History of Endodontics aae/abe



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Lindskog/Hammarstrom 1985 – Removal of the damaged PDL cells may inhibit dentoalveolar ankylosis and replacement resorption. Bone replacing the periodontal membrane grew from the alveolus towards the cementum.





  1. Lindskog/Hammarstrom 1985 – Necrotic PDL cells  Ankylosis between bone and cementum due to repair confusion (osteoblasts vs. cementoblasts). 2 Types: Ankylosis w/o root resorption (cementum-bone) & Ankylosis following inflamm. root resorption (dentin-bone)




  1. Trope 2002 – Damage to the pre-cemental layer due to traumatic injury + Inflammatory destruction of the cementum in response to dead PDL cells




  1. Andreasen 1975 – Need damage of >20% of root surface for progressive replacement resorption (vs. transient replacement resorption)



Discuss External Cervical Root Resorption


  1. Heithersay – 257 teeth, ECR associated with: orthodontic treatment (#1), trauma (#2), and intracoronal bleaching (#3), either alone or in combination. Recommends using 90% TCA for treatment

  2. Patel 2009 – Review of External Cervical Resorption

    1. Damage to precementum or gaps at CEJ, “aseptic resorption”

    2. Etiology: Ortho 24%, Trauma 15%, Internal bleaching 4%, Surgery, Periodontal Therapy (Sc/Rp)

    3. Most commonly: Maxillary Incisors/Canines, Mand Molars

    4. Histology: Hard base (Caries = sticky) profuse bleeding due to highly vascular granulomatous tissue (Pink spot in cervical area of crown, more common than in Internal root resorption)

    5. Pathophys: Osteoclasts, resorption lacunae, no acute inflam.cells

    6. Often mistaken as Internal inflamm resorption, outline of canal should be visible, ECR follows SLOB. Advocates use of CBCT.

    7. Treatment – Based on Heithersay Classifications: Treat Class I, II, III lesions Curretage, 90% TCA, Glass ionomer restoration

Discuss External Cervical Resorption
Heithersay Classifications:

Class I: Small invasive lesion near cervical area w/ shallow dentin penetration

Class II: Well defined lesion, penetration close to the coronal pulp with little or no extension into radicular dentin

Class III: Deeper invasion, involving the coronal dentin and coronal 1/3rd of root



Class IV: Large invasion, extending beyond the coronal 1/3rd of the root
Internal Bleaching and ECR:

  1. Rotstein – Internal bleaching & ECR – 30% H2O2 leakage through dentinal tubules at CEJ with no cemental layer (Neuvald; Papadapolous – 10%) – damages dentin, initiates inflamm/resorp.




  1. Heithersay EDT 1997 Hydroxyl radical was generated after thermocatalytic bleaching w/ 30% H2O2. This radical may be one mechanism underlying PDL breakdown and resorption after bleaching.

Orthodontic treatment, resorption and endodontics





  1. Mattison – No difference was seen in external root resorption between endodontically treated teeth and vital teeth when subjected to orthodontic forces.




  1. Reitan – Ortho movement too quickly = Pressure induced inflammatory Root Resorption (OIRR)




  1. deSouza 2006 – dog study - Ortho movement (5 months) delayed but did not prevent PA healing in comparison to NSRCT (2 stage) teeth without ortho movement


Discuss Apical Inflammatory Root Resorption (secondary to AP)

  1. Nair 2000; Trope 2002 - Dental hard tissues (dentin/cementum) are resorbed in apical periodontitis by multinucleated giant cells (odontoclasts)




  1. Felippe 2009 – Apical Inflammatory root resorption produces irregular apical root surfaces and can modify the AF, changing the working length and resulting in instrumentation beyond the AF (see Weiger – overinst. WL 0-2)




  1. Malueg/Wilcox/Johnson 1996 – SEM of external apical root resorption. Necrotic teeth w/ AP had more apical root resorption than Normal or I.P.




  1. Laux/Abbott 2000 – Radiographic/Histo correlation apical root resorption




  1. Vier 200475% of teeth with PARLs had apical internal inflammatory resorption, likely in conjunction with apical external inflammatory resorption of cementum; Vital teeth had significantly less resorption


CaOH2 & Intracanal Medicaments







CaOH2 Mechanisms of Action



Siqueira IEJ 2001

  • pH (12.5) alters enzyme activity/cellular metabolism

  • Hydroxyl (OH-) ions created in aqueous environment: Highly Oxidative Free Radicals (H.O.F.R.s):

    1. Cell Membrane Damage: OH- ions Remove H+ from Unsaturated Fatty Acids – Generating free lipid radicals and destroying phospholipids – key components of cell membrane

    2. Protein Denaturation: Alkalinization induces breakdown of ionic bonds maintaining tertiary structure of proteins = Loss of activity of the enzyme and Disruption of the cellular activity

    3. DNA Damage: OH- ions react with bacterial DNA and induce splitting of strands. Inhibits DNA replication and cellular activity.

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