History of Endodontics aae/abe



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Tronstad 1994 - LDF 91% accurate, more accurate than EPT (64%)



Pulse Oximeter

Pulse Ox = 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 = Oxyhemoglobin (HgO2) Saturation of Arterial blood




  1. 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




  1. 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

ASA Classification





  1. A normal healthy patient




  1. A patient with mild to moderate systemic disease




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




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




  1. A moribund patient not expected to survive 24 hours with or without an operation.


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


Mobility – Miller Index Classification


Class I - barely perceptible

Class II - < 1 mm movement



Class III - > 1 mm movement/depressible in socket

Does periodontal disease cause pulpal disease?


YES

  1. Seltzer – Yes, bacteria can pass through lateral/accessory canals

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

  3. Wong – Pulpitis adjacent to areas of scaling/root planing (Perio tx)


NO

  1. LangelandOnly when Apical Foramen involved

  2. Bergenholtz - No

  3. Mazur/Massler – found no relationship between pulpal & periodontal disease



Gutmann – 28% Molars – Furcation Canals (see also de Deus - 27% accessory)
AAE definitions:

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

Simon’s Classifications for Endo-Perio Lesions




  1. Primary Endo: Necrotic pulp, CAA drains into sulcus/furca = Narrow isolated PD; mimics VRF, Perio Abscess

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


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

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

  5. 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

  6. Concomittant Endo Perio Lesion (added later): Separate and Distinct Endo and Perio lesions w/ no influence on either; Prognosis depends on Perio Tx



Biologic Width

Gargiulo – 1. sulcus depth ~ 1mm

      1. epithelial attachment ~ 1mm

      2. connective tissue attachment ~ 1mm


Calcific Metamorphosis (aka PCO)

  1. 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.

  2. Gutmann –1-16% CM cases develop pulpal necrosis, do not treat cases of calcific metamorphosis unless AP or nonvital

  3. Andreasen22% trauma cases  Calcific metamorphosis

  4. Jacobsen – 70-90% horiztonal root fractures develop Calcific Metamorphosis

  5. Walton – No visible canal radiographically but ALWAYS present histologically

Calcific Metamorphosis (aka PCO)


  1. Trope – caused by luxation injury, uncontrolled reparative dentin or hemorrhage and clot formation act as a nidus for calcification, occurs in immature teeth.

  2. Robertson/Andreasen8.5% PCO cases  Necrosis; 50% PCO respond to vitality test (final recall: 16 years), 20 yr survival: 84%

  3. Holcomb/Gregory – 7% PCO cases  Necrosis

  4. Gutmann1-16% CM cases develop necrosis, do not treat CM unless AP or nonvital



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