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DENT 1520 > mini assessment 5-10 > Flashcards

mini assessment 5-10 Flashcards

1
Q

1-Leewenhoek

2-W.D. Miller

3-Clark

4-Fitzgerald

5-Loesche

6-Marsh

A

1-microscopic

2-chemo-parasitic theory

3-S. Mutans

4-S. Mutans from lesions

5-plaque theory

6-ecological plaque

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2
Q

Non Specific Plaque Hypothesis

A

Dental Plaque= dental disease but the decay= non specific because of overgrowth of acidogenic bacteria Prevent it by removing plaque

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3
Q

Oral Microbiology—Miller

A

1- plaque

2- susceptible host

3- fermentable carbohydrate

4-acid production

5- cavity (demineralization)

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4
Q

Caries are Initiated By

A

Time, Host (teeth), Biofilm (bacteria), Nutrients

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5
Q

Specific Plaque Hypothesis

A

-ONLY dental plaque colonized by SPECIFIC bacterial species

Within Caries= S. Mutans & Lactobacillus Caries are SUCROSE DEPENDENT

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6
Q

S. Mutans

A
  • most common in caries
  • reproduce + survive best in low pH
  • diff survival rates
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7
Q

S. Sanguis

A
  • Fimbriae attach to pellicle
  • Both S. mutans & S. sanguis
  • increase risk for caries
  • difficult to get rid of
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8
Q

Lactobacilli

A
  • not original colonizers, only secondary
  • acid via fermentation
  • come before teeth eruption
  • on the dorsum of the tongue
  • not needed for lesion development
  • comes with S. Mutans & S. sabrinus
  • demineralization once lesions begins
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9
Q

1- acidogenic

2-aciduric

3-glucansformation

4-extracellularpolysaccharides

5-intracellularpollysaccharides

A

1- transports sugars and converts them to acid

2- they thrive at low pH

3-GTF

4-adheres to tooth

5- provides energy when sugars aren’t available

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10
Q

Nutrient Sources

A

Sugars—so polysaccharides stick Sucrose—generate acid: pH decreases=demineralization of tooth and an increase in s.mutans= biofilm

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11
Q

Demineralization

A

Occurs below at 5.5—stephens curve

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12
Q

Cariogenicity

A

S. Mutans & sucrose combine to make glucans that will help with adhesion to tooth, and increase the energy source for bacteria (more acid)

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13
Q

Dental Plaque Formation

A

1- pellicle formation- acellular protein film from saliva

2-0-4 hours- single bacteria colonizes (sanguis. mitis. actinomyces)

3-4-24- microcolonies

4-1-14- microbial succession towards actinomyces

5- 2 weeks and plaque is mature

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14
Q

Biofilm

A

microorganisms attached to surface in matrix of extracellular polymers of host/bacteria (plaque) -resistant to antibiotics while individually it isnt

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15
Q

Biofilm Cycle

A

1-cell attaches and adheres

2- grows

3-Detaches and spreads

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16
Q

Biofilm Characteristics

A
  • Complex structure
  • responsive to environment
  • Detaches and sprads
  • Quorum Sensing
  • Resistant to antibiotics
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17
Q

Lactobacillus

S. Mutans

S. Sanguis

Actinomyces

Lactobacillus

A

acid via fermentation

caries

not needed for lesions

root caries

secondary colonizers

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18
Q

Restorative Model of Care

A

Exam cavity

remove

operate

replace with filling

recall

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19
Q
A

1- healthy enamel

2- initial, no cavity lesion

3- cavitation

4- root caries below filling

5- recurrent cavitation

6- loss of crown

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20
Q

Chewing Gum

A

Xylitol & Sorbitol

xyliotol- plaque reducing effect, attracts and then starves bacteria so it helps remineralize

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21
Q

Fluoride

A

inhibits enolase of S. Mutans

pentrates white spot lesions

—fluoride resistant S. Mutans are less cariogenic than fluoride sensitive

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22
Q

Chlorhexidine

A

Surface acting, S.mutans decrease by 50%

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23
Q

Transmission of Oral Flora

A

Vertically—mother to child

Horizontally—from environment (h20)

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24
Q

Window of Infectivity of S. Mutans

A

19-31 Mo. (26 mo mainly)

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25
Q

Proximal Caries

A

adjacent tooth surface—75% chance will spread to other tooth

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26
Q

Where do carious lesions occur

A

Time: at plaque retentive sites (build up over time)

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27
Q

Susceptibility to Dental Caries

A

1) mandibular 1st molars
2) Max First Molars/ max and mand 2nd molars
3) 2nd premolars, max incisors, 1st premolars
4) mandibular incisors, canines

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28
Q

Enamel Caries

A

aka. Smooth surface caries

Beneath plaque as areas of decalcification (white spots)

  • less inter rod and mucopolysaccharides
  • triangular pattern: APEX towards DEJ and BASE towards tooth SURFACE
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29
Q
A

Surface Zone

Body

Dark Zone

Transulcent Zone

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30
Q

White Spot Lesion

A

Dissolves tooth structure= loss of minerals= porosites= white spot lesion

internal loss of minerals but the external is still intact just porous

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31
Q
  • Surface Zone
  • Body of the Lesion
A
  • unaffected by caries, hypermineralized bc of saliva, pore volume= low
  • fluroapatite is formed in surfaceso most mineral loss in under the enamel surface

Bacteria if pores let them through

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32
Q

Dark Zone

A
  • tiny pores, blocking light, but make it opaque
  • loss of crystalline structure
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33
Q

Translucent Zone

A

Pores along the enamel rod

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34
Q
A

1-Reactive dentin

2- Sclerotic Dentin (Translucent Zone)

3- Zone of Demineralization

4- Zone of bacterial invasion and destruction (Turbid and Infected Dentin)

5-Peripheral rod direction

35
Q

Early Dentinal Changes

A

More common in chronic caries

Tubular Sclerosis(more crystals less structure)

calcification of dentinal tubules

36
Q

Dentinal Caries

A
  • Organic acides demineralize dentin
  • degenerates and dissolves
  • no more integrity=invasion of bacteria
37
Q

Zones of Dentinal Caries (5)

A

Zone 1- normal dentine

Zone 2- Subtransparent Dentine-demineralization/pain

Zone 3- Transparent Dentine- collagen=remineralization but there is still demineralization

Zone 4- Turbid Dentine- no self repair, bigger tubules, and more bacteria…extract it

Zone 5-Infected Dentine- lots of bacteria, no structure

38
Q

Pit and Fissure/Occlusal Caries

A

S. Mutans colonize better, no saliva flow/hygiene​

  • lesion under plaque in fissure
  • enamel in fissure= thin
  • caries follow direction of enamel rods
  • triangle shape: apex= surface of tooth and base towards DEJ
  • DEJ= more dentinal tubules= cavities
39
Q
A
40
Q

Occlusal Carie

Vs

Proximal Carie

A
  • Top triangle is at DEJ and goes towards surface but when it his the dentin it is opposite and the base is at the DEJ going towards the pulp.
  • The base is at the surface of the tooth and apex is towards the pulp, even when it hits the dentin
41
Q

Root Caries

A

root must be exposed to environment

actinomyces

invade cementum at sharpeys fibers

spreads laterally

  • destruction of matrix, and eventually pulp bc of tubules
  • slow bc there are less tubules
42
Q

Epithelial Outer Layer

Connective Tissue Layer

Fibrous Ligament

A
  • covers alveolar housing and seals to tooth
  • attaches to the rooth and periosteum covering the bone
  • supports the tooth to the alveolus
43
Q

Supra-crestal CT attachment

Biologic Width

A
  • always found—under junctional epi.
  • junctional epithelium and CT attachment
44
Q

Gingival Crevice

A

“gingival sulcus/pocket”

at the margin, gingiva inverts and forms a cuff around the neck of the tooth

45
Q

Oral Epithelium

Sulcular Epithelium

Junctional Epithelium

A
  • faces oral cavity on outer surface of free/attached gingiva
  • lines gingival sulcus
  • provides contact between gingiva and tooth= epithelial attachment
46
Q

Anatomy:

Oral Epithelium

Sulcular Epithelium

Epithelial attachment

A

-Keratinized strat squamous, resistant to forces + impermeable

  • resistant to forces + low perm. para keratinized
  • attachment apparatus, connect junctional to tooth surfacevia hemidesmosomes
47
Q

Junctional Epithelium

A

2 basal laminas: once facing the tooth (internal) and one facing the CT (external)

  • wider spaces in between cells
  • most permeable—how bacteria enter in
48
Q

Crevicular Fluid

A

CT flows into sulcus through enlarged intercellular. enlarged bc of the rupture of desmosomal junction + inflammation

49
Q

Perio Biofilm

A

1- pellicle—protein from saliva—first layer after teeth cleaning

2- bacteria will attach to that making a biofilm that is made up of dextran

50
Q

Asacchrolytic

Proteolytic

Sacchrolytic

A
  • dont need sugar
  • eat sugar
  • break down sugar for digestion
51
Q

Plaque Progression Perio

A

0-24hr-aquired pellicle, colonizers attach and organize

1-4 d-biolfim matures—fact. anaerobes

1-14 d= obligate anerobes + proteolytic/asacchro + motile + gram neg

52
Q

Socrabsky Color

A

Healthy to Disease

  • yellow
  • blue
  • purple
  • green
  • orange
  • red
  • yo boy put gaspedal on radio
53
Q

yellow

blue

purple

orange

green

red

A
  • -strep
  • actinomycess
  • veiolnella
  • fusobacterium
  • Aa
  • Pg- gingivalis, Tanerella, Treponema
54
Q

Plaque Induced Gingivitis

A

No Infllamatory Lesion or attachment loss. just plaque.

55
Q

Subclinical Gingivitis

A

Bacteria near gingival margin and PMN migrate to sulcus to fight infection

56
Q

Early Gingivitis

A

-bacteria penetrates through junctional epi into CT, releasing inflammatory cells to bring in PMN

57
Q

Established Gingivitis

A

plaque extends and disrupts coronal junctional epi.

PMN fights and Ab are produced…the immune response itself will destroy the healthy CT

58
Q

Hygiene Within Perio

A

Targets cervical and interproximal portions of teeth—where plaque accumulates first

59
Q

Bass Method Toothbrushing

A
  • 45 degree angle, short and rolling stroke
  • removes biolfilm from margin and sulcus
  • 2-3 teeth at a time with gentle back and forth
  • 30 s per quadrant—2 min
60
Q

Modified Stillmans Method Toothbrushing

A
  • 45 degree angle with bristles pressed to cause gingival blanching
  • rolling and repeated throughout mouth
  • stimulates gingiva
  • cleans coronal and interproximal well, but not sulcular
  • similar to bass
61
Q

Charters Toothbrushing

A
  • side of brush is against the tooth with the bristles occlusally
  • 45 degrees at gingival margin
  • bristles into proximal areas and vibrate for 10 strokes within areas of mouth (do rolling strokes prior)
62
Q

Rolling Stroke Toothbrushing

A
  • bristles against attached gingiva and at 45 angle
  • rolled slowly by flexing wrist—rolled 5ish times
63
Q

Flossing

A
  • arms length of floss
  • wrap most of it around middle finger of non dom hand and small amount wrapped around middle finger of dom hand
  • 4 inch of floss in between and then use index fingers and thumbs to grip
  • guid floss between teeth into a C shape around the tooth, side to side andup and down
64
Q

Toothrbushes

Powered

A

-flat, rippled, dome, multilevel, angled, bilevel

and change it every 3-4 months

—power=faster/better removal, has a timer, pressure sensor prevents tissue damage

65
Q

Dentrfice

A

-polish teeth, they are paste, powder gel or liquid

—like toothpaste

  • has detergent- fights plaque- sodium oral
  • antiplaque like against triclosan—substantive
  • tatar control- no supragingival calculus tetrasodium pyrophosphate
  • desensitizing- strontium or KNO-seals off dentin tubules
66
Q

Mouthrinses

A
  • kills the bacteria in plaque but only at biofilm surface
  • has alcohol
  • can get it with fluoride
  • can help with dry mouth
67
Q

Perio Diagnosis

A

Disease- Ginigivitis? Periodontitis? Systemic?

Etiology- Plaque induced? Non plaque induced?

Where- localized? generalized?

Severity

68
Q

Gingivitis

Periodontitis

A

No attachment loss/bone loss—intact crestal lamina dura + normal biowidth

attachment loss and bone loss- loss of crestal lamina dura and bigger biowidth

69
Q

Plaque Induced Gingivitis

A

-dental plaque only but can be modified by systemic, medication and malnutrition

dental plaque only- bc not brushing/flosisng. bleed w/ probe

systemic- endocrine (puberty), menstrual, preggo, diabetes, dyscrasis

Medication- enlargement bc of plaque w/ meds- phenytoin or Ca blockers

Malnutrition- ascorbic acid

70
Q

Non Plaque Induced Gingivitis

A

-of specific bacterial origin (or viral, fungal), can be genetic or from systemic/foreign/trauma reaction

71
Q

Chronic Periodontitis

A

not all gingivitis goes into this but all CP is from gingivitis

  • mainly in adults w/ subgingival calculus
  • slow progression
  • localized= less than 30% involved
  • slight= 1 - 2 mm loss
72
Q

CAL- clinical attachment level

A

Clinical Attachment loss

  • distance from CEJ to crevice base—pocket depth
  • lower #= better
73
Q

Localized Aggressive Periodontitis

A
  1. circumpubertal onset
  2. robust serum ab Response to agent
  3. usually molars or incisors (lower)

—plaque/calculus—less accumulation than there is attachment loss

74
Q

Generalized Aggressive Periodontitis

A

-people under 30

  1. poor serum ab response to agent
  2. pronounced destruction of attachment + bone
  3. affecting 3 perm teeth (not molars or incisors)
75
Q

Aggressive Perio Common features

A

—weird phagocyte function

  • hyperresponsive macrophages= inc PGE2
  • familial aggregation
  • rapid attachment loss
  • otherwise= clinically healthy
76
Q

Developmental or Acquired Deformities

A

Predisposition to plaque induced disease: poorly contoured restorations or anatomic variations

mucogingival deformities on teeth or around ridge

occlusal trauma

77
Q

Deformities: tooth, restoration, soft tissue

A

tooth- fracture, groove (lat. incisor), cemental tear, CEJ projections

restoration- contour, overhang, open contact

soft tissue- recession & frenum attachment

78
Q

mucogingival deformities

A
  • inadequate attached gingiva (too thin)
  • recession/attachment loss—restorations into thin, or poor hygiene/habits
79
Q

perio disease

A

inflammatory disease initated by bacterial infection

80
Q

Healthy Biofilm

Diseased Biofilm

A
  • light plaque, gram +, aerobic, cocci, non motile
  • mature plaque, gram -, anaerobic, spirochetes/filaments, motile
81
Q

Gingivitis Characteristics

A

red, swollen, smooth.

bleed easily and is tender

82
Q

Stage 1 subclinical gingivitis

A
  • increased blood flow
  • increased gingival fluid flow w/ PMN
  • collagen loss
  • beginning days, not detectable clincally but histologically
83
Q

Stage 2 Early Lesion

A
  • capillary loops
  • rete peg formation
  • lymphocytes= predom
  • collagen loss
  • 4-7 days
  • infllammation
  • erythema + edema + bleeding at probing
84
Q

Established Gingivities Stage 3

A

–plaque extends and disrupts junctional epithelium

  • PMN continues to fight
  • lymphoctes produce Ab
  • cytokines, pge, mmp
  • immune response can destroy healthy CT
  • engorged vessesl= bluish hue
  • erythema, edema, texture changes, no attachment/bone loss

DENT 1520 (8 decks)

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