Resorption Classification Guide

Resorption – Dr. Nithin Mathew
“What We Do Not See Does
Not Mean It Does Not Exist”
- Graber
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
3

• Mineralized tissues of teeth are protected
• In pulp cavity by : Predentine and odontoblasts
• On root surface by : Precementum and osteoblasts
• If protected structures are damaged / removed, multinucleated cells (osteoclasts) colonise root
surface and cause resorption.
[ Gulabiwala ]
4

Definitions – Tooth Resorption
• 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.
[ American Association of Endodontists ]
• Resorption affecting the cementum or dentin of the root of a tooth. [ Cohen ]
• Destruction of the cementum or dentin by cementoclastic or osteoclastic activity.
[ Medical Dictionary ]
5

Classification
1. Andreason
2. Lindskog
3. Cohen
4. Fuss et al
5. Based on histopathological presentation
6. AAE
7. AAE (modified by Cohen & Burns)
8. Weine
9. Ingle
10. Tronstad
11. Bakland
12. Maurice
13. Martin & Trope ( Seltzer & Bender)
14. Hartsfield
15. Gutmann
16. Heithersay
7

Andreason’s Classification
• Internal
• Inflammatory
• Replacement
• External
• Surface
• Inflammatory
• Replacement
8

Lindskog’s Classification
i. Trauma Induced Tooth Resorption
• Surface
• Transient
• Pressure
• Orthodontic
• Replacement
ii. Infection Induced Tooth Resorption
• Internal inflammatory (infective) resorption
• External inflammatory resorption
• Communicating internal-external inflammatory resorption
[ Australian Dental Journal Endodontic Supplement 2007 ]
9

Lindskog’s Classification
iii. Hyperplastic Invasive Tooth Resorption
• Internal (invasive) replacement resorption
• Invasive coronal resorption
• Invasive cervical resorption
• Invasive radicular resorption
[ Australian Dental Journal Endodontic Supplement 2007 ]
10

Cohen’s Classification
i. Based on nature
• Pathologic
• Physiologic
ii. Based on anatomical region of occurrence
• Internal
• External
iii. Based on causes
• Local
Inflammatory
 External
• Apical
• Lateral
• Cervical
 Internal
• Local
Pressure
• Orthodontic tooth movement
• Impacted tooth
• Tumours/cyst
Replacement or dentoalveolar ankylosis
• Systemic
• Idiopathic
11

Classification by Fuss et al
i. Pulpal infection
ii. Periodontal infection
iii. Orthodontic pressure
iv. Impacted tooth or tumour pressure
v. Ankylosis
vi. Idiopathic
[ Dental Traumatology 2003 ]
12

Classification based on Histopathological Presentation
i. Internal Root Resorption
• Metaplastic Resorption
• Inflammatory Resorption
ii. External Root Resorption
• Surface Resorption
• Replacement Resorption
iii. Invasive Root Resorption
iv. Idiopathic Root Resorption
[ Ne et al, Quintesscence International, 1999 ]
13

Classification by AAE
i. Internal Resorption
• Root Canal Replacement Resorption
• Internal Inflammatory Resorption
• Dentoalveolar Resorption
iii. Pathologic Root Resorption
14

Classification by AAE (Modified by Cohen & Burns – 1984)
i. Idiopathic Resorption
ii. Inflammatory Resorption
• External Root Resorption (Apical, Lateral, Cervical)
• Internal Root Resorption
iii. Pressure Resorption
• Orthodontic Tooth Movement Resorption
• Resorption Due To Impacted Tooth
• Resorption Due To Tumours/Cysts
iv. Dentoalveolar Ankylotic Replacement Resorption
v. Resorption Due To Systemic Causes
15

Tronstad’s Classification (1988)
• Inflammatory
• Progressive
• Transient
• Internal
• Perforating
• Non-perforating
16
[ Endod Dental Traumatol, 1988 ]

Bakland’s Classification (1992)
• Internal
• External
• Surface
• Replacement
• Inflammatory
• Pressure
• Systemic Conditions
• Cervical / Invasive
• Idiopathic
17

Weine’s Classification
• Internal
• Perforating
• Non Perforating
• External
• Mild Resorption
• Aggressive Resorption
18

Ingle’s Classification
i. Internal Resorption
• Infection 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
19

Maurice’s Classification (1999)
i. Physiologic Resorption
ii. Pathologic Resorption
• External Resorption Associated With Traumatic Injuries
• External Resorption From Pulp Necrosis & Periradicular Pathosis
• External Resorption From Pressure In Periodontal Ligament
• Cervical Resorption (Progressive External Inflammatory Resorption)
20

Martin & Trope’s Classification (Seltzer & Bender)
i. External Root Resorption
• Caused By Injury Restricted To External Root Surface
• Caused By Injury To External Root Surface + Inflammatory Component
ii. Internal Root Resorption
iii. Resorption Due To Systemic Factors
21

Hartsfield’s Classification (2004)
I. Based on anatomical region of occurrence and pathological correlation
i. Internal root resorption
 Internal replacement resorption (Metaplastic)
 Internal inflammatory resorption
• Transient
• Progressive
 Cervical root resorption
• With vital pulp
• Invasive cervical resorption
iii. External apical root resorption
22

Hartsfield’s Classification (2004)
II. Based on clinical and histological manifestations
i. External surface resorption
ii. External inflammatory root resorption
iii. Replacement resorption
iv. Ankylotic resorption
23

Gutmann’s Classification (1999)
I. Internal Resorption
 Root Canal Replacement Resorption
 Internal Inflammatory Resorption
II. External Resorption
 External Surface Resorption
 External Inflammatory Root Resorption
• Cervical
• Apical
 Ankylosis
 External Replacement Resorption
III. Transient Apical Breakdown
IV. Combined Internal And External Resorption
24
[ Quintesscence International, 1999 ]

Heithersay’s Classification (Invasive Cervical Resorption)
Class I
Small, invasive resorptive lesion near the cervical area with
shallow penetration into the dentin
Class II
Well defined, invasive resorptive lesion that has penetrated close
to the coronal pulp but with little or no extension into the
radicular dentin
Class III
Deeper invasion of root dentin by resorbing tissues that extend
into the coronal third of the root
Class IV
Large, invasive resorptive process that extend beyond the coronal
third of the root.
25

Factors Associated with Resorption of Dentoalveolar Complex
i. Physiologic resorption
ii. Local factors :
i. Periapical inflammation
ii. Dental trauma
iii. Tumors/cysts
iv. Excessive mechanical/ occlusal forces
v. Impacted teeth
vi. Intracoronal bleaching
vii. Periodontal procedures
iii. Systemic conditions :
i. Hormonal imbalance
ii. Paget’s disease
iii. Herpes zooster
26

Protective Mechanisms Against Resorption
• Remnants of HERS surround the root like a net.
• Imparting a resistance to resorption and subsequent ankylosis
• Based on the premise that the cementum and predentin covering the dentin are essential
elements in the resistance of the dental root to resorption.
27
[ Trope et al, Seltzer and Bender ]

• 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.
28

• 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.
29
RANKL : Receptor Activator of Nuclear Factor - kappaB Ligand

• 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.
31

• 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.
32

Prerequisites for Resorption
1. Loss / alteration of the protective layer ( Precementum / Predentin )
2. Inflammation must occur at the unprotected root surface.
33

Mechanism of Root Resorption
2 Phases
Injury Stimulation
34

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
35

Stimulation
• 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)
36

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
37

Sequence Of Events Leading To Root Resorption
38
• 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.

• Key Cells involved are
• Osteoclasts
• Odontoclasts
• Monocytes and Macrophages
39

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.
40

Osteoclasts
• For binding of osteoclast – various RGD – peptide containing proteins are necessary :
• Osteopontin
• Bone Sialoprotein
• Fibronectin
• Vitronectin
41

OSTEOPONTIN
• Important role in regulating osteoclast recruitment and activation by binding to the
osteoclast integrin receptor.
• 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
42
[ Seltzer & Bender ]

Odontoclasts
• Cells that resorb dental hard tissues
• Similar to the osteoclasts.
• Smaller in size
• Contain fewer nuclei than the osteoclasts.
43

Macrophages
• Similar structure to osteoclasts
• Can also become multinucleated giant cells
• Lack a ruffled border
• Do not create lacunae on the dentinal surface
44

Resorption
• Resorptive process is said to be a BIMODEL PROCESS :
• Dissolution of the Inorganic Crystal Structure
• Degradation of the Organic Structure of Collagen, Principally Type I
45

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.
46
CO2
H2CO3
CA II [ Proton pump provides steady source of H+ ions ]

ii. Degradation of the Organic Structure
• Three groups of Proteinase enzymes are involved:
• Collagenases (act at neutral pH)
• Matrix metalloproteinases (act at neutral pH)
• Cysteine proteinases (act at acidic pH).
47

ii. Degradation of the Organic Structure
• Cysteine proteinases appear to work closer to the ruffled border, where the pH is more acidic.
• Cysteine proteinases are secreted directly by the osteoclasts into the clear zone via the ruffled
border.
• Collagenases appear to be active at the resorbing bone surface, where the pH is closer to
neutral because of the buffering capacity of the dissolving bone salts.
48

Regulating Factors
• Systemic Regulating Factors:
• Parathyroid Hormone (PTH)
• 1,25-Dihydroxy Vitamin D3 [1,25(OH)2D3]
• Calcitonin
• Local Regulating Factors:
• Macrophage Stimulating Factor
• Interleukin 6
• Interleukin 1
• Tumor Necrosis Factor – α
• Prostaglandins
• Bacterial Toxins
49

Systemic Regulating Factors
• Parathyroid Hormone (PTH):
• Simulation of osteoblasts : Increase the production of neutral protease inhibitor and
matrix deposition.
• Direct action on the osteoclasts to increase CA II activity.
• Promotion of the fusion of marrow cells, leading to the formation of multinucleated
giant cell of osteoclastic phenotype.
50

Systemic Regulating Factors
• 1,25-Dihydroxy Vitamin D3 :
• Increases the resorbing activity of osteoclasts already present, without increasing
osteoclastic numbers
• Calcitonin:
• Inhibits resorption by inhibiting cytoplasmic mobility and producing cell retraction.
51

Local Regulating Factors
• Macrophage Stimulating Factor:
• Proliferation, differentiation and survival of osteoclasts
• Interleukin 6 :
• Acts on the osteoblastic stromal cells to induce osteoclast differentiation factor.
• Which recognizes osteoclastic progenitors and prepares them to differentiate into
mature osteoclasts.
• Serum levels of IL-6 are increased in several metabolic bone diseases.
52

• Interleukin 1:
• Osteoclast formation, differentiation and activation.
• Stimulates the production and release of prostaglandin E2 (PGE2)
• Tumour Necrosis Factor – alpha (TNF-α) :
• Stimulate osteoclastic activity
53

• Prostaglandins:
• PGE2
• Stimulates formation of osteoclasts
• Enhancing the fusion of osteoclastic precursors
• Increases the resorbing activity of existing cells
54

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.
55

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
57

Diagnosis
• Advanced Diagnostic aids includes
• Cone Beam Computed Tomography (CBCT)
• Dental Panoramic Tomography
• True Cephalometry Skull
• Optical Coherence Tomography
58

External Resorption
• Definition:
• Loss of cementum and/or dentin from the roots of the teeth originating in the PDL.
• 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
60
[ Chivian et al 1991 ]

EXTERNAL RESORPTION
61
External Surface Resorption (Repair Related)

• Small, superficial resorption cavities in the cementum and the outermost 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
• Subluxation
• Lateral luxation
• Intrusion
• Replantation of avulsed teeth
62
[ Andreason & Hjorting – 1966 ]
[ Ingle ]

• Resorption also occur frequently after
• 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
63

[ Seltzer & Bender ]
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
64
[ Ingle ]

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.
65

PRESSURE
• Due to excessive forces of
• Impacted teeth or from tumors or cysts.
• Pressure damages the cementum and provides the continuous stimulus for the
resorbing cells.
66

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
67

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.
68

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.
69

Endodontic Implication:
• Primarily periodontal injury – endodontic intervention not indicated
Treatment:
• If trauma/pressure eliminated – almost 100% repair
• If root apex resorbed - excessive mobility becomes a problem, if root is shorter than 12 mm
70
[ Ingle ]

EXTERNAL RESORPTION
71
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.
72
[ Ingle ]

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.
73
[ Ingle ]

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 )
74

Clinical Findings:
• Increased mobility
• Dull percussion tone
• Sometimes tooth extruded
• No response to sensibility testing
• Sometimes sinus tract develop
75

• Diagnoses 2-4 weeks after injury
• Appear as progressive cavitation involving root & adjacent alveolar bone
• Resorption progress rapidly - resulting in total loss of root structure after
only a few months (particularly in young children)
76
[ Ingle ]

77
Endodontic Implication:
• Resorption – combined periodontal & pulpal injury
• Require immediate endodontic therapy - to remove osteoclast promoting factors
(bacterial toxins)
Treatment:
• Remove /destroy bacteria in root canal & dentinal tubules.
• Allow healing in entire periradicular region.
• Bacteria in root canal best destroyed by Ca(OH)2.
• If Ca(OH)2- used for more than 30 days – weakening of root structure of immature teeth -
causes cervical root fracture.

78
Treatment:
• Mature teeth:
• Prophylactic extirpation of pulp in replanted avulsed teeth
• Biomechanical preparation
• Ca(OH)2 intra canal medicament- 2-3 weeks
• Obturation

79
Treatment:
• Immature teeth (open apex):
• Ca(OH)2 (apexification) – disadvantage – takes many months to obtain apical
barrier
• Long term use weaken dentin - by dissolving its organic component
• MTA – used as physical barrier apically – root canal filling can be placed
immediately without waiting for biologic response.
• In mature teeth – weakening does not occur.

Prognosis:
• Dentin lost by resorption cannot be replaced by new dentin
• Healing occurs – by arresting resorption process & replacement with either a layer of
new cementum & bone and establishment of new PDL
• Amount of healing – 88%
80
[ Abou et al 2007, Chadwick et al 2007 ]

EXTERNAL RESORPTION
81
External Trauma Related Replacement Resorption
(Ankylosis)

External Trauma Related Replacement Resorption (Ankylosis)
Etiology:
Severe Trauma :
• 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 root surface.
82

Moderate trauma :
• Initial ankylosis occurs
• If tooth is allowed functional mobility - non-rigid splint/no splinting
Small areas :
• Resorption can be replaced with new cementum and PDL (transient ankylosis).
Extensive Injury (>4mm2) :
• Progressive ankylosis occur
• Tooth becomes an integral part of bone
• Healing occurs by cells from alveolar wall (Ankylosis occur).
83

• Osteoclast is exposed to stimulating factors & other soluble molecules in dentin :
• Insulin Growth Factor
• Transforming Growth Factor
• Platelet Derived Growth Factor
• Bone Morphogenic Protein
• Fibroblast Growth Factor
• These molecules stimulate cementoblasts & osteoblasts.
84

• Younger Individuals :
• Progressive ankylosis - very active
• Lead to gradual infraocclusion
• Arrested development of alveolar process
• Loss of ankylosed teeth within 1-5 years
• Older Individuals :
• Replacement resorption is slower
• Allow tooth to function longer periods (5-20 yrs)
• Position of tooth in arch remains same
85

Clinical Findings :
• Appear firm in socket
• High metallic sound on percussion
• This can be demonstrated 4-6 weeks after trauma.
Radiographic Findings :
• Diagnosed radiographically within 2 months after injury.
• Clinically identified within one month – high percussion sound.
86

Endodontic implications :
• Endodontic therapy- cannot arrest progressive ankylosis related resorption
• In vital pulp - no endodontic procedure
• In pulp necrosis - root canal treatment
87
[ Ingle ]

Endodontic treatment:
• Thorough debridement and preparation of the root canal system
• Sequential use of
• 17% EDTAC (ethylenediaminetetraacetic acid plus cetavlon)
• 1% sodium hypochlorite and
• a final rinse with EDTAC solution
• most effective regimen resulting in a dentine surface devoid of smear layer.
• Facilitates the diffusion of medicaments (Ledermix paste) through dentine to the
external root surface
88
[ Australian Dental Journal Endodontic, 2007 ]

Treatment:
• Decoronation - to maintain & augment alveolar process
• Suitable in children & adolescence when significant remaining
alveolar growth expected.
• In adolescents – ankylosed tooth fail to erupt (infra
position)
• Younger the age – more pronounced infraposition
• Procedure:
 Removal of tooth crown (slightly below cervical bone
level) leaving remaining part of root
89
[ Dental Traumatology , 2007; 23: 87–94 ]

• 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.
90

• Treating The Root Canal
• Allow continued vertical growth of alveolus
• Remaining root maintain labiolingual content of alveolar process
91

EXTERNAL RESORPTION
92
External Spontaneous Ankylotic Resorption

Etiology:
• Ankylosis affect one or a few primary /permanent teeth
• Etiology unknown
• Suspected to be related to RANK- RANKL – OPG system.
Pathogenesis:
• Ankylosis related resorption causes -
• Infraposition of involved teeth in young individuals
• In all cases root substance is substituted with bone
93
[ Ingle ]
[ Ingle ]

Clinical Findings:
• Primary dentition
• Affects primary molars
• Mandibular second primary molar most affected (20%)
• Ankylosis – gradual infra position & tilting of neighbouring teeth
• Permanent dentition
• First & second permanent molars – most affected
• In young individuals - shows a gradual infraposition
• Percussion tone - high & metallic
94

• Ankylosis process starts at interdental area
• Gradually spreads to remaining part of root
• First molars – shows replacement resorption starting in intraradicular area
• Gradually spreads to remaining part of root
• Semi impacted /impacted third molar – shows ankylosis in rare cases
95
[ Ingle ]

Treatment:
• If diagnosed early - Decoronation
• If diagnosed late in adolescence - crown is rebuilt to prevent overeruption of antagonist
• If diagnosed early - extract ankylosed tooth
• In later stage - crown is rebuilt to achieve a functional occlusal level
96
[ Ingle ]

EXTERNAL RESORPTION
97
External Multiple Sites of Ankylosis
(Infection Related)

External Multiple Sites of Ankylosis (Infection Related)
Etiology:
• Rare type of root resorption
• Could be a defect in RANK – RANKL – OPG system
• Hereditary background - found in some cases
Pathogenesis:
• Any permanent tooth may involve
• Process takes place over 10-20 yrs
• Usually affect single group of teeth (premolar/molar) and gradually affects other group
of teeth.
98
[ Ingle ]

• Cervical invasive resorption cavities involving multiple teeth
• Resorption process expands over time in all directions
• Eventually it causes breakdown of involved teeth
99
[ Ingle ]

Endodontic Implications:
• Endodontic treatment not indicated
• Endodontic treatment promote resorption process
Treatment:
• Currently no treatment available
• Gradual replacement of involved teeth with implants are the only available treatment
100
[ Ingle ]

EXTERNAL RESORPTION
101
External Cervical Resorption

Heithersay’s Classification
Class I
Small, invasive resorptive lesion near the cervical area with
shallow penetration into the dentin
Class II
Well defined, invasive resorptive lesion that has penetrated close
to the coronal pulp but with little or no extension into the
radicular dentin
Class III
Deeper invasion of root dentin by resorbing tissues that extend
into the coronal third of the root
Class IV
Large, invasive resorptive process that extend beyond the coronal
third of the root.
102

Etiology:
• Defect in cementoblast layer in its RANK-RANKL-OPG system
• Heithersay et al – studied 259 teeth with invasive cervical resorption –
• 23% : related to orthodontic treatment
• 15% : acute trauma
• 14% : cervical restoration
103
[ Ingle ]

Predisposing Factors:
• Trauma
• Intracoronal bleaching
• Surgical procedures
• Periodontal therapy
• Other factors:
• Bruxism, intracoronal restorations, developmental defects, systemic diseases.
104

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
105

• Cervical bowl-shaped lesion is the start of invasive progression of
resorption in coronal & apical direction.
• Pulp canal not invaded in initial phase.
106

• 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)
107

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.
108
[ Ingle ]

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
109
[ JOE 35; 5; 2009 ]

Internal Resorption
• 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 surface resorption
• Internal infection related root resorption
• Internal replacement resorption
111
[ Shafer ]
[ Ingle ]

Internal Resorption
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”
112
[ Ingle ]

INTERNAL RESORPTION
113
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
114
[ Ingle ]

• Appears to be a temporary widening of root canal
• Resorption process - is a sign of progressing pulp healing.
• Any endodontic intervention may arrest this process.
Treatment:
• No treatment except periodic observation
115
[ Ingle ]

Transient Apical Internal Resorption
• Another form of trauma induced non-infective root resorption identified by Andreasen in 1986.
• Resorption follow luxation injuries
• Recognized by a confined periapical radiolucency which resolves within a few months.
• There may be associated colour change due to intra-pulpal haemorrhage.
• This resolve spontaneously if revascularisation to the coronal pulp chamber occurs
116
[ Australian Dental Journal Endodontic 2007 ]

Transient Apical Internal Resorption
• In the longer term, (transient process), the internally resorbed apex will close uneventfully.
117
Radiograph taken 1 year after the original
trauma shows resolution of the apical
internal resorption and no other signs of
periradicular pathosis

INTERNAL RESORPTION
118
Internal Infection Related Resorption

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 & diseased pulp
Pathogenesis:
• Resorption process – gradually expand – leading to fracture of
root
119
[ Ingle ]

Treatment:
• Endodontic treatment is appropriate
• Require technique that allows management of resorbed area
• Thermoplastic obturation
120
[ Ingle ]

• Internal inflammatory resorption may be classified according to location :
• Apical
• Intraradicular
Apical :
• Study showed that 74.7 % of teeth with periapical lesions had varying
degrees of apical internal resorption.
• Radiographically, apical internal resorption is difficult to diagnose when
the resorptions are of the lower grades.
121
[ Int Endod J 2004;37 ]

Intraradicular :
• Internal resorption fully contained within an intact root
• Round or oval shaped radiolucencies contained within the tooth root
122

Treatment:
• Defect not perforated the root to the periodontal ligament :
• Obturation with warm guttapercha technique.
• 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.
123
[ Cohen ]

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.
124
Radiograph taken 2 years later showing
periradicular repair and control of the root
resorption.

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.
125

INTERNAL RESORPTION
126
Internal Replacement Resorption

Etiology:
• Damage to pulp tissue usually related to trauma.
• When damaged pulp tissue replaced as a part of healing process – tissue
metaplasia occurs – formation of bone tissue in pulp canal
• Damaged pulp tissue – replaced with an ingrowth of new tissue, includes
bone derived cells.
Pathogenesis:
• Root will gradually be replaced with bone
• In some cases bone replacement will spontaneously arrest
127
[ Ingle ]

Clinical Findings:
• Teeth asymptomatic
• If ankylosis develop – teeth gradually develop infraocclusion
• A dissecting resorptive area- seen in root canal initially
• Root canal appears intact
128
[ Ingle ]

Treatment :
• Pulpectomy, curettage of the resorptive defect and root filling
• Generally control the resorptive process as soon as possible
129

Treatment :
In extensive cases:
• Resorptive tissue may communicate with the periodontal ligament
• Pulpectomy supplemented by the careful topical application of 90%
aqueous trichloracetic acid to the defect
• This inactivate any communicating resorptive tissue
• Insert conventional root filling
• In communicating lesions - MTA may be used to seal the defect prior to
the placement of a root filling.
130

Physiologic Root Resorption
• Entirely normal process
• Happens with the timely loss of deciduous teeth
• Occurs during the exfoliation of the primary dentition and eruption of
permanent successors
• Occurs in three separate phases
• Active
• Partial
• Reparative
131

Pathologic Resorption due to Systemic Causes
• Resorption occurs at the apex of several teeth and is bilateral
• Hypo parathyroidism
• Hyper parathyroidism
• Calcinosis
• Turner’s syndrome
• Paget’s disease
• Following radiotherapy
• Renal distrophy
• Genetic factors
132

Difference b/w Internal & External Resorption
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
133
Radiographic Features

Pharmacological Management of Inflammatory Response
• 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
134

Pharmacological Management of Inflammatory Response
• Combination of the two types of drugs
• Synergistic effect on the inhibition of root resorption
• Ledermix
• A drug combining tetracycline and corticosteroids
135

ART - Antiresorptive Regenerative Therapy (Pohl et al 2005)
• Comprises a combination of different treatment strategies for a synergistic effect :
• Local application of a glucocorticoid
• Systemic and local application of Tetracyclines
• Use of Enamel Matrix Derivative (EMD) e.g. Emdogain
• Emdogain (Enamel Matrix Protein)
• Makes the root more resistant to resorption
• Stimulates the formation of new periodontal ligament from the socket
136

AAE Guidelines (Management of External Root Resorption)
137
Unfavorable:
Structural integrity of the tooth or
root is compromised
• There are deep probing depths
associated with the resorptive
defect
• The defect is not accessible for
repair surgically
Favorable:
Minimal loss of tooth structure
• Located cervically but above
the crestal bone
• The lesion is accessible for
repair
• Apical root resorption
associated with a tooth
exhibiting pulp necrosis and
apical pathosis
Questionable:
Minimal impact on restorability of
tooth
• Crown lengthening or
orthodontic root extrusion may
be required
• The pulp may be vital or necrotic

Conclusion
• The diagnosis of dental resorptions and an understanding of the underlying pathosis is critical to
clinical management.
• Most infection related resorption respond well to endodontic treatment.
• Early diagnosis and prompt treatment are the key factors which determine the success of the
treatment.
138

References
• Ingle
• Cohen
• Seltzer & Bender
• Weine
• Gulabiwala
• Harty
• Nisha Garg
139

Resorption – Dr. Nithin Mathew 140

Resorption Classification Guide

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