BDS(NBI), CIBRD(KASADA), MDSc-Endo(Mal), Cert. In
Oral Implantology (Mal), FADI(USA) FICD(USA)
Senior Lecturer and Specialist Endodontist
Dept of Conservative Dentistry
University of Nairobi
E-Mail: tomdienya@uonbi.ac.ke or tomdienya@yahoo.com
DEFINATION
• Resorption : (AAE,1944 ) : Resorption
is a condition associated with either
physiologic or pathologic process resulting
in a loss of dentin, cementum or bone.
• Internal resorption : ( Grossman ): Internal
resorption is an idiopathic, slow or fast
progressive resorptive process, occurring in
the dentin of the pulp chamber or root canals
of teeth.
• External resorption : ( Grossman ):
External resorption is a lytic process,
occurring in the cementum or cementum and
dentin of the roots of teeth.
Causes of root resorption
A)Physiologic resorption as in decidous teeth
B)Local factors:
• Periapical inflammation
• Dental trauma
• Tumors/cysts
• Excessive mechanical/occlusalforces
• Impacted teeth
• Intracoronal bleaching
• Periodontal procedures
C)Systemicconditions:
• i.Hormonal imbalance
• ii.Paget’sdisease
• iii.Herpeszooster
PREREQUISITE FOR
RESORPTION
1. Loss/alteration of the protective
layer(Precementum/Predentin)
2. Inflammation must occur at the
unprotected root surface.
MECHANISM OF TOOTH RESORPTION
2 Phases
INJURY STIMULATION
INJURY
Concerns the non-mineralized tissues
covering the external(pre-cemental)
surface of the root or the internal(pre-
dentinal) surface of the root.
Injury can be
• Mechanical
• Chemical
Stimulation
• Stimulation concerns awide array of
factors:
1)Nature of cells present:
• At the time of injury
• Site of injury
2)Site of tooth involved(Cemental or
dentinal)
Sequence Of Events Leading
To Root Resorption
• Crushing and damage to PDL
• Loss of Precementum leading to
denudation of root surface
• Chemotaxisof hard tissue resorbing
cells
• Macrophages & Osteoclasts remove
damaged PDL & Cementum
Sequence Of Events
Leading To Root
Resorption
The situation gets further complicated by:
• Eventual exposure of dentinal tubules.
• Contents of the pulp i.e.Ischemic and
sterile or necrotic and infected.
• Presence/Absence of adjacent vital
cementoblasts.
• Resorptive process is said to be
aBIMODELPROCESS:
• Dissolution of the Inorganic Crystal Structure
• Degradation of the Organic Structure of
Collagen,Principally Type I
• i. Dissolution of the Inorganic Crystal
Structure
• pHlevels below 5,facilitate rapid
dissolution of hydroxyapatite.
• Polarised proton pump along the
ruffled border and the enzyme Carbonic
Anhydrase II play an important role.
• ii. Degradation of the Organic Structure
• •Three groups of Protein as enzymes are
involved:
• Collagenases(act at neutralpH)
• Matrix metalloproteinases(act at neutral
pH)
• Cysteine proteinases(act at acidicpH)
Diagnosis
Radiographs taken at different horizontal angulations
Vitality testing:
Vital:
• Sub epithelial external root resorption
• Internal root resorption
Non-Vital
• External inflammatory resorption involving an
infected pulp
• Internal root resorption with necrotic coronal pulp
Clinically:
• A pink spot present on the tooth surface
Advanced Diagnostic
aids includes:
• Cone Beam Computed
Tomography(CBCT)
• Dental Panoramic Tomography
• True Cephalometry Skull
• Optical Coherence Tomography
External Surface Resorption (Repair Related)
Small,superficial resorption cavities in the
cementum and the outer most layers of
the dentin without an inflammatory
reaction in the PDL.
Etiology:
Caused by injury restricted to external root surface.
Resorption can occur due to
• Concussion
• Sub luxation
• Lateral luxation
• Intrusion
• Replantation of avulsed teeth
Resorption also occur frequently after
• Orthodontic tooth movement
• Chronic injury affecting PDL
• Traumatic occlusion
• Pressure from developing
cyst/apicalgranuloma/ectopically
eruptingtooth
• •Whentrauma/pressure discontinued–
spontaneous healing occur–
• -typical feature of REPAIR RELATED
RESORPTION
PRESSURE
•Due to excessive forces of
Orthodontictoothmovement
Impacted teeth or from tumors or
cysts.
Pressure damages the cementum and
provides the continuous stimulus for
the resorbing cells.
Orthodontic movement
Endodontic Implication:
• Primarily periodontal injury–endodontic
intervention not indicated
Treatment:
• If trauma/pressure eliminated–almost
100%repair
• If root apex resorbed-excessive mobility
becomes aproblem, if root is shorter than
12mm
External Inflammatory Root Resorption
Etiology:
• Resorption presents acombined injury to pulp
and PDL
• Bacteria primarily located in pulp&dentinal
tubules trigger osteoclastic activity on root
surface.
• Resorption can affect all parts of root.
• Diagnosed 2-4 weeks after injury.
• Resorption rapidly progress–total root
resorption within few months.
• Most common after intrusion&replantation.
ClinicalFindings:
• Increased mobility
• Dull percussion tone
• Sometimes tooth extruded
• No response to sensibility testing
• Sometimes sinus tract develop
Endodontic Implication:
• Resorption–combined periodontal&pulpal
injury
• Require immediate endodontic therapy-to
remove osteoclast promoting
factors(bacterialtoxins)
Treatment:
• Remove/destroy bacteria in root canal&dentinal
tubules.
• Allow healing in entire periradicularregion.
• Bacteria in root canal best destroyed byCa(OH)2. If
Ca(OH)2-used for more than 30days–weakening of
root structure of immatureteeth-causes cervica l
root fracture.
Prognosis:
• Dentin lost by resorption cannot be
replaced by new dentin
• Healing occurs–by arresting resorption
process&replacement with either alayer of
new cementum&bone and establishment
of newPDL
• Amount of healing–88%
External Trauma Related Replacement
Resorption (Ankylosis)
• Etiology:
SevereTrauma:
• Lateral luxation
• Intrusions
• Replacement of avulsed tooth
• Healing takes place from adjacent healthy
PDL resulting in a normal PDL.
• Healing from bony alveolus–create bony
bridge between socket wall and rootsurface.
ClinicalFindings:
• Appear firm in socket
• High metallic sound on percussion
• This can be demonstrated 4-6 weeks after
trauma.
Radiographic Findings:
• Diagnosed radiographically within
2months after injury.
• Clinically identified within one month–high
percussion sound.
Endodontic treatment:
• Thorough debridement and preparation of the root canal
system
Sequential use of
• 17%EDTAC(ethylene diaminetetraacetic acid plus
cetavlon)
• 1% sodium hypochlorite and
A final rinse with EDTAC solution
• Most effective regimen resulting in adentine surface devoid of
smear layer.
• •Facilitates the diffusion of
medicaments(Ledermixpaste)through dentine to
theexternalrootsurface
•Treatment:
Decoronation-to maintain&augment
alveolar process
•Suitable in children&adolescence when
significant remaining alveolar growth
expected.
Inadolescents–ankylosed tooth fail to
erupt(infraposition)
Younger the age–more pronounced
infraposition
•Procedure:
Removal of tooth crown(slightly below
cervical bone level)leaving remaining part
of root which is then root treated
External Cervical Resorption
Etiology:
• Defect in cementoblast layer
• Heithersay et al–studied 259 teeth with
invasive cervical resorption–
• 23%:related to orthodontic treatment
• 15%:acute trauma
• 14%:cervicalrestoration
PredisposingFactors:
• •Orthodontic tooth movement
• •Trauma
• •Intracoronal bleaching
• •Surgical procedures
• •Periodontal therapy
• •Other factors:
• Bruxism,intracoronal
restorations,developmental
defects,systemic diseases.
ClinicalFindings:
• Expanding lesion-show as a“pinkspot”next
to cervical margin
Radiographic Findings:
• Cervical bowl-shaped lesion is the start of
invasive progression of resorption in
coronal&apical direction.
• Pulp canal not invaded in initial phase
Treatment:
• Essentially,treatment involves complete
removal of the resorptive tissue and
restoring the resulting defect with aplastic
tooth-coloured restoration.
• Endodontic treatment also be required in
cases in which the ECR lesion has
perforated the root canal.
Treatment:
• Heithersay recommended-topica l
application of a90% aqueous solution of
trichloroaceticacid,curettage,and restoration
with glass ionomer cement.
• Trichloroaceticacid causes coagulation
necrosis of the resorptive tissue
• No damage to adjacent periodontal tissues
• It also infiltrates the small channels and
recesses of tooth that otherwise be
unreachable by mechanical instrumentation
Internal Resorption
Definition:
• Internal resorption is an unusual form of
tooth resorption that begins centrally within
the tooth,apparently initiated in most cases
by apeculiar inflammation of the pulp
Internal Root Resorption—three types
• Internal surface resorption
• Internal infection related root resorption
• Internal replacement resorption
ClinicalFeatures:
• Asymptomatic until it has perforated and
become necrotic
• Detected through routine radiographs
• Pain:lesion perforates and tissue exposed to
oral fluids
• Can be found in all areas of root but most
commonly found in cervical region
• Common in maxillary central incisors
• Usually single tooth but can involve multiple
teeth
• Granulation tissue manifests as a“PinkSpot”
Internal Infection Related Root
Resorption
Etiology:
• Coronal to the resorption site in
pulp,necrotic infected tissue is found.
• Resorption site–represents resorbing
granulation tissue interposed between
healthy&diseasedpulp
• Pathogenesis:
• Resorption process–gradually expand–
leading to fracture of root
Treatment:
• Endodontic treatment is appropriate
• Require technique that allows
management of resorbed area
• Thermoplastic obturation
Treatment:
1)Defect not perforated the root to the periodontal
ligament:
• Obturation with warm gutta percha technique.
2)Defect perforated the root below bone level:
• A hard tissue barrier can be produced with long
term calcium hydroxide treatment,after which
obturation is carried out.
• •Defect perforates coronal to the epithelial
attachment or if an extremely large perforation is
present:
• A surgical approach is required to seal the
perforation.
Treatment(Apical):
• Extend instrumentation only to the position
of the resorption.
• With the removal of micro-organisms
followed by root canal filling,hard tissue
repair will occur in the resorbed apical
region.
• Treatment to the position of the resorption
help in achieving biological repair of the
resorbed apex.
Treatment(Intraradicular):
• Preparation of the canal to the apical
foramen.
• Particular emphasis on irrigation and
ultrasonication(resorbed area is cleansed
thoroughly).
• Thermoplastic obturation of canal.
ROOT RESORPTION BDS 5.ppt
ROOT RESORPTION BDS 5.ppt
ROOT RESORPTION BDS 5.ppt

ROOT RESORPTION BDS 5.ppt

  • 1.
    BDS(NBI), CIBRD(KASADA), MDSc-Endo(Mal),Cert. In Oral Implantology (Mal), FADI(USA) FICD(USA) Senior Lecturer and Specialist Endodontist Dept of Conservative Dentistry University of Nairobi E-Mail: tomdienya@uonbi.ac.ke or tomdienya@yahoo.com
  • 2.
    DEFINATION • Resorption :(AAE,1944 ) : Resorption is a condition associated with either physiologic or pathologic process resulting in a loss of dentin, cementum or bone.
  • 4.
    • Internal resorption: ( Grossman ): Internal resorption is an idiopathic, slow or fast progressive resorptive process, occurring in the dentin of the pulp chamber or root canals of teeth. • External resorption : ( Grossman ): External resorption is a lytic process, occurring in the cementum or cementum and dentin of the roots of teeth.
  • 5.
    Causes of rootresorption A)Physiologic resorption as in decidous teeth B)Local factors: • Periapical inflammation • Dental trauma • Tumors/cysts • Excessive mechanical/occlusalforces • Impacted teeth • Intracoronal bleaching • Periodontal procedures C)Systemicconditions: • i.Hormonal imbalance • ii.Paget’sdisease • iii.Herpeszooster
  • 6.
    PREREQUISITE FOR RESORPTION 1. Loss/alterationof the protective layer(Precementum/Predentin) 2. Inflammation must occur at the unprotected root surface.
  • 7.
    MECHANISM OF TOOTHRESORPTION 2 Phases INJURY STIMULATION
  • 8.
    INJURY Concerns the non-mineralizedtissues covering the external(pre-cemental) surface of the root or the internal(pre- dentinal) surface of the root. Injury can be • Mechanical • Chemical
  • 9.
    Stimulation • Stimulation concernsawide array of factors: 1)Nature of cells present: • At the time of injury • Site of injury 2)Site of tooth involved(Cemental or dentinal)
  • 10.
    Sequence Of EventsLeading To Root Resorption • Crushing and damage to PDL • Loss of Precementum leading to denudation of root surface • Chemotaxisof hard tissue resorbing cells • Macrophages & Osteoclasts remove damaged PDL & Cementum
  • 11.
    Sequence Of Events LeadingTo Root Resorption The situation gets further complicated by: • Eventual exposure of dentinal tubules. • Contents of the pulp i.e.Ischemic and sterile or necrotic and infected. • Presence/Absence of adjacent vital cementoblasts.
  • 12.
    • Resorptive processis said to be aBIMODELPROCESS: • Dissolution of the Inorganic Crystal Structure • Degradation of the Organic Structure of Collagen,Principally Type I
  • 13.
    • i. Dissolutionof the Inorganic Crystal Structure • pHlevels below 5,facilitate rapid dissolution of hydroxyapatite. • Polarised proton pump along the ruffled border and the enzyme Carbonic Anhydrase II play an important role.
  • 14.
    • ii. Degradationof the Organic Structure • •Three groups of Protein as enzymes are involved: • Collagenases(act at neutralpH) • Matrix metalloproteinases(act at neutral pH) • Cysteine proteinases(act at acidicpH)
  • 15.
    Diagnosis Radiographs taken atdifferent horizontal angulations Vitality testing: Vital: • Sub epithelial external root resorption • Internal root resorption Non-Vital • External inflammatory resorption involving an infected pulp • Internal root resorption with necrotic coronal pulp Clinically: • A pink spot present on the tooth surface
  • 17.
    Advanced Diagnostic aids includes: •Cone Beam Computed Tomography(CBCT) • Dental Panoramic Tomography • True Cephalometry Skull • Optical Coherence Tomography
  • 19.
    External Surface Resorption(Repair Related) Small,superficial resorption cavities in the cementum and the outer most layers of the dentin without an inflammatory reaction in the PDL. Etiology: Caused by injury restricted to external root surface. Resorption can occur due to • Concussion • Sub luxation • Lateral luxation • Intrusion • Replantation of avulsed teeth
  • 20.
    Resorption also occurfrequently after • Orthodontic tooth movement • Chronic injury affecting PDL • Traumatic occlusion • Pressure from developing cyst/apicalgranuloma/ectopically eruptingtooth • •Whentrauma/pressure discontinued– spontaneous healing occur– • -typical feature of REPAIR RELATED RESORPTION
  • 21.
    PRESSURE •Due to excessiveforces of Orthodontictoothmovement Impacted teeth or from tumors or cysts. Pressure damages the cementum and provides the continuous stimulus for the resorbing cells.
  • 22.
  • 23.
    Endodontic Implication: • Primarilyperiodontal injury–endodontic intervention not indicated Treatment: • If trauma/pressure eliminated–almost 100%repair • If root apex resorbed-excessive mobility becomes aproblem, if root is shorter than 12mm
  • 24.
    External Inflammatory RootResorption Etiology: • Resorption presents acombined injury to pulp and PDL • Bacteria primarily located in pulp&dentinal tubules trigger osteoclastic activity on root surface. • Resorption can affect all parts of root. • Diagnosed 2-4 weeks after injury. • Resorption rapidly progress–total root resorption within few months. • Most common after intrusion&replantation.
  • 26.
    ClinicalFindings: • Increased mobility •Dull percussion tone • Sometimes tooth extruded • No response to sensibility testing • Sometimes sinus tract develop
  • 27.
    Endodontic Implication: • Resorption–combinedperiodontal&pulpal injury • Require immediate endodontic therapy-to remove osteoclast promoting factors(bacterialtoxins) Treatment: • Remove/destroy bacteria in root canal&dentinal tubules. • Allow healing in entire periradicularregion. • Bacteria in root canal best destroyed byCa(OH)2. If Ca(OH)2-used for more than 30days–weakening of root structure of immatureteeth-causes cervica l root fracture.
  • 28.
    Prognosis: • Dentin lostby resorption cannot be replaced by new dentin • Healing occurs–by arresting resorption process&replacement with either alayer of new cementum&bone and establishment of newPDL • Amount of healing–88%
  • 29.
    External Trauma RelatedReplacement Resorption (Ankylosis) • Etiology: SevereTrauma: • Lateral luxation • Intrusions • Replacement of avulsed tooth • Healing takes place from adjacent healthy PDL resulting in a normal PDL. • Healing from bony alveolus–create bony bridge between socket wall and rootsurface.
  • 31.
    ClinicalFindings: • Appear firmin socket • High metallic sound on percussion • This can be demonstrated 4-6 weeks after trauma. Radiographic Findings: • Diagnosed radiographically within 2months after injury. • Clinically identified within one month–high percussion sound.
  • 33.
    Endodontic treatment: • Thoroughdebridement and preparation of the root canal system Sequential use of • 17%EDTAC(ethylene diaminetetraacetic acid plus cetavlon) • 1% sodium hypochlorite and A final rinse with EDTAC solution • Most effective regimen resulting in adentine surface devoid of smear layer. • •Facilitates the diffusion of medicaments(Ledermixpaste)through dentine to theexternalrootsurface
  • 34.
    •Treatment: Decoronation-to maintain&augment alveolar process •Suitablein children&adolescence when significant remaining alveolar growth expected. Inadolescents–ankylosed tooth fail to erupt(infraposition) Younger the age–more pronounced infraposition •Procedure: Removal of tooth crown(slightly below cervical bone level)leaving remaining part of root which is then root treated
  • 35.
    External Cervical Resorption Etiology: •Defect in cementoblast layer • Heithersay et al–studied 259 teeth with invasive cervical resorption– • 23%:related to orthodontic treatment • 15%:acute trauma • 14%:cervicalrestoration
  • 37.
    PredisposingFactors: • •Orthodontic toothmovement • •Trauma • •Intracoronal bleaching • •Surgical procedures • •Periodontal therapy • •Other factors: • Bruxism,intracoronal restorations,developmental defects,systemic diseases.
  • 38.
    ClinicalFindings: • Expanding lesion-showas a“pinkspot”next to cervical margin
  • 39.
    Radiographic Findings: • Cervicalbowl-shaped lesion is the start of invasive progression of resorption in coronal&apical direction. • Pulp canal not invaded in initial phase
  • 40.
    Treatment: • Essentially,treatment involvescomplete removal of the resorptive tissue and restoring the resulting defect with aplastic tooth-coloured restoration. • Endodontic treatment also be required in cases in which the ECR lesion has perforated the root canal.
  • 41.
    Treatment: • Heithersay recommended-topical application of a90% aqueous solution of trichloroaceticacid,curettage,and restoration with glass ionomer cement. • Trichloroaceticacid causes coagulation necrosis of the resorptive tissue • No damage to adjacent periodontal tissues • It also infiltrates the small channels and recesses of tooth that otherwise be unreachable by mechanical instrumentation
  • 43.
    Internal Resorption Definition: • Internalresorption is an unusual form of tooth resorption that begins centrally within the tooth,apparently initiated in most cases by apeculiar inflammation of the pulp Internal Root Resorption—three types • Internal surface resorption • Internal infection related root resorption • Internal replacement resorption
  • 44.
    ClinicalFeatures: • Asymptomatic untilit has perforated and become necrotic • Detected through routine radiographs • Pain:lesion perforates and tissue exposed to oral fluids • Can be found in all areas of root but most commonly found in cervical region • Common in maxillary central incisors • Usually single tooth but can involve multiple teeth • Granulation tissue manifests as a“PinkSpot”
  • 45.
    Internal Infection RelatedRoot Resorption Etiology: • Coronal to the resorption site in pulp,necrotic infected tissue is found. • Resorption site–represents resorbing granulation tissue interposed between healthy&diseasedpulp • Pathogenesis: • Resorption process–gradually expand– leading to fracture of root
  • 47.
    Treatment: • Endodontic treatmentis appropriate • Require technique that allows management of resorbed area • Thermoplastic obturation
  • 48.
    Treatment: 1)Defect not perforatedthe root to the periodontal ligament: • Obturation with warm gutta percha technique. 2)Defect perforated the root below bone level: • A hard tissue barrier can be produced with long term calcium hydroxide treatment,after which obturation is carried out. • •Defect perforates coronal to the epithelial attachment or if an extremely large perforation is present: • A surgical approach is required to seal the perforation.
  • 49.
    Treatment(Apical): • Extend instrumentationonly to the position of the resorption. • With the removal of micro-organisms followed by root canal filling,hard tissue repair will occur in the resorbed apical region. • Treatment to the position of the resorption help in achieving biological repair of the resorbed apex.
  • 50.
    Treatment(Intraradicular): • Preparation ofthe canal to the apical foramen. • Particular emphasis on irrigation and ultrasonication(resorbed area is cleansed thoroughly). • Thermoplastic obturation of canal.