resorption

1. ROOT
Resorption
Dr. SV.SATISH
Professor & HOD
Dept of Conservative Dentistry &
Endodontics
Navodaya Dental College

2. Introduction
• Multifactorial process – loss of tooth structure
• Due to different causes, it may vary, leading to several types of resorption.
• Treatment when
• Successful : only arrest the process
• Less Successful: slow down the resorptive process
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3. • Mineralized tissues of teeth are protected
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• In pulp cavity by
• On root surface by
: Predentine and odontoblasts
: Precementum and osteoblasts
• If protected structures are damaged / removed, multinucleated cells (osteoclasts) colonise root
surface and cause resorption.
[ Gulabiwala ]

4. Definitions –Tooth Resorption
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• A condition associated with either a physiologic or a pathologic process that result in loss of
substance from a tissue such as dentin, cementum or alveolar bone.

5. CLASSIFICATION
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6. Classification by AAE
i. Internal Resorption
• Root Canal Replacement Resorption
• Internal Inflammatory Resorption
ii. External Root Resorption
• Surface Resorption
• Inflammatory Resorption
• Replacement Resorption
• Dentoalveolar Resorption
iii. Pathologic Root Resorption
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7. Ingle’s Classification
i. Internal Resorption
• Surface Resorption
• Infection Resorption
• Replacement Resorption
ii. External Root Resorption
• Surface Resorption (Repair Related)
• Infection Related (Inflammatory Root Resorption)
• Trauma Related Replacement Resorption (Ankylosis)
• Spontaneous Ankylotic Resorption
• External Multiple Sites Of Ankylosis (Infection Related Resorption)
• Cervical Invasive Resorption
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8. Protective Mechanisms Against Resorption
• Remnants of HERS surround the root like a net.
• Imparting a resistance to resorption and subsequent ankylosis
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• Based on the premise that the cementum and predentin covering the dentin are essential
elements in the resistance of the dental root to resorption.
[ Trope et al, Seltzer and Bender ]

9. Protective Mechanisms Against Resorption
• Osteoclasts will not adhere to or resorb unmineralized matrix.
• Most external aspect of cementum is covered by a layer of cementoblasts over a non
mineralized cementoid.
• Osteoclasts bind to RGD peptides (Arginine-Glycin-Aspartic acid) bound to calcium salts on
mineralized surfaces.
[ Trope et al, Seltzer and Bender ]
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10. Protective Mechanisms Against Resorption
• Osteoprotegrin (OPG) : ability to inhibit osteoclasts mediated bone loss.
• RANKL : produced by osteoblasts
• RANKL liberated into tissue and attaches to receptors of macrophages
• Macrophages aggregate, fuse and form osteoclasts.
• OPG acts as decoy receptor by binding to the receptor activator of RANKL which reduces its
concentration which inhibits ability of RANKL to stimulate osteoclast production.
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[ Trope et al, Seltzer and Bender ]

11. Protective Mechanisms Against Resorption
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• Anti resorptive factors such as
• Estrogen
• Calcitonin
• Bone morphogenetic protein
• Tumor growth factor
• Interleukin -17
• Platelet derived growth factor
• Calcium, etc…
Depresses RANKL production and activate OPG production.
[ Trope et al, Seltzer and Bender ]

12. Protective Mechanisms Against Resorption
• Another function of cemental layer
• Ability to inhibit the movement of toxins if present in the root canal
space into the surrounding periodontal tissues.
• Intermediate cementum : acts as a barrier between the PDL and dentinal
tubules.
• Barrier damaged : inflammatory stimulators diffuse from pulp space to
PDL causing inflammatory response leading to root resorption.
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[ Trope et al, Seltzer and Bender ]

13. Prerequisites for Resorption
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Resorption – Dr. Nithin Mathew
1. Loss / alteration of the protective layer ( Precementum / Predentin )
2. Inflammation must occur at the unprotected root surface.

14. Mechanism of Root Resorption
2 Phases
Injury Stimulation
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15. 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
• Mechanical
• Chemical
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16. Stimulation
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Resorption – Dr. Nithin Mathew
• Stimulation concerns a wide array of factors:
i. Nature of cells present:
• At the time of injury
• Site of injury
ii. Site of tooth involved (Cemental or Dentinal)

17. Sequence Of Events Leading To Root Resorption
Crushing and damage to PDL
Loss of Precementum leading to denudation of root surface
Chemotaxis of hard tissue resorbing cells
Macrophages & Osteoclasts remove damaged PDL & Cementum
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18. Sequence Of Events Leading To Root Resorption
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Resorption – Dr. Nithin Mathew
• 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.

19. • Key Cells involved are
• Osteoclasts
• Odontoclasts
• Monocytes and Macrophages
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20. Osteoclasts
• Motile, multinucleated giant cells – responsible for bone resorption
• Derived from the hemopoietic cells of the monocyte-macrophage lineage, with a life span of
about 2 weeks.
• Recruited to the site of injury by the release of many proinflammatory cytokines.
• To perform their function, osteoclasts must attach themselves to the bone surface.
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21. Osteoclasts
• For binding of osteoclast – various RGD – peptide containing proteins are necessary :
• Osteopontin
• Bone Sialoprotein
• Fibronectin
• Vitronectin
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22. OSTEOPONTIN
• Important role in regulating osteoclast recruitment and activation by binding to the
osteoclast integrin receptor.
[ Seltzer & Bender ]
• Serves as linker molecule with one end bind to calcium crystals in exposed dentin and
other end bind to integrin protein (extending from the osteoclast plasma membrane)
• Binding of osteopontin to integrin protein - facilitate clastic cell adhesion
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23. Odontoclasts
• Cells that resorb dental hard tissues
• Similar to the osteoclasts.
• Smaller in size
• Contain fewer nuclei than the osteoclasts.
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24. Macrophages
• Similar structure to osteoclasts
• Can also become multinucleated giant cells
• Lack a ruffled border
• Do not create lacunae on the dentinal surface
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25. i. Dissolution of the Inorganic Crystal Structure
• pH levels below 5 , facilitate rapid dissolution of hydroxyapatite.
• Polarised proton pump along the ruffled border and the enzyme Carbonic Anhydrase II play an
important role.
CO2
H2CO3
CA II [ Proton pump provides steady source of H+ ions ]
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26. ii. Degradation of the Organic Structure
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• Three groups of Proteinase enzymes are involved:
• Collagenases (act at neutral pH)
• Matrix metalloproteinases (act at neutral pH)
• Cysteine proteinases (act at acidic pH).

27. Bacteria’s Role in Tooth Resorption
• Two possibilities exist for the mechanism of bacteria induced resorption:
1. Bacteria produce acids and proteases that destroy the bone matrix components
2. Bacteria stimulate the production of osteolytic factor, which promotes osteoclastic
activity
• Lipopolysaccharides present in the cell wall of gram negative bacteria stimulate
• Lysozymal enzyme release
• Collagenases release from macrophages
• Osteoblastic secretion of osteolytic factors IL-1, IL-6, M-CSF and PGE2.
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28. Diagnosis
• Radiographs taken at different horizontal angulations
• Vitality testing:
• Vital:
• Subepithelial 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
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29. Diagnosis
• Advanced Diagnostic aids includes
• Cone Beam Computed Tomography (CBCT)
• Dental Panoramic Tomography
• True Cephalometry Skull
• Optical Coherence Tomography
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30. External Resorption
• External Root Resorption
• Surface Resorption (Repair Related)
• Infection Related (Inflammatory Root Resorption)
• Trauma Related Replacement Resorption (Ankylosis)
• Spontaneous Ankylotic Resorption
• External Multiple Sites Of Ankylosis (Infection Related Resorption)
• Cervical Invasive Resorption
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• Definition:
• Loss of cementum and/or dentin from the roots of the teeth originating in the PDL.
[ Chivian et al 1991 ]

31. External Surface Resorption (Repair Related)
Etiology:
• Caused by injury restricted to external root surface.
• Resorption can occur due to
• Concussion
• Subluxation
• Lateral luxation
• Intrusion
• Replantation of avulsed teeth
• Small, superficial resorption cavities in the cementum and the outermost layers of the dentin
without an inflammatory reaction in the PDL.
[ Andreason & Hjorting – 1966 ]
[ Ingle ]
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32. External Surface Resorption (Repair Related)
• Resorption also occur frequently after
• Orthodontic tooth movement
• Chronic injury affecting PDL
• Traumatic occlusion
• Pressure from developing cyst /apical granuloma/ectopically erupting tooth
• When trauma/pressure discontinued – spontaneous healing occur –
- typical feature of REPAIR RELATED RESORPTION
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33. [ Seltzer & Bender ]
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External Surface Resorption (Repair Related)
Pathogenesis:
Injury causes :
• Attachment damage
• Loss of protective layer - serve as inflammatory stimulus
• Injured tissue – adjacent to root and surface cementum – removed by macrophages
& osteoclasts.
• Repair - by progenitor cells from adjacent PDL
• New cementum is formed with insertion of PDL fibres [ Ingle ]

34. External Surface Resorption (Repair Related)
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Pathogenesis:
• Small cavities on root surface - heal by new formation of cementum accommodating
the reformed PDL fibers.
• Resorption of soft tissue by macrophages and hard tissues by osteoclasts.
• Exposed cementum and dentin release growth factors which trigger periodontal
ligament specific cells to repair the site.

35. PRESSURE
• Root resorption increases with the period of force application.
• The severity of root resorption is highly influenced by the
• Amount of tooth movement and the force regimen.
• The more teeth are displaced, the more root resorption will occur.
• Intermittent forces cause less severe root resorption
External Surface Resorption (Repair Related)
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36. IMPACTED TEETH
• When impacted teeth attempt to erupt, resorb the roots or crowns of adjacent teeth by
pressure.
• Predentin and Odontoblastic layer is most resistant to this resorption and the pulps of these
teeth remain uninflamed.
• If impacted tooth is removed the resorption will stop.
External Surface Resorption (Repair Related)
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37. Radiographic Findings:
• After 2-4 weeks, localised widening of PDL space – seen due to loss of surface layer of
cementum and bony alveolar socket.
• Subsequently healing occurs – with reformation of PDL & deposition of hard tissue.
• Most repair related root surface resorption – have limited size and cannot be detected
radiographically.
External Surface Resorption (Repair Related)
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38. External Inflammatory Root Resorption
Etiology:
• Resorption presents a combined 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. [ Ingle ]
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39. External Inflammatory Root Resorption
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Pathogenesis:
• Initial resorption penetrate cementum & expose dentinal tubules.
• Toxins from bacteria in dentinal tubules /infected root canal diffuse to PDL.
• Osteoclastic process continue and associated inflammation in PDL- lead to resorption of
adjacent alveolar bone.
• Process progress & root dentin is resorbed until root canal is exposed.
[ Ingle ]

40. External Inflammatory Root Resorption
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Pathogenesis:
• If bacteria eliminated from root canal & dentinal tubules – resorptive process get arrested
• Resorption cavity gets filled with bone / cementum (according to the vital tissue available
adjacent to resorptive site )

41. External Inflammatory Root Resorption
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Clinical Findings:
• Increased mobility
• Dull percussion tone
• Sometimes tooth extruded
• No response to sensibility testing
• Sometimes sinus tract develop

42. External Trauma Related Replacement Resorption (Ankylosis)
• Treating The Root Canal
• Root canal - alternately instrumented & rinsed with saline until
bleeding from the surrounding tissues filled the empty root canal.
• This step is critical, as the blood clot will decrease the risk of
infection.
• Allows the ingress of osteoclasts and osteoblasts, thus inducing bone
formation at the inner surface of the root canal.
[ Dental Traumatology , 2007; 23: 87–94 ]
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43. External Trauma Related Replacement Resorption (Ankylosis)
• Treating The Root Canal
• Allow continued vertical growth of alveolus
• Remaining root maintain labiolingual content of alveolar process
[ Dental Traumatology , 2007; 23: 87–94 ]
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44. External Cervical Resorption
Pathogenesis:
• Initial cervical resorption cavity gradually spreads
• Progress in apical & coronal direction – leading to root fracture
Clinical Findings:
• Expanding lesion- show as a “pink spot” next to cervical margin
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45. External Cervical Resorption
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.
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46. External Cervical Resorption
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Endodontic Implications:
• Pathology entirely related to PDL defect
• Does not need endodontic treatment primarily
• When invasive nature finally encroaches pulp - need endodontic treatment.
Treatment Objectives:
• Arrest resorptive process
• Restore damaged root surface
• Prevent further resorption
• Improve esthetics of tooth (in cases where resorption has led to a pink spot)

47. External Cervical Resorption
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Treatment:
• Essentially, treatment involves complete removal of the resorptive tissue and restoring the
resulting defect with a plastic tooth-coloured restoration.
• Endodontic treatment also be required in cases in which the ECR lesion has perforated the
root canal.
[ Ingle ]

48. External Cervical Resorption
Treatment:
• Heithersay recommended - topical application of a 90% aqueous solution of trichloroacetic
acid, curettage, and restoration with glass ionomer cement.
• Trichloroacetic acid 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
[ JOE 35; 5; 2009 ]
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49. Internal Resorption
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Resorption – Dr. Nithin Mathew
• Definition:
• Internal resorption is an unusual form of tooth resorption that begins centrally
within the tooth, apparently initiated in most cases by a peculiar inflammation of
the pulp
• Internal Root Resorption
• Internal surface resorption
• Internal infection related root resorption
• Internal replacement resorption
[ Shafer ]
[ Ingle ]

50. Internal Resorption
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Resorption – Dr. Nithin Mathew
Clinical Features:
• 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 “Pink Spot”
[ Ingle ]

51. Internal Surface Resorption
Etiology:
• Found in areas where revascularisation occurs
• Fracture lines of root fracture
• Apical part of root canal of luxated teeth undergoing revascularisation
Pathogenesis:
• Osteoclastic activity is part of the process along with formation of granulation
tissue
[ Ingle ]
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52. Difference b/w Internal & External Resorption
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INTERNAL EXTERNAL
• Margins are smooth & clearly defined • Borders irregular & ill defined
• Root canal walls appear to balloon out
• Outline of root canal distorted • Outline of root canal is normal
• Root canal & resorptive defect appear
continuous
• Root canal is seen running through the defect
• Radiolucency confined to root (does not
involve bone)
• Almost always accompanied by resorption of
bone
• Bone lesion seen-only if resorption perforate
tooth
• Radiolucency appear in root and adjacent bone
• Lesion appear close to root canal in different
angulations
• Lesion moves away from canal as angulation
changes
Radiographic Features

53. Pharmacological Management of Inflammatory Response
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• Drugs that affects osteoclasts present at the site of resorption :
• Tetracyclines
• Sustained antimicrobial effect
• Anti-resorptive properties
• Direct inhibitory effect on osteoclasts and collagenase
• Significantly more cemental healing
• Drugs that affect the recruitment of osteoclasts to the injury site :
• Glucocorticoids
• Topical dexamethasone was found to be useful while systemic usage was not
• Bisphoshonates
• Alendronate
• Amino acids
• Taurine

54. Pharmacological Management of Inflammatory Response
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• Combination of the two types of drugs
• Synergistic effect on the inhibition of root resorption
• Ledermix
• A drug combining tetracycline and corticosteroids