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
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
3
Q
Oral Microbiology—Miller
A
1- plaque
2- susceptible host
3- fermentable carbohydrate
4-acid production
5- cavity (demineralization)
4
Q
Caries are Initiated By
A
Time, Host (teeth), Biofilm (bacteria), Nutrients
5
Q
Specific Plaque Hypothesis
A
-ONLY dental plaque colonized by SPECIFIC bacterial species
Within Caries= S. Mutans & Lactobacillus Caries are SUCROSE DEPENDENT
6
Q
S. Mutans
A
- most common in caries
- reproduce + survive best in low pH
- diff survival rates
7
Q
S. Sanguis
A
- Fimbriae attach to pellicle
- Both S. mutans & S. sanguis
- increase risk for caries
- difficult to get rid of
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
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
10
Q
Nutrient Sources
A
Sugars—so polysaccharides stick Sucrose—generate acid: pH decreases=demineralization of tooth and an increase in s.mutans= biofilm
11
Q
Demineralization
A
Occurs below at 5.5—stephens curve
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)
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
14
Q
Biofilm
A
microorganisms attached to surface in matrix of extracellular polymers of host/bacteria (plaque) -resistant to antibiotics while individually it isnt
15
Q
Biofilm Cycle
A
1-cell attaches and adheres
2- grows
3-Detaches and spreads
16
Q
Biofilm Characteristics
A
- Complex structure
- responsive to environment
- Detaches and sprads
- Quorum Sensing
- Resistant to antibiotics
17
Q
Lactobacillus
S. Mutans
S. Sanguis
Actinomyces
Lactobacillus
A
acid via fermentation
caries
not needed for lesions
root caries
secondary colonizers
18
Q
Restorative Model of Care
A
Exam cavity
remove
operate
replace with filling
recall
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
20
Q
Chewing Gum
A
Xylitol & Sorbitol
xyliotol- plaque reducing effect, attracts and then starves bacteria so it helps remineralize
21
Q
Fluoride
A
inhibits enolase of S. Mutans
pentrates white spot lesions
—fluoride resistant S. Mutans are less cariogenic than fluoride sensitive
22
Q
Chlorhexidine
A
Surface acting, S.mutans decrease by 50%
23
Q
Transmission of Oral Flora
A
Vertically—mother to child
Horizontally—from environment (h20)
24
Q
Window of Infectivity of S. Mutans
A
19-31 Mo. (26 mo mainly)
25
Proximal Caries
adjacent tooth surface---75% chance will spread to other tooth
26
Where do carious lesions occur
Time: at plaque retentive sites (build up over time)
27
Susceptibility to Dental Caries
1) mandibular 1st molars
2) Max First Molars/ max and mand 2nd molars
3) 2nd premolars, max incisors, 1st premolars
4) mandibular incisors, canines
28
Enamel Caries
aka. Smooth surface caries
## Footnote
Beneath plaque as areas of decalcification (white spots)
- less inter rod and mucopolysaccharides
- triangular pattern: APEX towards DEJ and BASE towards tooth SURFACE
29
Surface Zone
Body
Dark Zone
Transulcent Zone
30
White Spot Lesion
Dissolves tooth structure= loss of minerals= porosites= white spot lesion
internal loss of minerals but the external is still intact just porous
31
- Surface Zone
- Body of the Lesion
- 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
32
Dark Zone
- tiny pores, blocking light, but make it opaque
- loss of crystalline structure
33
Translucent Zone
Pores along the enamel rod
34
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
Early Dentinal Changes
More common in chronic caries
Tubular Sclerosis(more crystals less structure)
calcification of dentinal tubules
36
Dentinal Caries
- Organic acides demineralize dentin
- degenerates and dissolves
- no more integrity=invasion of bacteria
37
Zones of Dentinal Caries (5)
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
Pit and Fissure/Occlusal Caries
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
40
Occlusal Carie
Vs
Proximal Carie
- 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
Root Caries
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
Epithelial Outer Layer
Connective Tissue Layer
Fibrous Ligament
- covers alveolar housing and seals to tooth
- attaches to the rooth and periosteum covering the bone
- supports the tooth to the alveolus
43
Supra-crestal CT attachment
Biologic Width
- always found---under junctional epi.
- junctional epithelium and CT attachment
44
Gingival Crevice
"gingival sulcus/pocket"
at the margin, gingiva inverts and forms a cuff around the neck of the tooth
45
Oral Epithelium
Sulcular Epithelium
Junctional Epithelium
* faces oral cavity on outer surface of free/attached gingiva
* lines gingival sulcus
* provides contact between gingiva and tooth= epithelial attachment
46
Anatomy:
Oral Epithelium
Sulcular Epithelium
Epithelial attachment
-Keratinized strat squamous, resistant to forces + impermeable
## Footnote
- resistant to forces + low perm. para keratinized
- attachment apparatus, connect junctional to tooth surfacevia hemidesmosomes
47
Junctional Epithelium
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
Crevicular Fluid
CT flows into sulcus through enlarged intercellular. enlarged bc of the rupture of desmosomal junction + inflammation
49
Perio Biofilm
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
Asacchrolytic
Proteolytic
Sacchrolytic
- dont need sugar
- eat sugar
- break down sugar for digestion
51
Plaque Progression Perio
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
Socrabsky Color
Healthy to Disease
* yellow
* blue
* purple
* green
* orange
* red
* yo boy put gaspedal on radio
53
yellow
blue
purple
orange
green
red
* -strep
* actinomycess
* veiolnella
* fusobacterium
* Aa
* Pg- gingivalis, Tanerella, Treponema
54
Plaque Induced Gingivitis
No Infllamatory Lesion or attachment loss. just plaque.
55
Subclinical Gingivitis
Bacteria near gingival margin and PMN migrate to sulcus to fight infection
56
Early Gingivitis
-bacteria penetrates through junctional epi into CT, releasing inflammatory cells to bring in PMN
57
Established Gingivitis
plaque extends and disrupts coronal junctional epi.
PMN fights and Ab are produced...the immune response itself will destroy the healthy CT
58
Hygiene Within Perio
Targets cervical and interproximal portions of teeth---where plaque accumulates first
59
Bass Method Toothbrushing
- 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
Modified Stillmans Method Toothbrushing
- 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
Charters Toothbrushing
- 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
Rolling Stroke Toothbrushing
- bristles against attached gingiva and at 45 angle
- rolled slowly by flexing wrist---rolled 5ish times
63
Flossing
- 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
Toothrbushes
Powered
-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
Dentrfice
-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
Mouthrinses
- kills the bacteria in plaque but only at biofilm surface
- has alcohol
- can get it with fluoride
- can help with dry mouth
67
Perio Diagnosis
Disease- Ginigivitis? Periodontitis? Systemic?
Etiology- Plaque induced? Non plaque induced?
Where- localized? generalized?
Severity
68
Gingivitis
Periodontitis
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
Plaque Induced Gingivitis
-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
Non Plaque Induced Gingivitis
-of specific bacterial origin (or viral, fungal), can be genetic or from systemic/foreign/trauma reaction
71
Chronic Periodontitis
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
CAL- clinical attachment level
Clinical Attachment loss
- distance from CEJ to crevice base---pocket depth
- lower #= better
73
Localized Aggressive Periodontitis
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
Generalized Aggressive Periodontitis
-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
Aggressive Perio Common features
---weird phagocyte function
- hyperresponsive macrophages= inc PGE2
- familial aggregation
- rapid attachment loss
- otherwise= clinically healthy
76
Developmental or Acquired Deformities
Predisposition to plaque induced disease: poorly contoured restorations or anatomic variations
## Footnote
mucogingival deformities on teeth or around ridge
occlusal trauma
77
Deformities: tooth, restoration, soft tissue
tooth- fracture, groove (lat. incisor), cemental tear, CEJ projections
restoration- contour, overhang, open contact
soft tissue- recession & frenum attachment
78
mucogingival deformities
- inadequate attached gingiva (too thin)
- recession/attachment loss---restorations into thin, or poor hygiene/habits
79
perio disease
inflammatory disease initated by bacterial infection
80
Healthy Biofilm
Diseased Biofilm
- light plaque, gram +, aerobic, cocci, non motile
- mature plaque, gram -, anaerobic, spirochetes/filaments, motile
81
Gingivitis Characteristics
red, swollen, smooth.
bleed easily and is tender
82
Stage 1 subclinical gingivitis
- increased blood flow
- increased gingival fluid flow w/ PMN
- collagen loss
- beginning days, not detectable clincally but histologically
83
Stage 2 Early Lesion
- capillary loops
- rete peg formation
- lymphocytes= predom
- collagen loss
- 4-7 days
- infllammation
- erythema + edema + bleeding at probing
84
Established Gingivities Stage 3
--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
