:more in # = more infection
2. Metabolic substrates:
-qual: complex sugars vw/ simple sugars
-quant: more simple sugars = more infection
3.Teeth & their environment
-qual: environment (ex: use fluoride)
-quant: how many teeth, more # more caries can attack
4. Time
-qual: frequency (how often eating cookie, all at once or every couple hrs)
-quant: eaten sugary food & how long to develop
What can be done to limit the 4 factors in formation of caries?
1. Microorganism:
-add OHI
-xylitol
2. Metabolic substrates:
-limit soda and frequency
-OHI
-sugar substitues
3. Teeth & their environment:
-add fluoride
-sealants
-OHI
4. Time:
-eat 3 meals a day
-no snacking on simple sugars
Structure & Composition of Tooth Hard Tissues
1. Organic matrix: protein (collagen, other), and mucopolysaccharides
2. Mineral: hydroxyapatite
-Ca5(PO4)3(OH)2
3. Water
4. Cells (particularly in dentin)
Enamel

Dentin
Organic = 4
Mineral = 95
Water = 1

O = 20
M = 70
W = 10
Fluoride
-will bind to/replace missing OH-
-substitute for hydroxyapatite
-most electroneg. charge -1 in existence
-stronger magnet even tho same charge
-charge will hold structure together a little more firmly
-takes more H+ has more resistance to falling apart
Positive Ions:
-lead, zinc, strontium, silver, nickel, iron

-binds to Ca++ substitute
CO3 Carbonate (-2)
disadvantages:
-makes more sensitive to acid
~3% P substituted w/ CO3

advantages:
-kink: doesn't fit together perfectly
-if tooth fractures kinks give it a bit of flex (less fracture)
What happens to Hydroxyapatite in presence of acid?
-at neutral pH is insoluble
-dissolved; rxn is reversible
-acid = demineralization (structure held by ionized bond falls apart but reversible
-reverse = remineralization
Ca5PH4)3(OH)2 + 14H+
<-->
10Ca + 6(H2PH4) + 2H2O
What is critical pH?
pH below which dissolution predominates
~5.5

w/ fluoride critical pH = 4.9
stronger magnet, etc.
Sites of Caries
-gen. char: favorable plaque retention & limited access for saliva
1. pits and fissures
-occlusal surfaces of molars & premolars
-buccal pits of molars
(braces & limited saliva flow)
-palatal pits of maxillary incisors
2. Approximal surfaces of adj. teeth just cervical to contact point
3. Cervical margin just coronal to gingival margin
4. Exposed root surfaces
-in pt. w/ gingival recession
5. margins of deficient restorations
6. tooth surfaces adj to dentures & bridges
Sequence of Plaque Development
Salivary proteins
Pellicle
Plaque Biofilm
Calculus
Pellicle
acellular, homogeneous, organic film that forms on enamel and other hard surfaces by selective adsorption of salivary proteins and glycoproteins
Characteristics of Pellicle
-forms spontaneously on teeth
-bacteria not necessary for formation
-can be removed only by meticulous cleaning
-if removed rapidly forms again (min to hrs)
-protective fxns have suggested but not proben
-forms suitable environment for bacterial bioneer sps adherence & multiplication (plaque biofilm)
Plaque Biofilm
soft, non-mineralized bacterial deposit that forms on teeth
-suitable env. for acid producing bacteria & diminish saliva protection & mxn
-composition:
>plaque-tooth interface (generally pellicle)
>microbial layers and colonies
>intercellular matrix (insoluble)
Calculus
plaque biofilm in which inorganic deposits have caused mineralization
-greatly increased risk for developing periodontitis
Role of Bacterial Metabolism
Identification of Cariogenic bugs in Gnotobiotic Mice
-given human biofilm = caries
-given individual bugs at a time:
Required to cause caries:
>Strep mutans
>Strep
>Lactobacillus
>Actinomyces
Characteristics that suggest Strep Mutans dominant cause of caries.
S. mutans & S. sobrinus
-attach supra-gingival plaque
-sugar transport good at low pH
-acid production = homoplactic fermenter
-aciduricity = acidophilic (grows well at low pH)
-provides insoluble glucan (mutan) decrease buffer increase acid
-produce intracell polysacharide (snack) extracell levan (fructose polymers)
What do plaque bacteria use in our modern diet?
What do they do with it?
-sucrose=major consumed in our diet (dissach: glucose & fructose)
1. Invertase: breaks sucrose
-high affinity
2. can undergo glycolytic pathway -> Lactic Acid
3. Fructosyl-transferase
-low affinity
-fructose added to growing chain Levan
-snack food
4. Glucosyl-transferase
-low affinity
-glucose makes insoluble
What does Glucan or Dextran do?
makes insoluble
-difficult for saliva to wash away
-excludes saliva:
>keeps pH lower longer
>keep Ca & P away (difficult to remineralize)
What does Xylitol do?
non-metabolized sweetner
-bring X thru bacterial pores
-adds P doesn't metabolize
-bacteria needs to pump out or else toxic (use ATP)
How pH affect S mutans & L. Casei?
-poor competitor @ pH 7
-good competitor @ pH 5
(most extreme when buffer excluded = xerostomic)
Oral bacteria acid production based on pH
-pH 7 everyone produces acid
-pH 5 only cariogenic bacteria metabolize
Major bacterial sps responsible for these caries in major locations:
1. pits & fissures
2. smooth-surface (enamel)
3. dentin
4. Endodonic
6. Gingival & Perio
1. S. mutans
2. S. mutans
3. **Lactinobacilli, Actinomyces, S. mutans
4. Similar to dentin
-S. mutans, A. viscosus, A. ondontolyt. Lactobacilli
5. Gram neg rods (BPB - bacteriodes)
6. gram neg rods facultative & anaerobic
Role of dietary carbs in relation to caries.
-WWII down bc imported from denmark
-rised when sugar increased in diet
-down because of fluoride
-rise in US because diet
List acids produced by bacteria strongest to weakest:
1. Lactic acid (lowest pKa)
2. Formic acid
3. Succinic acid
4. Acetic acid
5. Popionic acid
Stephan Curve
-presence in diet of certian dietary cars leads to rapid & sustained pH drop
-when drops below critical pH w/ caries tooth = demineralization
What causes changes in pH below critical value?
-presence of plaque
-1st glucose rinse = pH drops dramatically in both w/ plaque
-1 person brushes teeth 2 doesn't
-1: in glucose rinse, mowed the lawn -> pH drop is less dramatic (not at critical pH)
-2: drop still the same
Effectiveness of given carbs in promoting caries depends on:
1. ability of cariogenic bacteria to metabolize the carb
2. ability of carb molecule to diffuse into plaque
3. frequency more important than amt
-higher freq: higher drop in critical pH more often
Saliva
-regulation
secretion of salivary glands (main source) & minor glands of the oral mucosa (minor source)
1. activated by autonomic reflexes
-para: increase flow, watery
-symp: low flow, thick
2. flow stimulated by: sight, smell, food in mouth, in stomach
3. flow rate
-stim 1-2 ml/min
-bw meals = small
-sleep: very small
Major Fxns of Saliva:
1. Aid in swallow/digest of food:
-lubricate food to swallow
-dissolve food = stim of taste bud sensory
-digest foods
2. Protective (chemical & thermal barrier)
-mucoid coating on oral mucous mem
-hot drink = mixes w/ acid & temp dispersed -> not as hot as compared to dry epith (skin)
3. Reduce tendency of caries
-flush away carbs
-contain Ca & P for remineralization
-antimicrobial agents
-acts as chemical buffer (maintain pH)
-source of recycled fluoride
Xerostomia
dry mouth, effects of lack of saliva:
-tendency to oral ulceration
-difficulty in swallow dry foods
-thermal & chemical sensitivity
-altered taste
-increased tend to caries
Why Xerostomia causes increased tendency to caries:
-disease
-drugs
-irradiation
-age
-sleep
Treatment for lack of saliva:
-artificial saliva
-increased oral hygiene
-dietary control (decreased sugars)
-fluoride therapy