Classification of root resorption Flashcards

1
Q

LIST ANDREASEN CLASSIFICATION OF ROOT RESORPTION

A
  1. Internal
    a. Inflammatory
    b. Replacement
  2. External
    a. Surface
    b. Inflammatory
    c. replacement
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2
Q

LIST LINDSKOG’S CLASSIFICIATION

A
  1. Trauma induced root resorption
    a. surface
    b. transient
    c. pressure
    d. orthodontic
    e. replacement
  2. Infection induced root resorption
    a. internal inflammatory (infection) resorption
    b. external inflammatory resorption
    c. communicating internal-external resorption
  3. Hyperplastic Invasive tooth resorption
    a. Internal (invasive) replacement resorption
    b. Invasive coronal resorption
    c. Invasive cervical resorption
    d. Invasive radicular resorption
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3
Q

LIST and DESCRIBE Heithersay’s classification (Invasive cervical root resorption)

A

• Class I-
o small, invasive resorptive lesion near the cervical area with shallow penetration into the dentin
• Class II
o well defined, invasive resorptive lesion that has penetrated close to the coronal pulp but with little or not extension into the radicular dentine.
• Class III
o Deeper invasion of root dentin by resorbing tissues that extend into the coronal thirds of the root
• Class IV
o Large, invasive resorptive process that extend beyond the coronal third of the root.

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4
Q

DISCUSS SEQUENCE OF EVENTS LEADING TO ROOT RESOTPION

A
  1. Crushing and damage to pdl
  2. Loss of precemtem leading to denudation of root surface
  3. Chemotaxis of hard tissue resorbing cells
  4. Macrophages and osteoclasts remove damaged PDL and cementum.
  5. Further complications:
    a. Eventual exposure of dentinal tubules
    b. Contents of the pulp is ischemic and sterile or necrotic and infected
    c. Presence/absence of adjacent vital cementoblast
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5
Q

Key cells involved in resorption

A
  1. Osteoclast
    a. Motile, multinucleated giant cells
    b. Responsible for bone resorption
    c. Derived from hemopoietic cells of monocyte- macrophage lineage
    d. Life-span of 2 weeks
    e. Recruited to site of injury by the release of many proinflammatory cytokines
  2. Odontoclast
    a. Cells that resorb dental hard tissues
    b. Similr to osteoclasts
    c. Smaller in size
    d. Fewer nuclei than osteoclasts
  3. Monocyte and macrophage
    a. Similar structure to osteoclasts
    b. Can also become multinucleated gint cells
    c. Lack a ruffled border
    d. Do not create lacunae on the dentinal surface
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6
Q

Discuss characteristic and management of trauma induced root resorption

A
1. SURFACE
•	Shallow resorption on cementum
•	Small dentine involvement
•	Self limiting
•	Follows trauma/ortho
MX- Self limiting. Heals uneventfully with deposition of reparative dentine. 
  1. PRESSURE AND ORTHO
    • Pressure of a crypt of unerupted/erupting tooth/neoplasm
    MX- Removal of “trauma”, resorption becomes inactivated and uncomplicated repair occurs
  2. TRANSIENT
    • Identified by Andreasen 1986
    • Associated with transient internal apical resorption
    • Occurs from history of traums
    • Colour change due to intrapulpal haemorrhage
    • May resolve spontaneously, 50% of time
    MX- No treatment. Elective endo for bleach
  3. REPLACEMENT
    • Most serious
    • Progressive replacement of the tooth by alveolar bone
    • Ultimately tooth loss
    • Occurs following death of PDL cells due to compression or drying of ligament cells
    • On rare occasions, intact cementum/cementoid layer acts as a barrier so that ankyloses (union with bone) is not accompanied by replacement resorption
    • Total lost of mobility
    • High metallic percussion sound
    • Tooth could be infra-occluded
    • Symptom free
    MANAGEMENT:
    Developing dentition
    • Disrupts arch form
    • Surgical repositioning with emdogain can be attempted to restore arch integrity
    • Decoronate and submerge

Adult dentition
• Nothing can stop the resorption
• Usually occurs at a slow rate, so no treatment required
• Plan for eventual replacement

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7
Q

Discuss characteristic and management of infection induced root resorption

A
  1. INTERNAL
    A. Apical
    • 74.7% of teeth with PA lesion have some degree of apical internal resorption
    B. Intraradicular
    • Resorption in an otherwise intact root
    • Round/Oval shaped radiolucency
    • Commonly accessory canal found communicating from PDL to resorptive area
    • This may have allowed for the passage of blood supply which plays an important role in developing and maintaining resorption
    MANAGEMENT:
    1.Instrument to position of resorption
    2.Instrument to apical terminus
    Long term CaOH medicament used to induce hard tissue barrier prior to obturation/MTA

Intraradicular
Prepare and instrument to the apical foramen
Irrigation + U/S

  1. EXTERNAL
    • Infection is superimposed on a traumatic injury- avul/lux
    • Damage to normal protective cementum/cementoid which then initiates surface resorption exposing underlying dentine to the passage of bacteria or metabolites from the root canal to the external root surface
    • Inflammatory response ensues activating clastic cells which results in resorption of bone and tooth
    MANAGEMENT:
    • Stabilised with endo tx
    • Ledermix x6 weekly for 3 months
    • Signs of healing- caoh
  2. COMMUNICATING
    • Communicating internal and external resorption
    • Radiolucency extending to the exterior
    MANAGEMENT;
    • Endo tx is carried out in the coronal segment to the resorptive area
    • Caoh to induce calcification
    • Another approach is 90% TCA to the resorptive defect after endo
    • This will induce sterile coagulation necrosis forming a scaffold
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8
Q

DISCUSS PATHOGENSIS OF EXTERNAL ROOT RESORPTION

A

• Resorption presents as a combined injury to pulp and PDL
• Bacteria primarily located in pulp & dentinal tubules trigger osteoclastic activity on root surface
• Diagnosed 2-4 weeks after injury
• Resorption rapidly progress – total root resorption within a few months
• Most common after intrusion and replantation
Pathogenesis:
o Initial resorption penetrates cementum and expose dentinal tubules
o Toxins from bacteria in dentinal tubules/infected root canal diffuse to PDL
o Osteoclastic process continue and associated inflammation in PDL – lead to resorption of adjacent alveolar bone
o Process progress and root dentine is absorbed until root canal is exposed
o If bacteria is eliminated, resorptive process is arrested
o Resorption cavity gets filled with bone/cementum

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9
Q

Discuss characteristic and management of invasive root resorption

A
  1. INVASIVE CORONAL TOOTH RESORPTION
    • Rare
    • Localised coronal defect allows invasion of aggressive hyperplastic resorptive tissue
    • Usually in erupting teeth
    • Pink lesion in hypomineralised
    • Has been observed in teeth that have been injured by instrusion of primary teeth
    MANAGEMENT:
    • Total removal of inactivation of all resorptive tissue and restoration of coronal defect
    • Curettage/TCA
    • Endo is pulp affected
  2. INVASIVE CERVICAL
    • Can occur in any permanent tooth
    • Resorptive lesion leaves pinkish colour on crown (highly vascular resorptive lesion visible t’ru thin residual enamel)
    • Occasionally, no visible signs
    • Usually painless, unless superimposed by infection
    • Cause-unknown, trauma, ortho, bleaching
    MANAGEMENT:
    • In absence of tx, lesion is progressive and destructive
    • Management varies according to severity
    • Aim is total removal or inactivation

CLASS I & CLASS II
• Resorptive tissue is fibrovascular
• Pulp is walled off by a protective predentine and dentine barrier
Mx
• Curette resorptive defect and restore
• TCA (trichloroacetic acid)
o Causes coagulation necrosis resorptive tissue is avascular (helps with haemorrhage control) decreases recurrence/occurrence due to deactivation of resorptive cells and adjacent tissues

CLASS III
• Ectopic bone like deposits can be observed within the lesion and the interface with resorbed dentine
• Resorptive tissues creates a series of channels that encircle the root canal and infiltrate into the radicular dentine
• Interconnection between infiltrate channels and the Periodontal ligament
Mx
o Curettage and TCA deactivation. 90% TCA forms coagulation necrosis that deactivates resorptive cells
o Restoration

CLASS IV
• Poor succss rate
• Tx option to do nothing
• Or surgical intervention and deactivation with TCA
May require ortho extrusion if tooth survives

3. INVASIVE/INTERNAL REPLACEMENT 
•	Rare
•	Pink area in crown (pink indicative of highly vascular resorbing tissue)
•	Irregular outline
•	Oval radiolucency

MANAGEMENT:
• Pulpectomy
• Curettage resorptive defect
• RF

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