Classification of root resorption Flashcards
LIST ANDREASEN CLASSIFICATION OF ROOT RESORPTION
- Internal
a. Inflammatory
b. Replacement - External
a. Surface
b. Inflammatory
c. replacement
LIST LINDSKOG’S CLASSIFICIATION
- Trauma induced root resorption
a. surface
b. transient
c. pressure
d. orthodontic
e. replacement - Infection induced root resorption
a. internal inflammatory (infection) resorption
b. external inflammatory resorption
c. communicating internal-external resorption - Hyperplastic Invasive tooth resorption
a. Internal (invasive) replacement resorption
b. Invasive coronal resorption
c. Invasive cervical resorption
d. Invasive radicular resorption
LIST and DESCRIBE Heithersay’s classification (Invasive cervical root resorption)
• 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.
DISCUSS SEQUENCE OF EVENTS LEADING TO ROOT RESOTPION
- Crushing and damage to pdl
- Loss of precemtem leading to denudation of root surface
- Chemotaxis of hard tissue resorbing cells
- Macrophages and osteoclasts remove damaged PDL and cementum.
- 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
Key cells involved in resorption
- 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 - Odontoclast
a. Cells that resorb dental hard tissues
b. Similr to osteoclasts
c. Smaller in size
d. Fewer nuclei than osteoclasts - 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
Discuss characteristic and management of trauma induced root resorption
1. SURFACE • Shallow resorption on cementum • Small dentine involvement • Self limiting • Follows trauma/ortho MX- Self limiting. Heals uneventfully with deposition of reparative dentine.
- PRESSURE AND ORTHO
• Pressure of a crypt of unerupted/erupting tooth/neoplasm
MX- Removal of “trauma”, resorption becomes inactivated and uncomplicated repair occurs - 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 - 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
Discuss characteristic and management of infection induced root resorption
- 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
- 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 - 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
DISCUSS PATHOGENSIS OF EXTERNAL ROOT RESORPTION
• 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
Discuss characteristic and management of invasive root resorption
- 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 - 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