Caries.txt

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emm64
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Caries.txt
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2012-08-31 03:31:38
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Caries200
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Caries200
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  1. what is diagnosis?
    • ID disease from signs & symptoms
    • 1. recognize SS
    • 2. Hx, Phys
    • 3. Diff Diag
    • 4. Hypothesis
    • 5. Diagnostic tests
    • 6. Diagnosis
    • 7. Treatment
  2. What is the protocol for caries diagnosis?
    • 1. Detect lesions: differentiate caries-free v caries-affected
    • 2. Factor RISK
    • 3. Determine caries management options
    • * avoid unjustified (overtreatment)
    • * classifying carious lesions corresponding to the best management options for each lesion type
  3. Which questions should management options consider?
    • pts benefit?
    • OH improve?
  4. What is the difference between detection and diagnosis?
    detetion is part of diagnosis
  5. What are the caries lesion classifications?
    • cavitated: RESTORATIVE management, form and function, proper OHI, NOT disease mgt
    • Non-cavitated: non-restorative (control plaque, diet, Fl, CPP-ACP, monitor), cost concerns of professional application (usually if active)
    • active: ongoing mineral loss (professional non-restorative or lesion specific OHI)
    • arrested: no active mineral loss: professional intervention not needed
  6. What does cavitated lesion imply?
    • Restorative: form, function, facilitate OH
    • NO MGT OF DISEASE
  7. What are the essentials for proper visual tactile clincal caries assessment?
    • light: anterior interproximals, shadows
    • DRY, clean
    • 3-way syringe: dry
    • mirror: retract tissue, reflect light
    • sharp explorer: remove plaque with side, assess roughness w/tip & gentle pressure(vibrations), do not EXPLORE STICK(NOT valid detection)
    • magnification
    • systematic (isolate/dry quadrants)
  8. Why dry teeth before clinical exam?
    • Dry w/ 3 way syringe to increace refractive index between sound and carious enamel
    • allows visualization of surface texture
    • look for white spots, lines, shadwows beneath enamel
  9. What are the features of an active non-cavitated lesion?
    • white (or yellow)
    • opaque, chalky (neon-like)
    • Rough texture
  10. What are the features of an arrested non-cavitated lesion?
    • variable color (whitish to black)
    • shiny
    • smooth texture
  11. What are the features of an active cavitated lesion?
    • soft, leathery
    • dull, not shiny
  12. What are the features of an arrested cavitated lesion?
    hard & shiny
  13. What are differential diagnosis of white enamel lesions?
    • caries: arch, banana, kidney-shaped (plaque accululation along present of former FGM)
    • fluorosis: symmetric distribution of fine horizontal stiae (perichymatal enamel pattern)
    • developmental defect(non Fl): round or oval, clearly defined from adjacent enamel on single teeth
  14. What are the visual features of mild flurosis?
    • white lesions w/ symmetric distribution & fine horizontal striae reflective of perichymatal enamel pattern
    • perikyma: pits around the long prisms of tooth enamel. They indicate the places where enamel-producing cells used to make contact to neighboring cells and are the result of normal enamel apposition.
  15. What white lesion is round or oval and usually appears on single teeth?
    developmental, non-flouride
  16. What are the various scores of flourosis?
    • TF1: thin, white, opaque lines corresponding to perikymata, may include white areas along cusp tips, incisal edges or marginal ridges
    • TF2: more pronounce lines appear as bands
    • TF3: entire surface cloudy, white, opaque w accentuated perikymata
    • perikymata: pits around the long prisms of tooth enamel. They indicate the places where enamel-producing cells used to make contact to neighboring cells and are the result of normal enamel apposition.
  17. What is CAMBRA?
    Caries Management by Risk Assessment
  18. What is the 1st step of CAMBRA?
    Risk Asessment
  19. What is PREVTX1?
    • caries risk assessment: Preventive Dentistry Consultation Notes
    • MBI/PI categories
    • OHI
    • Fl trays
    • Prevention Plan
  20. What is PREVTX2 of caries risk assesment?
    • High Risk categories
    • Visible caries/ dentin caries radiograph
    • Restorations last 3 yrs
    • frequent snaacks
    • saliva reducing factors (meds, radiation, systemic)
    • visually inadequate saliva
    • Appliances
  21. What is meant by high risk for caries?
    • YES” on visible cavitations or dentin in radiograph or on any two of:
    • Restorations last 3 yrs
    • frequent snaacks
    • saliva reducing factors (meds, radiation, systemic)
    • visually inadequate saliva
    • Appliances
  22. What is asssesed in PREVTX3?
    • Moderate risk & Protective factors
    • exposed roots
    • dev defects: deep pits/fissures
    • interprox lesions, radiolucenies
    • enamel white spots/discoloration
    • recreational drug use
    • Protective: Fl H2O, Fl toothpaste, mouthwash, salivary flow, xylitol (4x/day), CHX
  23. What is PREVTX4 in GSD?
    Treatment recommendations
  24. What is WREC of CAMBRA?
    • Disease Indicators
    • White spots
    • Restorations <3yrs
    • Enamel lesions
    • Cavities/dentin
  25. What is BAD of CAMBRA?
    Risk Factors: Bacteria, absent saliva, diet(poor)
  26. What is SAFE of CAMBRA?
    Protective: sealants, antibacterials, Fl, Effective diet
  27. Steps of CAMBRA?
    • Hx & clinical exam
    • enter notes
    • assign category
    • treatment reccomendations
    • explain
    • instruct (writing)
    • provide test results
    • reassess in 3-6 months
  28. CAMBRA low risk clinical guidlines?
    • Radio: BW 24-36 months
    • Recall: 6-12 month
    • Fl:
  29. What was the 1st caries detection dye?
    • fuschin: Fusayama (1972) histologic stain for protein, discovered 2 layers(affected, infected) of carious dentin
    • partially carcinogenic: replaced by 1% acid red
  30. What product replaced fuschin?
    1% acid red in propylene glycol or polypropylene glycol
  31. What is the difference between affected and infected dentin?
    • infected w/bacteria, affected by acid
    • infected (outer): highly-decalcified, fuschin stainable, irreversibly denatured collagen, unrecalcifiable
    • affected (inner): partially-decalcified and recalifiable, no fuschin stain, sound collagen
  32. What are the features of caries detection dyes?
    stain only infected dentin to enhance removal, prevent over-excavation, improve accuracy
  33. What was the traditional tactile and visual criteria for dentin?
    • sound: Rock hard, not discolored
    • Low specificity= High FP rate
    • often over-removed
  34. How do CDDs work?
    • stain organic matrix (collagen) of less-mineralized dentin(not enamel), more stained, more disease
    • don't stain bacteria (NOT RELATED TO PENETRATION OR ELIMINATION)
    • must know limitations
  35. What are the statistical features of CDD?
    • Low specificity = high FP
    • especially in DEJ, near pulp because higher organic matrix comp
  36. What are common sites of CDD FP(false positives)?
    DEJ, near pulp where more organics(collagen)
  37. Do CDDs work on enamel?
    NO, nonspecific protein, will stain food, pellicle and other organics trapped in pits & fissures
  38. What is FO Transillumination
    • Non ionizing, EARLY caries detection (3D-view) via scattering light principles
    • Sound tissue: more light transmission
    • Demineralized tissue:more scattering, more absorption
  39. What does sound tissue do to light?
    transmits (no shadows, scattering)
  40. What do enamel and dentin lesions look like when transilluminated?
    • enamel: gray shadow
    • dentin: orange-brown or bluish
  41. What are the stats on FOTI?
    • High specificity for both FOTI and BW
    • Lower sensitivity for FOTI vs BW
    • another study showed high specificity and no sensitivity vs BW
    • High Spec = Low FP
    • Low sensitivity = misses a lot (High FN)
  42. How well does FOTI work on occlusal?
    better than visual but steep learning curve, low performance w/stains
  43. What is DIFOTI?
    FOTI w/CCD intraoral
  44. How does DIFOTI perform on proximal lesions?
    • Higher sensitivity in detection of early lesions not apparent in conventional radiography
    • use of DIFOTI in conjunction with radiographs improves diagnostic accuracy
    • NOT for depth
    • Adjuntive(not replacement) diagnostic tool
  45. What are the main strenths of (DI)FOTI?
    • EARLY lesions
    • visualizing suspicious fissures and confirming enamel or dentin cracks
  46. How is a crack visuallized with FOTI?
    light transmission is blocked at crack planes
  47. What is fluoresence and how is it used in dentistry?
    • phenomenon where absorption of light of a given wavelength by a molecule is followed by
    • the emission of light at longer (visible) wavelengths.
    • Direct relationship between fluorescence and mineral content (distinguish sound and demineralized enamel)
  48. What is Quantitative Light-induced Fluorescence(QLF)?
    • arc lamp to analyze sound vs demin enamel via 370nm (blue) wavelength
    • lesion area(mm2), depth(% fluoresence loss), volume (area*depth)
  49. What are the stats for QLF?
    • good corr btwn % fluoresence loss and lesion depth in vitro (0.85)
    • smooth surfaces: sensitivity: .76 specificity .85
    • occlusal: sensitivity .68 specificity .7
  50. What are the QLF advantages?
    • early lesion detection & quantification
    • storable/tranmittable data
    • over time comparisons of remin & preventive tx
  51. What is laser fluorescence(diagnodent)?
    • IR light and has a 655 nm wavelength (red) reades moment(real time)/peak(max)
    • probe uses 2-way FO system
    • must be used on CLEAN DRY to reduce FP
    • rotate & pivot to improve accuracy
  52. How is diagnodent technique improved?
    • CLEAN/DRY (stains/plaque->FP)
    • rotate & pivot tip
  53. What do moment peak values of diagnodent(laser) mean?
    • 0-10 sound enamel
    • 10-20 outer enamel caries
    • 20-30 lower enamel caries
    • >30 dentinal caries
  54. What are the stats for Diagnodent(laser)?
    • high sensitivity for dentinal caries but wide range
    • higher sensitivity, lower specificity than visual (more FP)
    • adjunct
  55. How does LED reflectance/refraction used in dentistry?
    • Δ in optical signature of healthy vs.demineralized tooth structure
    • healthy(green) ->more translucent than decalicied(red)
    • used on WET tooth surface
    • tool must be calibrated (ceramic)
  56. How is Midwest ID (LED) used interproximally?
    directed down long axis
  57. What are the Midwest ID (LED) stats?
    • 80% sensitivity IP
    • 92% occlusal
  58. What causes FPs in LED(MW) and lasers(diagnodent)?
    • atypical enamel morph
    • restorations or sealants
    • Calculus or plaque
    • Stains (thick, dark brown)
    • Food debris
    • Contaminants on probe tip
    • Probe not being in contact with tooth surface
    • Tooth is dry (Midwest Caries I.D.) or tooth iswet (DIAGNOdent)
  59. How does Spectra Fluoresence work?
    Six LEDs emitting blue light @ 405nm
  60. How does CarieScan work?
    • AC impedance spectroscopy
    • Sound enamel =high electrical resistance.
    • Demineralization = ↑enamel permeability = ↓electrical resistance
    • By the time caries has reached dentin the resistance has dropped by a factor of 30.
  61. What is the efficacy of Fl?
    • only drug proven to prevent
    • dental caries lesions
    • higher conc (5000 vs 1500) enhanced remineralization and inhibited demineralization
  62. What is the ACP mechanism?
    • Amorphous Calcium Phosphate Free & available for incorporation into tooth structure
    • Best for pts. w/mild remin probs and high motivation
    • Two-phase delivery system
    • Prevents the calcium and phosphate from reacting
  63. What is the drawback of ACP?
    • low substantivity
    • acid challenge (pH<5.5) breaks down ACP and not available after
  64. What is CPP?
    • Casein Phosphopeptides (CPP)
    • tooth-protective activity
    • bind calcium and phosphate and keep them in a soluble, amorphous state
    • provides SUBSTANTIVITY to ACP
    • penetrate into the tooth enamel, work synergistically with fluoride and repair demineralized areas
  65. What is enamelon?
    insoluble calcium phosphate crystals
  66. How is MI paste applied?
    • pea-sized on finger
    • smear on teeth
  67. What are the indications for MI paste?
    • High caries risk
    • Infants & Children
    • Expectant Mothers
    • Orthodontics
    • Whitening sensitivity
    • Root exposure
    • Chemotherapy, radiation
  68. What is the composition/chemical features of MI Paste?
    • CPP-ACP: 10%
    • •NaF: 900 ppm* (OTC toothpaste: 1000 ppm*)
    • •ph: 7.2
  69. Why is Fl added to CPP-ACP?
    • superior anti-caries effect than Fluoride alone
    • high risk for dental caries and dental erosion
    • Remineralized(thickened) through the body vs surface only of Fl alone
  70. What is the forumulation of MI Paste Plus?
    • 5 :3 :1
    • 5 / Calcium
    • 3 / Phosphate
    • 1 / Fluoride
  71. What do studies say about CPP-ACP?
    • CT evidence insufficient to make conclusions regarding the longterm effectiveness of casein derivatives, specifically CPP-ACP, in preventing caries in vivo and treating dentin hypersensitivity or dry mouth
    • not yet been substantiated
    • Topically applied fluoride remains the standard for anti-caries effectiveness
  72. What is Tri-calcium phosphate?
    • anticavity toothpaste 1.1 (5000ppm F-) blended/milled with organic materials
    • • Calcium – phosphate bonds are broken
    • • Calcium oxides become ‘protected’ by the organic materials
    • • TCP ingredient can coexist with fluoride ions in an aqueous dentifrice base  High fluoride availability
    • • Organic carry the calcium to the tooth surface, protected from fluoride ion  High fluoride bioavailability during application
    • • Saliva activates the calcium compound degrading the protective coating, releasing calcium at the tooth surface  Calcium bioavailability during application
  73. What activates tri-calcium phosphate?
    saliva at tooth surface increase bioavailability
  74. What is Novamin?
    • Particulate “bioactive glass” material
    • attach to tooth surface,
    • → react with water
    • → release Ca2+ and PO43- ions
    • → new HA forms on tooth surface
    • Found in NUPRO Sensodyne Prophylaxis Paste with NovaMin (5000ppm F- too)
  75. How do HA nanocrystals(pHluorigel) work?
    • Foundational Principles
    • • Resting saliva pH = 6.75
    • • Stimulated saliva pH = 7.8
    • • HA dissociates into Ca2+ and PO4 3- ions at pH < 5.5
    • • Fluorapatite (FA) dissociates at pH < 4.5
    • ∴ Saliva environment favors presence of HA and FA nanocrystals over ions
  76. How properties of O3 make it good for the mouth?
    • Powerful oxidant, disinfectant (CONFLICTING)
    • unstable releases nascent oxygen
    • Disinfection of endodontic systems (CONFLICTING)
    • Promote soft tissue healing (e.g. apthous ulcers)
    • Tooth whitening (oxidation)
    • HALT/REVERSAL OF CARIES LESIONS (NO EVIDENCE)
  77. what are Ozone medical uses?
    • • Wound healing – long history
    • • Gangrene, infection, burns
    • • Ocular diseases
    • • Kills microorganisms, safe for human tissue cells (GOOD EVIDENCE)
  78. What were the original uses of O3 in dentistry?
    • promote haemostasis
    • • enhance local oxygen supply,
    • • inhibit bacterial proliferation
  79. What is the intraoral mechanism of O3?
    • • Oxidizing action drives O2 beneath surface of lesion to
    • kill bacteria
    • • Neutralization of acids creates hostile environment for
    • cariogenic bacteria
    • • Lesion is populated with non-cariogenic bacteria
    • (probiotic effect)
    • • Remineralization from salivary or topically-applied
    • sources of F, Ca, and PO is facilitated
  80. What was really the only good evidence for O3 dentistry?
    prophy for restorative prior to etching
  81. What is Icon (DMG)?
    • Diffusion barrier for proximal lesion infiltration of NON-CAVITATED, smooth surface lesions
    •  Interproximal
    •  White spot lesions
    • Infiltrate the porous body of lesion with low-viscosity resin
    •  Block diffusion pathways INSIDE vs surface sealant for cariogenic acids
    • Procedure: Acid-etch, rinse, dry  Drying solution (ethanol)  Infiltrate with resin  Light-cure
    • Stats: higher penetration coefficient
  82. How was infiltration methods evaluated?
    digital subration images of radiographs
  83. Is complete removal of all infected and affected dentin necessary?
    • strong evidence for the advisability of leaving behind infected dentin…”
    • cariogenic bacteria isolated by a restoration pose no risk…”
    • removing all vestiges of infected dentin from lesions approaching
    • the pulp is not required for caries management
  84. What was the historical evidence for AgF?
    • black surfaces of amalgam-restored teeth
    • had no caries progression
    • • Knew of silver nitrate use for sensitive teeth
    • • Showed 61% decay inhibition at 3 years w/silver nitrate
    • Arrest of active lesions
    • • Prevention of new lesions
    • • May be more effective than fluoride varnish!*
  85. What is the mechanism of AgF?
    • AgF: HA->FA (hydroxy apatite to fluoroapetite(less acid soluble)
    • in infected area AgPO4s go into Thiols of AA and nucleic acids that aren't metabollically active for bacteria
    • also only darkens infected areas
  86. What chemical can reduce discoloration of AgF?
    KI (potassium Iodide)
  87. What is main advangtage of radiography?
    preclinically evident detection of demineralization
  88. What is an acceple range of overlap for bitewings?
    less than 1/3rd of enamel
  89. What is sensitivity?
    • TP/(TP+FN)
    • correct test result for all with disease
    • ability to detect presence of disease when it’s actually present
  90. What is specificity?
    • TN/(TN+FP)
    • ability to rule out disease when it’s not present
  91. What are stats of radiographs?
    • low sensitivity & high specificity
    • False negatives more likely than false positive
    • miss more than incorrect diagnos
  92. What factors contribute to radiographic accuracy?
    • size: low accuracty for small proximal lesions, increases w/ lesion depth
    • must be combined with clinical exam (visual/tactile)
  93. Do digital radiograph receptors (CCD/CMOS/PSP) perform as well as film?
    yes
  94. Where do proximal caries usually appear?
    • between contact and gingival margin
    • therefore do not superimpose teeth
    • must be at least 30-40% to be radiographically visible
  95. What are the false positives of radiographs causes?
    • cervical burnout: illusion of radiolucency of a radiopaque object as a radiolucent area or band between two extremely radiopaque areas.
    • hypoplastic enamel
    • morhological variation: lingual concavity, enamel hypoplasia (look like erosion)
  96. What are reasons for false negatives in radiographs?
    • needs to be 30-40% demineralized
    • overlap: less than 1/3rd ideal
    • about 50% of proximal caries aren't detected
  97. What are the stats for early enamel lesions of radiographs?
    • DEPENDS ON RISK!!
    • incidence = 10%, (50% sensitive, 95% specific, PPV = 53%)
    • incidence = 50%, (PPV = 90%)
    • Therefore PPV is better for high risk groups
  98. What are radiographic reccomendations for high risk pts?
    • 6-12 months (children,adolescents)
    • 6-18 adults
  99. What are radiographic reccomendations for low risk?
    • 12-24 months children
    • 18-36 adolescents
    • 24-36 adults
  100. What are the radiographic false positives of occlusal?
    • Deep buccal pits
    • minimize by correlating w/ clinical exam
  101. What are the radiographic false negatives of occlusal?
    • superimposition of tooth structure
    • insufficient radiographically detectable demineralization
  102. What are limits of CBT with caries diagnosis?
    • Beam hardening "scatter" artifacts from metallic restorations
    • artifacts interfere w/ caries diagnosis
    • typically only used for high risk

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