1. Normal Pulp
    A clinical diagnostic category in which the pulp is symptom free and normally responsive to vitality testing.
  2. Reversible pulpitis
    A clinical diagnosis based upon subjective and objective findings indicating that the inflammation should resolve and the pulp return to normal.
  3. Irreversible pulpitis
    A clinical diagnosis based on subjective and objective findings indicating that the vital inflamed pulp is incapable of healing.

    Symptomatic – Lingering thermal pain, spontaneous pain, referred pain

    Asymptomatic – No clinical symptoms but inflammation produced by caries, caries excavation, trauma, etc.
  4. Pulp necrosis
    A clinical diagnostic category indicating death of the dental pulp.

    The pulp is non-responsive to vitality (sensibility) testing.
  5. Previously Treated
    A clinical diagnostic category indicating that the tooth has been endodontically treated and the canals are obturated with various filling materials, other than intracanal medicaments.
  6. Normal apical tissues
    Teeth with normal periradicular tissues that will not be abnormally sensitive to percussion or palpation testing.  The lamina dura surrounding the root is intact and the periodontal ligament space is uniform.
  7. Symptomatic apical periodontitis
    Inflammation usually of the apical periodontium, producing clinical symptoms including painful response to biting and/or percussion or palpation.  It may or may not be associated with an apical radiolucent area.
  8. Asymptomatic apical periodontitis
    Inflammation and destruction of apical periodontium that is of pulpal origin, appears as an apical radiolucent area, and does not produce clinical symptoms.
  9. Acute apical abscess
    An inflammatory reaction to pulpal infection and necrosis characterized by rapid onset, spontaneous pain, tenderness of the tooth to pressure, pus formation and swelling of associated tissues.
  10. Chronic apical abscess
    An inflammatory reaction to pulpal infection and necrosis characterized by gradual onset, little or no discomfort and the intermittent discharge of pus through an associated sinus tract.
  11. Ludlow 2006 / AAE 2011

    CBCT Radiation

    Measured in what unit?
    • Effective dose measured in μSv
    • Kodak:
    • Max Ant:  4.7μSv
    • Max Post: 9.8μSv
    • Mand Post: 38.3μSv
  12. Ludlow 2006 / AAE 2011

    What is the effective dose of:
    One Digital PA
    One Day of Background Radiation
    • One Digital PA: 6μSv
    • FMX: 171μSv
    • One Day of Background Radiation: 7-8μSv
  13. CBCT vs. PA (PARL Detection)
    Velvart 2011
    Lofthag-Hansen 2007
    Bornstein / Von-Arx 2011
    Tsai / Torabinejad 2012
    • Velvart 2011:
    • Mandibular Molars: 100% vs. E Speed PA 78%

    • Lofthag-Hansen 2007:
    • CBCT 100% vs. F Speed PA 62%

    • Bornstein / Von-Arx 2011
    • Mandibular Molars: 100% vs. F Speed PA 75%

    • Tsai / Torabinejad 2012:
    • Simulated Lesions (0-1.4mm): CBCT > Digital
  14. CBCT vs. PA Radiograph (Mandibular canal detection):
    Velvart 2001
    Bornstein/Von Arx 2011
    • Velvart 2001:
    • Mandibular Molars: CBCT 100% vs. E Speed PA 61%

    • Bornstein/Von Arx 2011:
    • Mandibular Molars: CBCT 100% vs. F Speed PA 35.3%
  15. CBCT vs. PA Radiograph (Working Length)
    Jeger/Bornstein 2012
    Jeger/Bornstein 2012: No significant difference when using CBCT and Digital PAs for Final Working Length
  16. Vitality Testing = Sensibility Testing

    What does sensibility testing assess?
    Sensibility testing assesses pulpal nerve status.

    Sensibility testing does not evaluate blood/vascular supply.
  17. When may sensibility testing be unreliable?
    Immature developing teeth respond unreliably  to EPT.  Immature teeth possess higher EPT thresholds/late innervation of plexus of rashkow.

    Thermal (Cold) testing should be performed instead.
  18. When may sensibility testing be unreliable?
    • Trauma cases:
    • EPT, cold and heat tests are unreliable (due to nerve damage without alteration of blood supply.
  19. When may sensibility testing be unreliable?
    EPT unreliable in the presence of large restorations.
  20. EPT - Mode of Action
    Low threshold Aδ fibers (prepain sensation) – ionic fluid shift
  21. EPT - Technique
    Abdel Wahab
    Slowly increasing the current may lead to more accurate results.
  22. EPT and Pulpal Histopathology
    There is no relationship between EPT value and pulp histopathology.
  23. EPT - Where to place probe?
    Bender - Test the incisal edge in anterior teeth

    Jacobson - Test the facial middle 1/3rd on incisors; occlusal 1/3rd on premolars
  24. Heat Test
    Used on refractory (persistent AP) cases to identify missed canals or late stage of irreversible pulpitis.
  25. ASA Classification
    ASA Classification 

    I. A normal healthy patient.

    II. A patient with mild to moderate systemic disease.

    III. A patient with severe systemic disease that limits activity but is not incapacitating.

    IV. A patient with severe systemic disease and is a constant threat to life.

    V. A moribund patient not expected to survive 24 hours with or without an operation.
  26. Glickman Classification of Furcation Involvement
    Class I: Incipient lesion

    Class II: Bone destroyed on one or more aspects of furca, partial penetration of probe into furcation.

    Class III: Interradicular bone absent but orifice of furca is occluded by gingival tissue, complete penetration of probe through furcation.

    Class IV: Furca opening visible
  27. Mobility - Miller Index Classification
    I: Barely perceptible

    II: < 1 mm movement

    III: > 1 mm movement/depressible in socket
  28. Does Periodontal Disease cause Pulpal Disease?  Yes.
    Rubach / Mitchell
    Seltzer – Yes, bacteria can pass through lateral/accessory canals.

    Rubach/Mitchell – Yes, bacteria can pass through lateral/accessory canals.

    Wong – Pulpitis adjacent to areas of scaling/root planing (Perio tx).
  29. Does Periodontal Disease cause Pulpal Disease?  Yes.
    Langeland – Only when Apical Foramen involved.

    Bergenholtz - No

    Mazur/Massler – Found no relationship between pulpal & periodontal disease.
  30. Simon’s Classifications for Endo-Perio Lesions
    1. Primary Endo
    2. Primary Perio
    3. Primary Endo + Secondary Perio
    4. Primary Perio + Secondary Endo
    5. True Combined
    6. Concomitant Endo Perio Lesion
    Primary Endo:  Necrotic pulp, CAA drains into sulcus/furca = Narrow isolated PD; mimics VRF, Perio Abscess

    Primary Perio:  Vital pulp, Wide PD defect, Angular/may involve several teeth; Prognosis depends on Perio Tx

    Primary Endo + Secondary Perio:  Necrotic pulp, CAA drains into sulcus/furca + Plaque/calculus at gingival margin = solitary, wider PD

    Primary Perio + Secondary Endo:  (Controversial) Wide PD defect extending to AF → IP/PN; Prognosis depends on Perio Tx

    True Combined: PN + Perio = Endo lesion (apically) meets perio lesion (cervically); Extensive bony destruction, Wide defects, May involve multiple teeth; Prognosis depends on Perio Tx

    Concomittant Endo Perio Lesion (added later): Separate and Distinct Endo and Perio lesions w/ no influence on either; Prognosis depends on Perio Tx
  31. Biologic Width
    • 1. Sulcus depth ~ 1mm
    • 2. Epithelial attachment ~ 1mm
    • 3. Connective tissue attachment ~ 1mm
  32. Calcific Metamorphosis
    Trowbridge / Kim
    Trowbridge/Kim – caused by luxation injury, obliteration of pulp by mineralized tissue.  Occurs in immature teeth, pulpal infarct, connective tissue from PDL proliferates and replaces pulp.

    Gutmann: 1-16% CM cases develop pulpal necrosis, do not treat cases of calcific metamorphosis unless AP or non-vital

    Andreasen: 22% trauma cases → Calcific metamorphosis

    Jacobsen: 70-90% horiztonal root fractures develop Calcific Metamorphosis

    Walton: No visible canal radiographically but ALWAYS present histologically
  33. Calcific Metamorphosis
    Robertson / Andreasen
    Holcomb / Gregory
    Trope: caused by luxation injury, uncontrolled reparative dentin or hemorrhage and clot formation act as a nidus for calcification, occurs in immature teeth.

    Robertson/Andreasen: 8.5% PCO cases → Necrosis; 50% PCO respond to vitality test (final recall: 16 years), 20 yr survival: 84%

    Holcomb/Gregory: 7% PCO cases → Necrosis

    Gutmann: 1-16% CM cases develop necrosis, do not treat CM unless AP or non-vital
  34. Dystrophic Calcification
    Diffuse foci of calcification frequently found in the aging pulp; usually described as being perivascular or perineural.
  35. Pulp Stones / Pulp Calcification
    Bernick - Caused by Aging
    Hendricks-Klyvert - Incidence

    Reduction in vascular supply, innervation (loss of plexus of rashkow), cellularity (odontoblasts deterioration), and pulp chamber size (due to deposition of dentin).

    Increase in calcified masses and collagen (relatively) to pulp.

    Hendricks-Klyvert – incidence of calcifications 8-90%

    Pulp stones – calcifications

    Denticles – composed of dentin
  36. Pulp Stones: Types
    Free, attached, embedded

    Normal or Inflamed

    Old or Young

    Occurs in 50% of pulps; asymptomatic; no detrimental effect on the pulp.
  37. Cracked Tooth
    Cameron: coined term "Cracked tooth syndrome."  Most commonly found in the mandibular second molar  (#1- biting pain, #2-acute onset thermal sensitivity)

    Hiatt: Mand 2nd Molar > Mand 1st Molar > Max PMs = Max 1st Molar;  70%: non-restored or minimally restored.

    Abou-Rass: Transillumination and Staining for diagnosis of Cracked Tooth

    Rivera – Classified longitudinal tooth fractures

    • 1. Craze lines
    • 2. Cuspal fracture
    • 3. Cracked tooth
    • 4. Split tooth
    • 5. Vertical root fracture

    Ehrmann: Ortho band – eval 2-4 wks → symptomatic →RCT/Crown
  38. Cracked Tooth
    Krell / Rivera
    • Krell / Rivera
    • 20% Reversible Pulptitis/Cracked teeth treated with full coverage crown required NSRCT by 6 months due to IP or PN.

    9.7% incidence.
  39. Cracked Tooth
    Berman / Kuttler
    Berman / Kuttler

    Fracture necrosis: 27 teeth with Pulp Necrosis and M-D crack (no or shallow rest.) were extracted and evaluated with micro CT.  Cracks extended deep onto the root surface.

    Recommendation: Teeth with no or shallow restoration that exhibit fracture necrosis should be extracted.
  40. Cracked Tooth
    Tan 2006
    1st longitudinal crack retrospective outcome study (49 patients).

    RCT/Crown – 85.5% survival at 2 years.

    Significant Outcome Factors: terminal tooth, multiple cracks, pre-op probing depth.

    Location/extent of crack not significant factor.
  41. Cracked Tooth Syndrome Misnomer
    Abbott / Leow 2009
    Cracked Tooth Syndrome is not a "syndrome."
  42. Cracked Tooth Cuspal Coverage
    Opdam - Cuspal Coverage Composite

    Signore - Cuspal Coverage Amalgam
  43. Vertical Root Fracture
    Tamse / Fuss 1999
    1. “J-shaped” lesions on PA.

    2. Etiology - Intraradicular Posts, Lateral condensation. 

    3. #1- Max 2nd PM, #2- Mesial root Mand Molar.

    4. 67% had isolated buccal perio defect; 34% sinus tract closer to gingival margin than apex
  44. VRF Etiology
    Holcomb / Pitts
    Holcomb / Pitts: VRF from lateral condensation  - 84%

    Peters: VRF from occlusal loading of Posts
  45. VRF and Posts
    Carbon fiber, parallel sided posts least likely to cause VRF
  46. VRF Exploratory Surgery
    Pitts / Natkin
    • Pitts/Natkin:
    • Exploratory Surgery reveals “Punched out” bony lesion(dehisc/fenest); granulomatous tissue; periodontal abscess; multiple sinus tracts (pathognomonic)
  47. VRF and Narrow Periodontal Defect
    Rud / Omnell
    Rud/Omnell: 79.8% VRFs had isolated narrow periodontal pocket
  48. VRF and susceptible teeth
    Cohen / Berman
    Cohen/Berman 2006: VRFs more prevalent in  maxillary premolars and mandibular first molars; Endodontically treated teeth; >40 years of age
  49. Periapical Index
    Orstavik 1986 - Five Categories
    • Radiographic size of periapical lesion
    • 1. Healthy - Normal
    • 2. Uncertain - Small bony changes, not pathognomic for AP
    • 3. Uncertain - Bony changes with mineral loss, characteristic of AP
    • 4. Diseased - AP with well-defined radiolucent area
    • 5. Diseased - Severe AP with exacerbating features
  50. Periapical Index for CBCT
    Estrella 2008 (0-5)
    Score + E
    Score + D
    0: Intact periapical bone structures

    1: Diameter of PARL > 0.5 – 1.0 mm

    2: Diameter of PARL > 1.0 – 2.0 mm

    3: Diameter of PARL > 2.0 – 4.0 mm

    4: Diameter of PARL > 4.0 – 8.0 mm

    5: Diameter of PARL > 8.0 mm

    + E: Expansion of periapical cortical bone

    + D: Destruction of periapical cortical bone
  51. Differential Diagnosis for a Periapical Radiolucency:
    1. Periapical Granuloma, Cyst, Abscess

    2. Periapical Scar

    3. Keratocystic Odontogenic Tumor (KCOT) aka OKC (multilocular)

    4. Central Giant Cell Granuloma  (multilocular)

    5. Ameloblastoma (multilocular)

    6. Metastatic carcinoma (breast, prostate, kidney)

    7. Nasopalatine duct cyst (Anterior Maxilla only- between centrals)

    8. Benign fibro-osseous lesions (early stages): Periapical/Florid/Focal cemento-osseous dysplasia, Central Ossifiying Fibroma

    9. Lateral periodontal cyst (Lateral RL demarcated RO border, premolars/max lat)

    10. Traumatic Bone cyst (men, 1st/2nd decade, RL demarcated/scallops roots)

    11. Brown’s tumor (HPT), Multiple Myeloma, LHC Histocytosis, FD/Paget’s
  52. Multilocular Radiolucencies (MACHO)
    • Myxoma
    • Ameloblastoma
    • Central Giant Cell Granuloma
    • Hemangioma
    • OKC

    Multiple Keratocystic Odontogenic Tumor = Basal Cell Nevus Syndrome
  53. Differential Diagnosis for a Periapical Radiopacity:
    1. Condensing Osteitis (Focal sclerosing osteomyelitis) – LEO

    2. Idiopathic osteoscleroses (aka Dense Bony Islands)

    3. Benign fibro-osseous lesions (later stages): Periapical/Florid/Focal cemento-osseous dysplasia, Central Ossifying Fibroma

    4. Odontoma 

    5. Cementoblastoma

    6. Osteoma

    7. Central Ossifying Fibroma (COF)

    8. Calcifying odontogenic cyst (COC) – mixed (Gorlin’s cyst)

    9. Calcifying epithelial odontogenic tumor (CEOT) – mixed (Pinborg)

    10. Adenomatoid odontogenic tumor (AOT) - mixed
  54. What percentage of condensing osteitis resolve following NSRCT?

  55. Histological Biopsy Reviews:
    Bhaskar 1966: No distinction radiographically between cyst/granuloma.

    Simon: “Bay cyst”; CBCT able to differentiate Cyst/Granuloma – Grey value

    Nair 1996: Granulomas 50%, Abscesses 35%, Cysts 15% (True 9%, Pocket 6%)

    Spattafore (WVU) 1990: 1659 biopsies- Granulomas 52%, Cysts 42%, Scars 2%, Other 4%, “rule of 2s”

    Koivisto (Minn) 2012: 9723 biopsies - Granulomas 40%, Cysts 33%, Others 20% (KCOTs 8%, CGCGs 1.3%, Ameloblastomas 1.2%, Metastatic <1%)
  56. Does heat damage the pulp?
    Zach / Cohen OOO 1965 (Monkey Study)

    Critical Increase of intrapulpal temperature for Irreversible Pulpitis?  Pulpal Necrosis?
    4C – 100% pulps recovered

    10C – 85% recovered; 15% necrotic

    20C – 40% recovered; 60% necrotic

    >20C – none recovered

    5.5C = Irreversible Pulpal Injury

    11C = Pulpal Necrosis
  57. Critical Increase of intrapulpal temperature for Irreversible Pulpitis?  Pulpal Necrosis?
    5.5C = Irreversible Pulpal Injury

    11C = Pulpal Necrosis
  58. Without water coolant, what is the average intrapulpal temperature rise?
    > 5.5C
  59. Effect of Restorative Dentistry on Pulpal Health
    Abou-Rass: Stressed pulps = Multiple restorations, Slow test results; NSRCT before restoration

    Felton: Full coverage restorations led to a higher incidence  (10-18%) of Pulp Necrosis

    Zach: Heat is capable of causing Irreversible Pulpitis (10C lead to Irreversible Pulpitis in 15% of subjects) and Pulpal Necrosis (20C lead to Pulpal Necrosis in 60% of subjects).

    Bergenholtz: Resultant Pulpal Necrosis after preparation of abutments: 15%; non-abutments: 3%.
  60. Pulp vitality after full coverage crown preparation

    • At 10 yrs: 84%
    • At 15 yrs: 81%

    FPD abutment:

    • At 10 yrs- 70%,
    • At 15 yrs- 66%

    At 10 years, 15% PFMs / 30% FPD were necrotic and required NSRCT.

    At 10 years, 50% Anterior FPD abutments are Necrotic requiring NSRCT.
  61. Murray / Smith: What is the number one factor determining pulp vitality after preparation?
    Remaining Dentin Thickness

    Other Factors: Type of restoration placed, drill speed, coolant, and preparation method
  62. Pashley - Dentinal Tubules
    The number, size of lumen, and surface area of dentinal tubules ↑ closer to the pulp


    0.8→2.5 μm

  63. Murray / Smith
    Remaining Dentin Thickness
    1. Pulpal inflammation was most severe when RDT < 0.25 mm.

    2. Cavity RDT and Bacterial leakage affect survival of odontoblasts/pulp.

    3. Pulpal inflammation was highly correlated with bacterial leakage.
  64. Murray
    Odontoblast Injury
    1. Preparations within 0.5 mm of Pulp leads to Odontoblast injury

    2. Survival of Odontoblasts is critical for Pulp vitality and dentin repair.

    3. Caries → host-derived MMPs (collagenases, etc) → Soluble growth factors released from dentin (i.e.: TGF-β, BMP, NGF, VEGF) → stimulation of odontoblastic reparative dentin formation.
  65. Reeves / Stanley

    Caries within ___ of the pulp or reparative dentin will result in irreversible pulpitis.
  66. Direct Pulp Cap

    Tronstad - DPC only 50% successful

    Barthel - 40% failure rate at 5 years; 80% failure rate at 10 years
  67. Cold Test and Pulp Injury

    Rickoff / Trowbridge
    No pulp injury when cold CO2 is applied for 5 minutes.

    No pulp injury when heat is applied for 10 seconds.
  68. Cold Test Accuracy


    • Overall Accuracy 86%
    • Sensitivity (Diseased) 83%
    • Specificity (Health) 93%
    • PPV 89%
    • NPV 90%


    • Overall Accuracy 81%
    • Sensitivity (Diseased) 71%
    • Specificity (Health) 93%
    • PPV 88%
    • NPV 84%


    • Overall Accuracy 71%
    • Sensitivity (Diseased) 86%
    • Specificity (Health) 41%
    • PPV 48%
    • NPV 83%
  69. Sensibility Testing Accuracy and Reproducibility

    Villa-Chavez 2013
    Cold > Heat > EPT
  70. COLD + EPT

    Peters / Baumgartner
    Cold Neg + EPT Neg = True Necrosis
  71. Barodontalgia - Pain caused by change in pressure

    Senia / Cunningham
    Senia/Cunningham – inflammed vital pulp tissue

    Fenjensick – 86% faulty restorations
  72. Histopathologic Correlation with testing and clinical symptoms

    Seltzer / Bender; Dummer
    No correlation between diagnostic tests and histopathological status of the pulp except for pulp necrosis.
  73. Localization of Pain

    EPT stimulation – Vital teeth

    Friend / Glenwright
    EPT stimulation – Vital teeth

    37% patients could localize symptoms to offending tooth.

    80% patients could localize symptoms to 3 teeth.
  74. Localization of Pain

    McCarthy / McClannahan

    Perc (+)
    Perc (-)
    73% of patients could localize symptoms to the offending tooth (irreversible pulpitis).

    • 90% - Perc (+)
    • 30% - Perc (-)

    Pain never crossed the midline.

    ↑pain (VAS) = ↓ localization
  75. Mechanical Allodynia - Percussion Sensitivity

    Khan / Hargreaves

    • 67% Irreversible Pulpitis
    • 57% Pulp Necrosis


    • 57% Irreversible Pulpitis
    • N/A Pulp Necrosis
  76. Laser Doppler

    Index of pulpal blood flow
    Use of infared beam of light – scatters by Doppler principle when interacting with moving RBCs – photodetector reads this Doppler shifted backscattered light

    Index of pulpal blood flow
  77. Laser Doppler

    Yanpiset / Trope
    Dog Study
    Avulsion / Re-implantation
    Yanpiset/Trope 2001

    • Dog study
    • Avulsion/reimplantation
    • Detect return of pulpal blood flow by 4 wks
  78. Laser Doppler

    Gazelius 1988
    Case Report
    Lateral Luxation of 4 lower incisors
    Gazelius 1988

    • Case report
    • Lateral luxation 4 lower incisors
    • Detected blood flow 6 wks (partially), 9 mos (complete)
  79. Laser Doppler

    Chandler / Sundquist 1999
    Case Report
    Laser doppler used to diagnosis PCOD.
  80. Laser Doppler vs. EPT

    LDF Accuracy 91%

    EPT Accuracy 64%
  81. Pulse Oximiter

    Oxyhemoglobin (HgO2) saturation of arterial blood
    2 light emiting diodes at 2 wavelengths (red, infared) transmit light through vascular tissue, absorbed selectively by oxygenated and deoxygenated hemoglobin, photodetector reads unabsorbed light
  82. Pulse Oximeter vs. Cold vs. EPT

    Gopikrishna 2007
    Compared Pulse Ox to EPT and Cold tests for recently traumatized (uncomplicated crown fractures, concussions, subluxations only)

    Maxillary incisors (day 0 to 6 months post trauma)

    Pulse Ox signficantly improved ability to detect pulp vitality (intact vascular supply) day 0 – 1 month
  83. Pulse Oximeter

    Setzer 2012
    Evaluated Pulse Ox for determining pulpal conditions: Normal pulp, Reversible pulpitis, Irreversible pulpitis, and Pulp necrosis. 

    Statistically significant differences in mean pulp oxygenation levels for each pulpal condition – possible method to determine pathological process within pulp.
  84. Furcation Canals

    Gutmann 28% molars contained furcation canals
  85. Accessory vs. Lateral Canals
    Accessory Canal – Any branch of the main pulp canal or chamber that communicates with the external surface of the root

    Lateral Canal – Accessory canal located in the coronal or middle third of the root
  86. What lines a sinus tract?


    • 100% of sinus tracts are lined with epithelium to the level of the rete ridges (epithelium/CT barrier)
    • 67% had granulomatous tissue lining the tract past the rete ridges
    • 33% had epithelium lining the entire way
  87. What is the overall incidence of patients exhibiting sinus tracts?

  88. What lines a sinus tract?

    Harrison / Larson
    10% lined with epithelium

    90% lined with granuation tissue
  89. Lamina Dura

    Kaffe - Lamina dura is the most consistent feature to aid in diagnosis of apical periodontitis

    Strinberg - PDL width / shape aids in diagnosis of apical periodontitis
  90. Radiographic Interpretation

    Tewary / Hartwell

    • Accuracy increases with added films
    • One Film - 74%
    • Two Film - 87%


    • 6-8 month
    • Interobserver - 47%
    • Intraobserver - 75%

    Tewary / Hartell

    • Digital PAs
    • 35% interobserver
  91. Which technique allows for better working length determination?

    Paralleling or Bisecting Angle?

    Paralleling > Bisecting Angle

  92. What percentage of radiation reduction occurs when using digital radiography?

  93. CBCT Applications

    Patel 2007
    Detection of PA changes & Diagnosis (PRE-OP)

    Anatomical anomalies (i.e.: Dens), Resorptive lesions

    Treatment complications – Perforations, VRFs, sep instruments

    Pre-surgical planning

    Healing/Treatment Outcomes (POST-OP)
  94. VRF

    CBCT vs. Digital PA

    Bernardes / Acevedo 2009; Ozer 2010
    Ozuk 2011
    Ee / Johnson 2014
    Blattner 2010
    Bernardes/Acevedo 2009; Ozer 2010

    • VRF detection
    • CBCT > Digital PA

    Ozuk 2011

    • Accumoto
    • 93% accuracy VRF (confirmed via Sx/RETX)

    Ee/Johnson 2014

    • CBCT>Digital PA Diagnosis
    • VRFs, Resorption, Perforations, PARLs- 83% vs 36%.
    • CBCT resulted in a change to initially proposed treatment 60% of time

    Blattner 2010

    • MB2 detection
    • CBCT = Sectioning (gold standard)
  95. Which view is the best for the detection of VRF?


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