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Risk Assessment > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Periodontium-what does it conist of? What are the 2 main functions?

A

Consists of: gingiva, periodontal ligament, alveolar bone proper, cementum

2 main functions: attach the tooth to the jaw bone and maintain the integrity of the surface of the masticatory mucosa of the oral cavity

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2
Q

Masticatory gingiva

A

gingiva and the covering of the hard palate

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3
Q

Specialized mucosa

A

covers the dorsum of the tongue

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4
Q

Lining mucosa (alveolar mucosa)

A

(the remaining part) loose, dark red

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5
Q

Gingiva/mucosa: coronal to apical

A

free gingiva: the part of the gingiva that surrounds the tooth and is not directly attached to the tooth surface

attached gingiva: the portion of the gingiva bound to the tooth and to the alveolar bone, extending apically to the mucogingival junction

mucogingival junction: the junction of the gingiva and the alveolar mucosa

alveoler mucosa: mucosa covering the basal part of the alveolar process and continuing without demarcation into the vestibular fornix and the floor of the mouth–> it is loosely attached to the periosteum and is movable

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6
Q

Periodontal health requirements

A

BoP < 10%

PD= 3mm for non-periodontics pt (in stable periodontitis pt: =4mm)

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7
Q

Gingivitis definition

A

inflammation of the gingiva caused by the interaction between dental plawue and the host immune response and is REVERSIBLE by reducing levels of dental plaque at and apical to the gingival margin

DENTAL PLAQUE INDUCED

radiographs cannot be used to diagnose

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8
Q

Gingivitis requirements

A
  • BOP>/=10%
    • localized: 10-30% BOP sites
    • generalized: >30% BOP sites
  • PD<3mm
  • No radiographic bone loss!
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9
Q

Periodontitis definition

A

Inflammation of the supporting tissues of the teeeth–>usually a progressively destructive change leading to loss of bone and periodontal ligament

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10
Q

Periodontitis requirements

A

BOP>/= 10%

PD>3mm

varying degree of radiographic bone loss

clinical attachment loss

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11
Q

Periodontitis staging vs grading

A

staging-severity and complexity of an individual based on currently measurable extent of destroyed and damaged tissue attributable to periodontitis

grading-as an indicator of the rate of disease progression–>provides supplemental info. about the biological feature of teh diease, anticipated treatement response

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12
Q

3 main bacteria in periodontitis

A

porphyromonas gingivalis

tanerella forsythia

treponema denticola

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13
Q

Non-surgical periodontal treatments

A
  • scaling and root planing
    • scaling:instrumentation of the crown and root surfaces of teeth to remove plaque, calculus and stains from these surfaces
    • root planing: a treatment procedure designed to remove cementum or surface dentin that is rough, impregnated wiht calculus or contaminated wiht toxins or microorganisms
  • Chemotherapeutics
    • adjunctive therapy the ScRP
      • Systemic
        • Abx (amoxicillin w/ or w/o metronidazole, azithromycin)
      • local
        • topical antimicrobials or antiseptics
        • antimicrobial mouthrinse
        • local drug delivery system
  • Perio maintenance–> procedures at selected time intervals (3 months)
  • Oral prophylaxis (prophy) on pts with no history of periodontal disease
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14
Q

Surgical periodontal treatments

A

periodontal flap surgery

periodontal plastic surgery

regenerative surgery

implant therapy

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15
Q

What is the most common chronic childhood disease

A

Dental caries

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16
Q

Etiological factors of dental caries

A

cariogenic microflore, susceptible host tooth, carbohydrate-rich diet

…and time

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17
Q

Dental erosion versus dental caries

A
  • dental caries-acids that result from the metabolism of dental plaque bacteria
  • dental erosion-acids that come from the diet (lemon juice) or body (stomach acids)
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18
Q
A

Erosion

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19
Q
A

Erosion

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20
Q
A

Dental caries

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21
Q

Can minerals be lost from the tooth without the role of acids?

A

Yes-tooth wear

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22
Q
A

Abrasion

e.g. harsh tooth brushing

wearing away of dental hard tissue through abnormal mechanical processes involving foreign objects

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23
Q
A

Attrition

“tooth against tooth”

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24
Q
A

Abfraction

Abfraction is the loss of tooth structure where the tooth and gum come together. The damage is wedge-shaped or V-shaped and is unrelated to cavities, bacteria, or infection

wedge shaped defects at CEJ

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25
Q

What is dental caries?

A
  1. chronic
  2. site specific
  3. multifactorial, diet mediated
  4. dynamic (but not necessarily continuous)
  5. disease process that invilves the shift of the balance between protective factors (that aid in remineralization) and destructive factors (that aid in demineralization) to favor demineralization of the tooth structure over time
  6. the disease can be arrested at any time point
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26
Q

Caries lesion

A

The manifestation of the stage of the process at one point in time (active or inactive)

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27
Q

Incipient Caries

A

Incipient, initial caries lesion or non-cavitated caries lesion

demineralization without evidence of cavitation

reversible by biochemical means

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28
Q

Cavitated lesion

A

Cavity

a caries lesion that has lost the outer surface leading to a discontinuity in the surface)

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29
Q

What is the most susceptible time to get a lesion?

A

2 years after eruption

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30
Q

Caries progression rate (initial and cavitation)

A

initial: >2 years
cavitation: >4 years

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31
Q

Remineralized lesion

A
  • a lesion which not only exhibits convincing evidence of lesion arrest, but also one or more of other definite changes including:
    • increased mineral concentration
    • increased radiodensity
    • decreased size of white spot lesion
    • increased hardness of the surface
    • increased surface sheen compared to a previous matte surface texture
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32
Q

How do we detect caries lesions?

A
  • visual
    • tactile
    • light
    • drying
    • magnification
    • tooth separation
  • radiographs
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33
Q

What is dental fluorosis?

A

Hypomineralization of the dental enamel caused by excessive ingestion of fluoride during the post secretory maturation phase (immediate pre-eruptive phase) of amelogenesis (e.g., 15 months for maxillary anterior teeth). it is one of a variety of causes of defective enamel formation

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34
Q

5 different types of caries (based on location)

A

Smooth surface

Occlusal surfaces (pit and fissure)

aproximal (surface that forms a contact with adjacent teeth)

root surface

secondary/recurrent caries

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35
Q

Classes I-V

A

Have to do with restorative treatment site

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36
Q

Early Childhood Caries Etiology and other names

A

It happens in little children that go to sleep while sucking intermittently from a bottle containing liwuid and sugar

AKA baby bottle syndrome, nursing bottle caries, rampant caries

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37
Q

Radiation caries

A

Caries of the cervical regions of the teeth, incisal edges, and cusp tips secondary to xerostomia induced by radiation therapy to the head and neck

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38
Q

Rampant caries

A

multiple active caries lesions occurring in the same pt–> involves surfaces not usually common for the development of caries

AKA bottle or nursing caries, baby bottle, ECC, radiation caries, drug induced caries, meth caries, Mountain Dew caries

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39
Q

“Traditional” Assumptions on Caries Etiology (all are wrong)

A
  • Dental plaque is the causative of caries (non-specific hypothesis)
    • Prevention was based on continuous plaque control
    • Patient was responsible for caries lesions appearance
    • Everybody is at high risk
    • No diagnosis required
    • Everyone treated the same way
  • Lesion progression relatively fast
  • Irreversible sequence of events
    • Enamel demineralization
    • Collagen degradation
  • Logical treatment
    • Restorations planned at first apt.
    • Surgical excision of the pathological tissue
    • Extension for prevention (G.V. Black’s Philosophy)
    • Placement of a “definitive” restoration
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40
Q

Residual caries

A

Caries left over by the dentist during restorative treatment (partial excavation)

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41
Q

Secondary or recurrent caries

A

restorations repaur the tooth structure, but do not stop caries and have a finite lifespan. they themselves are susceptible to disease since the caries can reoccur around a restoration

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42
Q

Primary caries or primary cavitated or non cavitated lesion

A

Initial lesions produced by direct extension from an external surface

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43
Q

Examples of Therapeutic/Biological (Non-Surgical) Approaches for Caries Management

A
  • Stimulation of salivary glands
  • Fluorides
  • Mechanical plaqu control
  • Diet control
  • Antimicrobial therapies
  • Dental sealants
  • Resin infiltration
  • Behavioral management

Not new ideas–>from G.V. Black

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44
Q
A
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45
Q

Enamel composition by weight and volume

A

85 vol% inorganic (hydroxyapatite)

12 vol% water

3 vol% protein

95 wt% inroganic (hydroxyapatite)

4 wt% water

1 wt% protein

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46
Q

What is the basic unit of enamel?

A

Enamel rod (enamel prism)

It is tightly packed, highly organized mass of hydroxyapatite crystals

Ca10(PO4)6(OH)2

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47
Q

Chemical composition at different depths of enamel

A

Outer surface: Ca, PO4, F

Inner surface: Mg, CO3, Cl

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48
Q

Dentin composition

A

55 vol% inorganic (hydroxyapatite)

20 vol% water

25 vol% protein

75 wt% inorganic (hydroxyapatite)

5 wt% water

20 wt% protein

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49
Q

What does dentin resemble?

Odontoblasts in dentin?

Harder or softer than bone and enamel?

A

Physically and chemically similar to bone

odontoblasts cell bodies are outside of dentin but their processes exist in tubules within dentin

harder than bone but softer then enamel

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50
Q

Primary, secondary, and tertiary dentin

A

primary-formed before eruption, forms the bulk of the tooth

secondary, begins formation after eruption

tertiary-formed in response to irritation and appears as a localized deposit on the wall of the pulp chamber

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51
Q

Factors of dental caries

A
  1. Host factor: tooth, saliva, pellicle
  2. diet
  3. dental biofilm/plaque (cariogenic bacteria)
  4. time
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52
Q

Main contributing factors to demineralization

A

Diet + plaque= plaque acids

Reduction in salivary flow

Low buffering and oral clearance

Acidic saliva–>erosive acids

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53
Q

Main remineralization factors

A

Salivar buffering capactiy

Ca2+ and PO43- levels

buffering and remineralization

oral clearance proteins/glycoproteins

fluoride contact developmental topical application

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54
Q

5 stages of the caries process

A
  1. pellicle formation
  2. biofilm/plaque formation
  3. production of acid
  4. diffusion of acid
  5. demineralization
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55
Q

5 parts of pellicle/plaque formation

A
  1. pellicle formation
  2. attachment of early bacterial colonizers (0-24hrs)
  3. co-adhesion and growth of attached bacteria leading to the formation of microcolonies (4-24hrs)
  4. microbial succession leading to increased species diversity concomitant with continued co-adhesion and growth of microcolonies (1-7days)
  5. climax community/mature dental plaque/biofilm (1 week or older)
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56
Q

Host factor: tooth location/morphology

What are areas of stagnation where plaque (biofilm) can accumulate undisterubed?

A
  • occlusal surfaces of posterior teeth
  • lingual pits and maxillary incisors
    • pit and fissure
    • approxial surface
    • gingival margin
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57
Q

What increases stability of crystals and increases solubility of enamel?

A

CO32-

(the larger and more uniform the crystals, the less the specific surface area dn reactivity (solubility))

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58
Q

When is caries susceptability of the enamel the greatest?

A

immediately after eruption and tends to decrease with age

during eruption, more soluble carbonate-rich apatite is preferentially lost and replaced by apatite lower in carbonate and higher fluoride

the reprecipitated crystals may grow to be larger than the original crystals–>hypermineralization

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59
Q

What is Sjögren’s Syndrome?

A
  • chronic or lifelong autoimmune disease (immune system attacks body instead)
  • attack typically starts on moisture producing glands–> exocrine glands
  • 9/10 are women with avg age of symptom onset in the 40s
  • dryness symptoms worsen during menopause
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60
Q

What is the aquired pellicle?

A
  • promotes plaque/biofilm formation and is selective bacterial adhesion, as well as to the movement of dissolution products from apatite out of the tooth
  • acellular, essentially bacteria free organic film deposited on teeth
  • between enamel surface and dental plaque
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61
Q

Which more cariogenic: Simple sugars (sucrose,glucose,fructose) or complec carbs (starches)

A

Simple sugars with sucrose being the main source of sugar

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62
Q

Name 3 endogenous oral microorganisms found in the dental biofilm/plaque that can contribute to caires

A

mutans streptococci

lactobacillus species

actinomyces species

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63
Q

critical pH

definition

and what it is for enamel and dentin

A
  • Critical pH is the pH at which a solution is just saturatedwith respect to a particular mineral
    • if pH of solution>critical pH–>supersaturated–>precipitate
    • if pH of solutionundersaturated–>mineral will dissolve until the solution becomes saturated
  • Critical pH of caries formation in enamel is often referred to as pH between 4.5 - 5.5 (5.5)
  • Critical pH of caries formation in dentin is often referred to as pH between 6.0 - 6.9 (6.6)
  • This range coincides with pH of acids formed when plaque bacteria ferment carbohydrates
  • Critical pH is not a fixed value, it depends on the levels of calcium and phosphate in plaque fluid
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64
Q

2 theories that explain intact surface zone overlying intact non-cavitated lesions

A
  1. greater acid resistance of the surface layer due to compositional characteristics of the surface enamel
  2. reprecipitation of minerals from dissolving sub-surface lesions
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65
Q

What are the arrows pointing to?

A
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66
Q

Progression of dentinal lesion

A
  1. first reaction: tubular sclerosis
  2. change in refractive index
  3. demineralization continues: sclerosis continues
  4. transparant dentin
    • major portion of inner carious dentin
    • tubule lumina fills with Ca and PO4
      • Saturation with Whitlockite-grow to form gigantic rhomboidal crystals
    • reduced permeability
  5. Demineralization continues
  6. Sclerosis continues
  7. reactive dentin (tertiary dentin) is formed
    • pulp reaction
    • starts even before dentin bacterial invasion
    • irregular mineralization
    • irregular dentinal tubules
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67
Q

What is secondary caries?

A

caries lesion that exists adjacent to restorations

there is an outer lesion and a wall lesion

outer lesion caused by plaque accumulation in a manner similar to the initiation of primary lesion

the wall lesion was thought to be the result of microleakage

68
Q

Who is the father of modern dentistry?

A

Albucasis

69
Q

Materia Alba

A
  • soft, loose
  • white cheeselike accumulation
  • soft accumulation of salivary proteins, some bacteria, many desquamated epithelial cells, and occasional disintegrating food debris
  • easily displaced with a water spray
70
Q

Dental plaque

A
  • synonymous with plaque biofilm
  • resilient clear to yellow-grayish substance
  • more structured than materia alba
  • primarily composed of bacteria in a matrix of salivary glycoproteins and extracellular polysaccharides
  • considered to be a biofilm
  • impossible to remove by rinsing or the use of sprays
71
Q

Calculus

A
  • hard deposit that forms by mineralization of dental plaque
  • generally covered by a layer of unmineralized dental plaque
72
Q

Formation of calculus

A
  1. salivary pellicle phase-salivary pellicle forms on tooth surface
  2. plaque formation phase-initial adhesion and attachment of earlier colonizers to salivary pellicle–> start of biofilm formation
    • note: as biofilm matures, there is a shift in microbial profile: gram positive cocci–>gram negative filamentous species
  3. Mineralization (calculus) phase:
    • calcification of plaque has been reported to occur in as little as 4-8 hours and persists for 1 to 14 days
    • plaque is hardened by the precipitation and incorporation of insoluble mineral salts
73
Q

Supragingival calculus: how removed? appearance? common locations?

A
  • can be removed off the tooth surface using a sharp curette
  • appears chalky and hard
  • common surfaces
    • lingual surfaces of mandibular incisors
      • saliva from Wharton’s Duct (submandibular gland) and Bartholin’s Duct (sublingual gland) empties onto the lingual surfaces of the mandibular incisors
    • buccal surfaces of the maxillary molars
      • saliva from stensen’s duct (parotid gland) empties directly onto the buccal surfaces of the maxillary molars
74
Q

Subgingival calculus: how it is detected? appearance?

A
  • can only be detected by fine, careful tactile detection with a delicate dental instrument, such as an explorer
  • appearance
    • appears dark brown due to being exposed to gingival crevicular fluid, blood, or blood breakdown products
    • may be burnished on the root surface due to previous inadequate scaling
    • firmly attached to the root surface
    • supragingival calculus and subgingival calculus generally occur together, but one may be present without the other
75
Q

How to visualize supra and subgingival calculi

A
  • Supragingival-can be visualized by use of compressed air
  • Subgingival calculus can sometimes be detected by blowing air down the gingival crevice
    • usually detect sub g by probing the gingival sulcus with a fine tipped explorer
  • Radiographs
    • radioopaque deposits noted on the tooth surface
    • note that less than 50% of surfaces with actual calculus is detected radiographically
      • doesn’t show lingual or labial calculi
76
Q

Microscopic composition of supragingival calculus

A
  • predominantly inorganic–> mostly minerals
  • crystaline in nature
  • organic content (10-30%)
    • carbohydrates (galactose, glucose, mannose)
    • salivary proteins
    • lipids
    • desquamated epithelium
    • microorganisms
    • leukocytes
  • inorganic content (70-90%)
    • calcium phosphate salt
    • calcium carbonate
    • trace minerals
    • over 2/3 of the inorganic component is crystalline in nature–> there are 4 main crystal forms:
      • hydroxyapatite, 58%
      • magnesium whitlockite, 21%
      • octacalcium phosphate, 12%
      • brushite, 9%
77
Q

Composition of subgingival calculus

A
  • inorganic (70-90%)
    • calcium phosphate salt
    • calcium carbonate
    • trace minerals
    • over 2/3 of the inorganic component is crystalline in nature-there are 4 main components
      • hydroxyapatite, 58%
      • magnesium Whitlockite, 21%
      • octacalcium phosphate, 12%
      • brushite, 9%
  • organic 10-30%
    • carbohydrate (galactose, glucose, mannose)
    • lipids
    • desquamated epithelium
    • microorganisms
    • leukocytes

salivary proteins found in supragingival calculus is not typically foudn in subgingival calculus but supra and sub g calculus have similar inorganic composition

78
Q

What is the source of mineral content for supragingival calculus?

A

saliva

79
Q

source of mineral content for subgingival calculus?

A

gingival crevicular fluid (GCF)- an inflammatory exudate that accumulates within the gingival margin

exudate: an inflammatory infultrate that has left the blood vessels

80
Q

Four modes of calculus attachment

A
  1. attachment by means of an organic salivary pellicle–> calculuse attachment is superficial because no interlocking or penetration into the tooth surface occurs
  2. mechanical locking into surface irregularities (e.g. palato-lingual grooves extending to the root surface, mesial root concavity on maxillary premolar, furcation flutings, CEJ)
  3. attachment into areas of resorption bays (i.e. mechanical damage to the surface of the tooth)
    • itrogenic: caused by dentist
  4. direct penetration fo the calculus bacteria into the cementum
81
Q

What is the salivatory pellicle?

A

thin acellular layer of adsorbed proteins and macromolecules on the dental enamel surface formed within seconds of cleaning the surface

82
Q

Role of salivary pellicle in health

A
  • protective effect-protects enamel from attrition and/or abrasion
    • buffering capcity
    • diffusion barrier
    • lubrication
83
Q

How do you remove calculus?

A

Scaling and root planing

devices used: universal curette, ultrasonic tips, gracey curette

84
Q

What is the primary bacteria covering the outer surface of calculus?

A

predominantly viable gram-negative rods and cocci

85
Q

What kind of bacteria covers the calculus deposit?

A

nonviable

86
Q

relationship between plaque and periodontal disease

A

The non-mineralized plaque on calculus is the primary irritant, but the underlying calcified portion Cementum
Calculus
may be a significant contributing factor to periodontal disease. By itself, it does not irritate the gingiva directly, but provides a fixed reservoir for the continued accumulation of plaque and retains it in close proximity to the gingiva.

TA K E -HOME MESSAGE: Calculus is a contributing factor for periodontal inflammation, not the primary etiology!

87
Q

Pathway of formation for biofilms

A
  • start as free floating cells until they find a surface they have an affinity for adn attach
  • once attached–>multiply–>form microcolonies
  • at some point, the bacteria will pack and disperse and find other surfaces
  • once organized communities are formed, they stop growing and metabolism is low
    • most abx work while cell is growing so not good for these cells
  • they have a matrix to protect them and help them survive
88
Q

quorum sensing

A

when bacteria in one part of the biofilm send chemical signals to the other side of the biofilm

89
Q

the good and bad of biofilms

A
  • good
    • bioreactors
    • waste-water treatment
    • environmental clean up
  • bad
    • corrosion
    • fouling
    • diseases
90
Q

factors affecting growth of microorganisms in the oral cavity

A
  • redox potential-oral bacteria are mostly:
    • facultative anaerobes (grow in the presence or absence of oxygen)
      • these will be supragingival
    • obligate anaerobes (oxygen is toxic)
      • these will be subgingival
  • pH: 6.75-7.25 in saliva
    • acidogenicity
    • aciduricity
    • changes of pH in inflamed sites
    • sometimes saliva can;t penetrate biofilm to act as a buffer and decrease pH
  • nutrients:
    • endogenous-provided by saliva, or by other bacteria
    • exogenous–>dietary
  • adherence
91
Q

Pellicle formation

A
  • the surfaces are bathed with salivary fluids
  • salivary glycoproteins adsorb to the surfaces
  • the glycoproteins lose their solubility
  • the glycoproteins may become altered by the action of the bacterial enzymes
92
Q

Co-aggregation and co-adhesion

A
93
Q

What type of bacteria is present in enamel and dental caries?

A

Enamel: streptococcus

Dentin: streptococcus and veillonella

94
Q

Is caries an infectious disease?

A

No

biofilm is sugar dependent–> bacteria fermentation of sugar lowers pH

95
Q

Why is sucrose important?

A

sucrose is the substrate for the production of the polysaccharide matrix

96
Q

Roles of extracellular polysaccharide, intracellular storage compounds, energy pathway

A

extracellular polysaccharide (glucan or fructan): adherence, protection; intracellular storage compounds: energy resources for tough times; energy pathway: provides energy and carbon sources

97
Q
A
98
Q

Koch’s postulate

A
  • Defines what an infectious disease should have
  • causative agent must do the following
    • be routinely isolated from disease individuals
    • be grown in pure culture in the lab
    • produce a similar disease when inoculated in susceptible lab animals
    • be recovered from lesion in a diseased lab animal
99
Q

Non-specific plaque hypothesis and specific plaque hypothesis

A

Non-specific: age and amount of plaque-when only small amounts of plaque are present, the noxious products are neutralized by the host; similarly, large amounts of plaque would cause a higer production of noxious products, which would essentially overwhelm the host’s defences

Specific:recognition of the differences in plaque at sites of different clinical status led to a renewed search for specific pathogens in periodontal diseases and a conceptual transition from nonspecific to specific plaque hypothesis

100
Q

Requirements of visual/tactile examination for dental caries

A

good lighting and clean, dry surface

101
Q
A
102
Q

When to use explorer?

A

clean/remove debris using side of explorer

confirm and assess cavitations (breaks in teh continuity of the surface)

check margins of restorations.crowns

check cavity preparations

feel the texture (roughness) of no-cavitated lesions (determination of caries lesion activity)

103
Q

DMFT

A

D component: decayed (cavitated) teeth/surfaces

M component: missing teeth/surfaces due to dental caries

F component: filled teeth/surfaces due to dental caries

  • a tooth may have several restorations but it counted as one tooth as filled F
  • a tooth may have restoration on one surface and caries on teh other it should be counted as decayed D
  • no tooth must be counted more than once, D M F or sound
  • non-cavitated lesions count as sound
104
Q

DMFS

A
  • each tooth was recorded as 4 surfaces for anterior teeth and 5 surfaces for posterior teeth
    • retained root was recorded as 4D for anterior teeth, 5D for posterior teeth
    • missing tooth was recorded as 4M for anterior teeth, 5M for posterior teeth
    • tooth with crown was recorded as 4F for anterior teeth, 5F for posterior teeth
105
Q
A
106
Q

Appearance of active caries lesion (enamel)

A

dull/opaque white area and feels rough

107
Q

Appearance of inactive caries lesion (enamel)

A

appears shinier and feels smooth

108
Q

Appearance of active caries lesion (dentin)

A

leathery/soft for probing, cavitationa and light borwn/yellowish

109
Q

Appearance of inactive caries lesion (dentin)

A

smooth for probing and dark brown/black

110
Q

Fluorosis

A
  • whit areas on smooth surfaces, and as white patches on occlusal surfaces, often close to fissures; bot not extending into the fissure
  • can be
    • bilateral
    • on multiple teeth
    • more straight across smooth surfaces
    • does not follow the gingival contour
    • shinier
    • diffuse
    • less opaque
111
Q

Which is fluorosis and which is dental caries?

A

left-fluorosis and right-dental caries

112
Q

Difference between erosion and caries

A

Erosion-caused by gastric acid or food

Caries- demineralizationa cid caused by dental plaque

113
Q

What is this?

A

erosion

114
Q

What is this?

A

Attrition

115
Q

MIH

A
  • molar incisor hypomineralization
    • developmental condition caused by the hypomineralization of enamel during its maturation phase, due to interruption to the fxn of ameloblasts but the cause is unknown
    • only choldhood illness, fever in particular seems to be associated
116
Q

Electrical Conductance Measurement

A
  • enamel is electrically isolated material–>does not go through the electrical flow
  • when a lesion develops, crystals shrink and start to crate space–>filled by saliva–>mostly water–>highly electrically conductive –>lesion has high conductance and low resistance

can use carise scan PRO

enamel maturation can be monitored

117
Q

Transillumination

A
  • light propagates across tooth tissue to nonilluminated surfaces (examination surface)
  • when lesion exists light is not going to pass through the area
  • can use carivu or diagnocam
118
Q

Fluorescence by blue-green light

A

when there is a caries lesion the intensity of the light is lower than in the sound structure

119
Q

Fluorescence by infrared

A

Diagnodent detects chromophore (bacteria by-product, not necessarily bacteria)

120
Q

Photothermal radiometry and modulated luminescence

A

PTR/LUM

canary heats up the tooth surface–> creates heat and luminescence

machine picks up the luminescence from the tooth structure

company claimed it could detect caries with this info

121
Q

Sensitivity

A

true positive ratio:the proportion of diseased patients correctly identified as positive

122
Q

Specificity

A

true negative ratio: the proportion of disease-free patients correctly identified as negative

123
Q

What percentage of adults in the US have signs of gingivitis?

A

>75%

124
Q

What percent of US adults had periodontitis?

A
  • 46%
    • 8.7% mild
    • 30% moderate
    • 8.5% severe
125
Q

Difference between bacteria in health vs disease

A
  • health
    • gram positive
    • non motile
    • aerobic
  • disease
    • gram negative
    • motile
    • anaerobic
126
Q

What is the dental plaque biofilm formed by?

A

salivary glycoproteins and extracellular ploysaccharides

(very dense and non-mineralized)

When it become mineralized it becomes a calculus

127
Q

Roles of dental plaque

A
  • barrier against acids
  • prevents drying of surfaces
  • aids in the adherence of microorganisms
  • (one) mode of attachment for calculus
128
Q

What type of biofilm are arrows pointing to?

A
129
Q

Four key periodontal pathogens

A
130
Q

Five main stages of dental plaque biofilm development

A
  1. Acquired pellicle coats the tooth surface
    • occurs immediately after the tooth is erupted or after prophy
  2. initial colonizers attach to tooth
  3. bacteria coaggregation
  4. formation of the extracellular slime layer
    • protects the whole mass–>don’t want to use systemic abx w/o disrupting the plaque first
  5. mature biofilm
    • can potentially detach and flow through other areas
131
Q

What is the bridging organism in the dental plaque biofilm development?

A

fusobacterium nucleatum

132
Q

Tooth-surface-attached bioflim

Unattached biofilm

Epithelium-attached biofilm

A
  • Tooth-surface-attached bioflim
    • next to tooth
    • associated with root caries, calculus formation and root resorption
  • Unattached biofilm
    • b/w the two (tooth-surface; and epithelium)
    • a fluid biofilm that contains many WBCs
  • Epithelium-attached biofilm
    • pocket epithelium
    • gram-negative bacteria, WBCs infiltrate
133
Q

Experiment with dental students

A
  • cleaned teeth at beginning and didn’t brush for 21 days
  • not everyone will develop gingivitis at the same rate
  • teeth showed gingivitis as a dental plaque accumulation
  • once dental plaque removed–> reverse process
  • avg of 21 days for gingivitis to develop
  • about one week of good oral hygeine to reverse process
134
Q

Major characteristics of initial gingivitis

A
  • these initial inflammatory changes occur in response to microbial activation of resident leukocytes and the subsequent stimulation of endothelial cells in respinse to bacterial plaque
  • the first manifestations of gingival inflammation are vascular changes consisting of dilated capillaries and increased blood flow
  • subclinical

PMN is the polymorphonuclear leukocyte which is a neutrophil

you can see the fusobacterium bridging bacteria here

JE=junctional epithelium

135
Q

Major characteristics of early gingivitis

A
  • clinically noticeable: signs of inflammation (erythema along gingival margin: proliferation of capillaries and increased formation of capillary loops), bleeding on probing may be evident
  • histologically: rete pegs forming while some of the coronal epithelium is disappearing, more vascular proliferation
136
Q

Major characteristics of established gingivitis

A
  • clinically: blood vessels are engorged and congested
  • microscopic:
    • intense chronic inflammatory reaction
    • predominance of plasma cells and B lymphocytes
    • plasma cells invade deep into the connective tissue
    • JE reveals widened intercellular spaces and develops rete pegs or ridges that protrude into the connective tissue
  • plasma cells produce ABs, mainly IgG
  • shift from gram + to gram - and from aerobic to anaerobic
  • may have spontaneous bleeding
137
Q

Major characteristics of advanced gingivitis–>periodontitis

A
  • micro
    • widespread manifestations of inflammatory and immunopathologic tissue damage
  • clinically characterized by periodontal breakdown and the extansion of the lesion into alveolar bone
138
Q

Equation for CAL (clinical attachment loss/level)

A

CAL= PD + CEJ-gingival margin distance

139
Q

ADA: Sound

A

ICDAS=0

no clinically detectable lesion

dental hard tissue appears normal in color, translucency and gloss

140
Q

ADA: initial lesions

A

ICDAS=1-2

earliest clinically detectable lesion compatible with mild demineralization

mildest forms detectable only after drying

lesions may be white or brown and enamel has lost its normal gloss

visually non-cavitated

141
Q

ADA: moderate lesions

A

ICDAS=3-4

visible signs of enamel breakdown or signs the dentin is moderately demineralized (shadow)

established, early cavitated, localized enamel break down (microcavitation)

142
Q

ADA: advanced lesion

A

ICDAS=5-6

enamel is fully cavitated and dentin is exposed–> dentin lesion is deeply/severely demineralized

spread/disseminated, late cavitated, deep cavitation

143
Q

ICDAS=1

A

hard to distinguish from normal enamel when it is wet–>air-dry for 5 seconds–>become more opaque and can be detected visually (white)

on approxiaml surfaces, can onlu be detected from the buccal or lingual/palatal direction

144
Q

ICDAS=2

A
  • When wet, code 2 lesions exhibit either:
    • white spot lesion (caries opactity) and/or
    • brown caries discoloration
  • for occlusal surfaces, white opacity (white line) and/or brown caries discoloration is wider than the base of the natural fissure/fossa and has an appearance which is not consistent with the clinical appearance of sound enamel
145
Q

ICDAS=3

A

enamel surface begins to break down and surface discontinuity can be visualized

in the pits and fissures, this is wider than the natural fissure/fossa

this breakdown can appear substantially and unnaturally wider than normal

DENT HA NOT BEEN EXPOSED

a ball ended probe can be used gently acorss a tooth surface to confirm the presence of breakdown

146
Q

ICDAS=4

A
  • appear as shadows of discolored dentin visible through apparently intact enamel which may or may not exhibit localized enamel breakdown
  • shadow is often more noticeable when wet, and may appear as gray, blue or brown
  • if a tooth is restored with amalgam, can be difficult to distinguish the shine-through of the restoration from a caries shadow
147
Q

ICDAS=5

A
  • cavitation present due to caries in opaque or discolored enamel exposing the dentin beneth
  • in pits and fissures, there is visual evidence of demineralization (white, brown or dark brown walls) at the entrance to or within the pit or fissure, and dentin is exposed
  • involve less than half of the surface of the tooth
  • ball ended probe can confirm the presence of a cavity in dentin
148
Q

ICDAS=6

A
  • at least half the tooth surface is cavited to expose dentin
  • cavity is deep and wide
149
Q

Difference between stain and cavity in fissure system?

A
  • in stains you tend to see only the bottom of the fissure system and it’s a very fine thin line
  • cavity is wider and might be less dark on the outer edges
150
Q

A difference between coronal caries and root surface caries?

A

root surface caries can become softened and bacteria penetration further into tissue at an earlier stage of lesion development

151
Q

ICDAS Code E

A

Exclusion

if patient has healthy gingiva that means root has not been exposed–>cannot asses root caries because there is no root exposed–>E

when calculus covers a lot og gingiva and you cannot see the root surface–>E

152
Q

ICDAS root surface Code 0

A

does not exhibit any discoloration

has a natural anatomical contour

153
Q

ICDAS root surface Code 1

A
  • there is a clearly demarcated area on the root surface or at the cemento-enamel junction that is discolored (light/dark brown, black)
  • there is no cavitation present
  • loss of anatomical contour <0.5mm
154
Q

ICDAS root surface Code 2

A
  • a clearly demarcated area on the root surface or at the cemento-enamel junstion that is discolored
  • there is cavitation present (loss of anatomical contour >/= 0.5mm)
155
Q

Why take radiographs?

A

To see things we cannot see on visual inspection

156
Q

See things like what on radiographs?

A

posterior interproximal caries, possible bone loss due to periodontal disease, incidental odontogenic and bony pathosis

157
Q

Limitations of radiographs

A

soft tissues

2D images of a 3D person

static view vs dynamic process

technique errors (spring)

158
Q

periapical radiograph

A

shows the entire tooth and at least 2mm of surrounding bone

want to see around apices

159
Q

Bitewing

A

display upper and lower teeth, OPEN interproximal spaces, and bone levels

160
Q

Occlusal

A

capture the “3rd dimension”: helps to localize foreign objects, impacted teeth, etc. Common before CBCT, still used in pediatrics

161
Q

panoramic (extra oral)

A

“broad overview” of general structures in the dentition, alveolar bone, sinuses, airway, TMJ, cervical vertebrae, and surrounding soft tissues

162
Q

lateral cephalometric (extraoral)

A

commonly used in ortho to determine skeletal/dental developmental and maxillomandibular relationships

163
Q

CBCT (extraoral)

A

complete 3D view of the head and neck

only aquired when 2D images are inadequate due to high radiation dose

164
Q

Posterior interproximal caries

A

ideal: bitewings

should always be correlated with visual clinical findings

small lesions that are not evident clinically, usually present as dark triangles between teeth

limitation: only visible once 30-50% of demineralization has occured

radiographically smaller than it looks clinically

165
Q

how to describe radiographic caries

A
  • mention tooth #, surface(s) involved, and depth (ex:12M-D2)
    • E1: outer half of enamel
    • E2: inner half of enamel
    • D1: outer third of dentin
    • D2: middle third of dentin
    • D3: inner third of dentin/pulpal invasion
166
Q

Periodontic radiographs

A
  • ideal: bitewings
  • look at bone levels in between teeth
    • normal: about 1-2mm from CEJ
  • complete periodontal diagnosis is not based on radiographs
    • PD, recession, attachment loss, BOP, calculus plaque scores, gingival color, etc.
167
Q

Periodontal radiograph descriptors

A
  • horizontal
  • vertical
  • generalized
  • localized
  • mild (cervical third of root)
  • moderate (middle third of root)
  • severe (apical third of root)
  • Special considerations
    • furcation involvment
    • apical involvement
    • calculus

Risk Assessment (1 decks)

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