History of Endodontics aae/abe



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Give a 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

MACHO – Multilocular RLs – Myxoma, Ameloblastoma, Central giant cell granulomas, Hemangioma, OKC (KCOT)

*Multiple KCOTs – Basal cell nevus syndrome

Give a differential diagnosis for a periapical radiolucency

Histological Biopsy Reviews:




  1. Bhaskar 1966 – No distinction radiographically between cyst/granuloma

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

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

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

  5. Koivisto 2012 – U of Minnesota (9723 biopsies):

    1. Granulomas 40%

    2. Cysts 33%

    3. Others 20%: KCOTs 8%, CGCGs 1.3%, Ameloblastomas 1.2%, Metastatic <1%



Give a 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

Cemento-osseous dysplasia (cementoma) forms - Florid, Focal, Periapical

Odontomas - Compound, Complex (“little teeth”)



Condensing Osteititis - 85% resolve following NSRCT (Eliasson)

Stressed pulp syndrome & effect of restorative dentisty




  1. Abou-Rass – Stressed pulps = Multiple restorations, Slow test results; NSRCT before restoration




  1. Felton – Full coverage restorations led to a higher incidence (10-18%) of PN




  1. Zach – Heat is capable of causing Pulpal Necrosis (20 deg = 60% necrosis)




  1. Bergenholtz – Pulpal Necrosis: abutments: 15%, non-abutments: 3%



  1. Cheung 2005 –Pulp vitality: Full coverage crown @ 10 yrs- 84%, 15 yrs- 81%; FPD abutment: 10 yrs- 70%, 15 yrs- 66% (At 10 yrs- 15% PFMs/30% FPD/50% Anterior FPD abutments are Necrotic requiring NSRCT)





  1. Murray/SmithRemaining Dentin Thickness = #1 Factor for pulpal vitality (vs. type of restoration placed, drill speed, coolant, and preparation method)

Effects of restorative dentistry on the pulp

Murray

  1. Preparations within 0.5 mm of Pulp = 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-, BMP, NGF, VEGF)  stimulation of odontoblastic reparative dentin formation


Murray/Smith

  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!


Pashley

  1. The number, size of lumen, and surface area of dentinal tubules  closer to the pulp (18,00045,000/mm2, 0.82.5 m, 522%)

Does heat damage the Pulp?
Zach/Cohen OOO 1965 – Monkey study, effect of temp increase on pulp


  1. 4 C – 100% pulps recovered

  2. 10 C – 85% recovered; 15% necrotic

  3. 20 C – 40% recovered; 60% necrotic

  4. >20 C – none recovered




  • Critical increase of intrapulpal temperature:

    • 5.5 C = Irreversible pulpal injury

    • 11 C = Pulpal necrosis




  • Without water coolant, Avg intrapulpal temperature rise > 5.5 C



Facial Space Infections:

Laskin; Hohl 1983

Mandible/Below:


Fascial Space

Source

Borders

Buccal Vestibule

Any Mand. Tooth; B cortical plate; Apex lies above Mentalis (ant) or Buccinator (post)

Buccal cortical plate, alveolar mucosa, Mentalis (anterior), Buccinator (posterior)

Mental Space

Mand. Anterior; B cortical plate; Apex lies below attachment of Mentalis

Mentalis (superiorly), Platysma (inferiorly)

Submental Space

Mand. Anterior; L cortical plate; Apex lies below attachement of Mylohyoid m.

Mylohyoid (superiorly), Platysma (inferiorly)

Sublingual Space

Any Mand. Tooth; L cortical plate; Apex lies above attachement of Mylohyoid m.

Mucosa of Floor of Mouth (superiorly), Mylohyoid (inferiorly), Mandible (laterally)

Submandibular Space

Mand. Posterior; L cortical plate; Apex lies below attachment of Mylohyoid m.

Mylohyoid (superiorly), Platysma (inferiorly), Mandible (laterally)

Facial Space Infections (cont.):

Lateral Face/Cheek:


Fascial Space

Source

Borders

Buccal Vestibule (maxillary)

Max Posterior; B cortical plate; Apex lies below Buccinator

Buccal cortical plate, alveolar mucosa, Buccinator (superiorly)

Buccal Space (max/mand)

Max Posterior:B cortical plate; Apex lies above Buccinator

Mand Posterior: B cortical plate; Apex lies below Buccinator



Buccinator (medial), Skin of cheek (lateral), Zygomatic arch/Buccinator attachment (superior), Mandible/Masseter attachment (inferior)

Submasseteric

Impacted 3rd Molar

Ramus (medial), Masster (lateral)

Temporal Space

Infection spread superiorly from the pterygomandibular or inferiorly submasseteric spaces

Deep Temporal: Skull (medial), Temporalis (lateral)

Superficial Temporal: Temporalis (medial), Fascia




Facial Space Infections (cont.):

Mid-Face:


Fascial Space

Source

Borders

Palate

Any Max tooth; Apex near Palate

Palate (superior); Periosteum (inferior)

Base of Upper Lip

Max C.I.; B cortical plate; Apex above Orbiularis oris

Mucosa upper lip; Orbicularis Oris (inferior)

Canine Space (Infraorbital)

Max Can.-1st PM; B cortical plate; Apex above Levator Anguli Oris

Levator Anguli Oris (inferior); Levator Labii Superioris (superior)

AOLS

Peri-Orbital Space

Infection spread from Canine or Buccal spaces

Lies deep to Orbicularis Oculi


Additional spaces:

- Pterygomandibular space (Moderate – Severe Trismus): 2nd or 3rd molar drains directly into space or Infected IAN B. Borders: Medial Ptergyoid (medial), Lateral Pterygoid (superiorly) Lateral surface of Ramus of Mandible (lateral)
Fascial Space Infections

Complications:

  1. Ludwig’s Angina = Sublingual + Submental + Submandibular spaces bilaterally  pharyngeal/cervical spaces  Airway closure (life threatening cellulitis)




  1. Cavernous sinus thrombosis = Infection of midface (spread from canine or periorbital spaces)  Inflammation/Pressure within the Infratemporal spaceReverse direction of venous blood flow & stasis within the Cavernous sinusThrombi formation within cavernous sinus. Symptoms: Unilateral periorbital edema, headache, bulging of eye, blindness, fever


Signs of Infection:

Extraoral: Swelling, Dysphagia, Trismus, Lymphadenopathy

Lymphadenopathy: Submental (lower incisors), Submandibular (all other teeth)

Intraoral: Swelling, Sinus Tract



Treatment:

Surgical (I&D, decompression), Antibiotics (Pen VK, Clindamycin), Supportive (Analgesics, Heat, Fluids)



Morphology

Morphology


Max Anterior Teeth

1

2

3

4




Vertucci ‘84

100










Dye: decalc/dye/clear

Max 1st Premolar
















Hartwell/Belizzi ‘85

6

91

3




Retrospective chart review: 514 1st PMs (over 13 yrs)

Vertucci ’79

25

70

5




Dye: 400 1st PMs – decal/dye/clear

Max 2nd Premolar
















Hartwell/Belizzi ‘85

40

59

1




Retrospective chart review: 630 2nd PMs (over 13 yrs)

Vertucci ‘79

75

24

1




Dye: 400 2nd PMs – decalc/dye/clear


Morphology


Max 1st Molar

1

2

3

4




Neaverth ‘87







23

77

Retrospective chart review: 228 1st Molars

Type II: 36%, III: 61%



Stropko ‘99







27/7

73/93

Retrospective chart review: 1096 1st Molars ( MB2 after 6 yr)

Type II: 45%, III: 55%



Wolcott ‘02










60

Prospective clinical cases: 3578 RCT/Retxs (6 Endodontists)

Max 2nd Molar
















Fogel/Peikoff/Christie ‘96

3

7

57

23

Retrospective chart review: 520 2nd Molars (3 Endodontists)

Wiene/Eskoz ‘95







60

40

In Vitro: 73 Ext teeth, Burs and files, Radiograph

Type II: 21%, III: 16%, IV: 3%



Wolcott ‘02










35

Prospective clinical cases: 2038 RCT/Retxs (6 Endodontists)

Morphology


Mand Incisors

1

2

3

4




Henry/Rankine-Wilson ‘65

60

40







Radiographs/Histo Sectioning

Type III: 13%



Benjamin/Dowson ‘74

59

41







#15 kfile/Radiographs

Type III: 1.3%



Mand Canine
















Vertucci ‘84

80

20







Dye: decalc/dye/clear

Mand 1st Premolar
















Cleghorn ‘07

76

24







Literature Review: 6700 1st PMs

Trope ‘86

66/86

34/14







Retrospective Radiographic Evaluation: 400 AA/400 White

Mand 2nd Premolar
















Cleghorn ‘07

91

9







Literature Review: 7700 2nd PMs

Trope ‘86

92/97

8/3







Retrospective Radiographic Evaluation: 400 AA/400 White

Morphology


Mand 1st Molar

1

2

3

4




Hartwell/Belizzi ‘82




0.1

65

35

Retrospective chart review: 846 1st Molars

M root: Type II: 36%, III: 62%



Skidmore/Bjorndal ‘71




7

63

28

Plastic resin casts of internal anatomy

M root: Type II: 40%, III: 60%

D root: Type II: 60%, III: 40%


Mand 2nd Molar
















Hartwell/Belizzi ‘82

1

4

89

5

Retrospective chart review: 420 2nd Molars

Weine ‘88

1

4

81

11

PA radiographs and k-files

(75 teeth, C shape = 2.7%)

M root: Type II: 52%, III: 40%


Morphology
C-shaped canals:

Fan – Classifications:

Type I: C

Type II: Semicolon

Type III: 2 or 3 dots

Type IV: No discernable canal

Cook/Cox 1979 (U of Washington) – 8% Incidence
Middle-Mesials:

Dean Baugh/James Wallace1-15% Incidence, Mesial root Mand 1st Molars
Radix:

Radix Entomolaris: Distolingual Supernumerary Root in Mandibular Molars



Radix Paramolaris: Mesiobuccal Supernumerary Root in Mandibular Molars

Calberson 1-5% (AA, Indian), 5-30% (Mongoloids – Chinese, Eskimo, AI)

Morphology
Classifications:

  1. Weine - Type I (1-1), II (2-1), III (2-2), IV (1-2)

  2. Vertucci - Type I (1-1), II (2-1), III (1-2-1), IV (2-2), V (1-2), VI (2-1-2), VII (1-2-1-2), VIII (3-3)

MB2:

  1. Weine- Classic histological study of canal morphology

  2. Neaverth- Access should be extended from triangular to rhomboidal for MB2


Accessory/Lateral Canals:

  1. De Deus27% incidence of lateral canals, 19% Apical 1/3rd

  2. Gutmann28% incidence of furcation canals, 10% extend to PDL

Isthmuses

  1. Weller – MB root Max 1st Molars, 4 mm- 100% incidence isthmus (3-5 mm from apex highest)

  2. Von Arx – M root Mand 1st Molars, 90% incidence isthmus 3 mm from apex

Morphology

Dens Evaginatus:


  1. Definition: Developmental anomaly resulting in an accessory cusp (enamel tubercle) on the occlusal surface of posterior teeth or lingual surface of anterior teeth; thin enamel layer covering dentin core with slender pulpal extension

  2. Prevalence:

    1. Levitan/Himel 2006 – Review Article: Asian descent 0.5-4.3%, Lower Premolars/bilateral, Higher in Chinese/Eskimo/Native Americans –Mongoloids (up to 15%, see also Radix)

  3. Dental Treatment:

    1. Augsburger 1996 – Pulpal management of Dens Evaginatus

    2. Levitan/VanHimel - Cover with composite. NSRCT (mature) or MTA Pulpotomy (vital/inflammed/immature), MTA apexification/REP (necrotic/immature)


Morphology

Dens Invaginatus (Dens in Dente):

  1. Definintion: Developmental anomaly resulting in invagination of an enamel-lined tract extending into the root, with or without exposure of the dental pulp

  2. Types: Oehlers 1957: Type I: occuring within confines of crown, not extending beyond CEJ; Type II: invades root but remains confined as a blind sac w/in root canal, no separate foramen;Type III: penetrates thru the root and exits as separate AF, No communication with the pulp

  3. Prevalence:

    1. Hulsmann IEJ 1997 (review)0.3-10%; bilateral 43%, Max Lats

    2. Hovland 1977 0.4-10% overall incidence, Max Lateral incisors

  4. Dental Treatment:

    1. Narayana/Hartwell JOE 2012 – Case report (11 yo #7), Type III, case specific, removal of dens in dente and pulpal revascularization

    2. Hulsmann 1997 – RCT of dens tract when separate AF; WV obturat.

    3. Alani/Bishop IEJ 2008 – Case specific; RCT of dens only (Type III) or both dens/pulp; Removal of dens tract and tx as 1 canal (Type III)

Orifice Location

Krasner/Rankow 2002Laws of Pulp chamber anatomy:


  1. Law of Centrality – Floor of Pulp chamber located in center of tooth at CEJ

  2. Law of Concentricity – Walls of Pulp chamber are concentric to external surface of tooth at CEJ

  3. Law of CEJ – CEJ is most consistent landmark for locating pulp chamber

  4. Law of Symmetry 1 (Except Max Molars) – Orifices are equidistant from line drawn M-D direction through pulp chamber floor

  5. Law of Symmetry 2 (Except Max Molars) – Orifices lie on line perpindicular to line drawn in M-D direction through pulp chamber floor

  6. Law of Color Change – Color of pulp chamber floor is darker than walls

  7. Law of Orifice location 1 – Orifices are located at junctions of floor-wall

  8. Law of Orifice location 2 – Orifices are located at angles of floor-wall junctions

  9. Law of Orifice location 3 – Orifices are located at terminus of root developmental fusion lines

Wilcox/Walton 1989 – In vitro – related location of canal orifices to occlusal landmarks (cusp tips, grooves) – Max molars – Avoid mesial marginal ridges, Mand molar access too far lingual
Tooth Developmental Anomalies


  1. Fusion: 1 crown/2 roots; joining of 2 developing tooth germs during root formation; may be complete or incomplete fusion w/ separate or joined pulps




  1. Gemination: 2 crowns/1 root; single enamel organ attempts to create 2 teeth




  1. Concrescence: Adjacent teeth are joined by cementum only (form of fusion)




  1. Amelogenesis Imperfecta: 3 types: Hypoplastic, Hypocalcified, Hypomaturation, Hereditary defects in enamel formation/maturation; yellow-brown discoloraiton; Radiographically: Dentin thin/normal roots


Tooth Developmental Anomalies (cont.)


  1. Dentinogenesis Imperfecta: Opalescent Dentin; Autosomal Dominant; 3 types: 1- Osteogenesis Imperfecta, 2- Dental only, 3- Brandywine: Type 2 + Huge pulp chambers/canals (shell teeth), Periapical Radiolucencies; Clinical features: Opalescent translucency, yellow-brown discoloration, easily fractured enamel, blunted roots




  1. Dentinal Dysplasia: Autosomal Dominant; 2 types: 1- Radicular: Crowns Normal, SHORT roots, Obliterated pulps, PARLs; 2- Coronal: Crowns Normal, SHORT roots, Large pulps



Anatomy Studies

  1. Classic Studies:

    1. Hess – 1920s – Original morphology studies (sectioning/dye studies)

    2. Walton - Canal not seen radiographically is present histologically on sectioning

    3. Kuttler 1955 – Distance from the major to the minor diameters:

      1. 0.525mm (18-25y/o)

      2. 0.659mm (>55 y/o)

    4. Burch 1972 – Measured from the occlusal aspect of the major diameter to the apex. Average distance for all roots = 0.59 mm

    5. Vertucci – Decalcification/Dye/Clearing studies on canal anatomy

    6. Stein – Measured from the minor diameter (CDJ) to the major diameter = 0.72mm average. Foramen width increases with age but CDJ width does not

    7. Dummer 1984 – 270 Ext. teeth - Mean A-F distance: 0.38 mm, Mean A-C distance: 0.89 mm; 4 types of ACs described
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