Guide to Tooth Resorption: Causes, Types, Mechanisms

CONTENTS
 INTRODUCTION
 DEFINITIONS
 CLASSIFICATION OF TOOTH RESORPTION
 CELLS INVOLVED IN TOOTH RESORPTION
 ETIOLOGY
 FACTORS REGULATING TOOTH RESORPTION
 MECHANISM OF TOOTH RESORPTION
 EXTERNAL RESORPTION

 EXTERNAL SURFACE RESORPTION
 EXTERNAL INFLAMMATORY ROOT RESORPTION
 EXTERNAL REPLACEMENT RESORPTION
 EXTERNAL CERVICAL RESORPTION
 INTERNAL RESORPTION
 APICAL ROOT RESORPTION
 IDIOPATHIC APICAL ROOT RESORPTION
 TRANSIENT APICAL BREAKDOWN
 CONCLUSION
 REFERENCES

INTRODUCTION
Tooth resorption can be physiological or pathological
Physiologic resorption is seen in primary teeth that results in their exfoliation and
allows eruption of their permanent successors.
Pathologic resorption can occur following traumatic injuries, orthodontic tooth
movement, or chronic infections of the pulp or periodontal structures.
Pathologic resorption if untreated will result in the premature loss of the affected teeth

TOOTH IS NORMALLY RESISTANT TO RESORPTION
HOW?
Trope et al, Seltzer and Bender. Root Resorption due to Dental Trauma Endodontic Topics 2002, 1,
79–100
Remnants of HERS surround the root like a net - imparting a resistance to
resorption and subsequent ankylosis
HYPOTHESIS I
HERS cells produce specific matrix proteins like osteopontin, ameloblastin and bmp –
imp role in cemental repair and are antiresorptive factors

HYPOTHESIS II
Cementum and Predentin covering on dentin are
essential elements in the resistance of the dental root
to resorption
Prevents External Root Resorption

If an injury removes or alters the (protective) pre-dentin or pre-
cementum, inflammation of the pulp or periodontium will induce
root resorption with multinucleated clastic cells similar to those
seen in bone resorption

HYPOTHESIS III
OSTEOPROTEGRIN (OPG)
Ability to inhibit osteoclasts mediated bone loss.
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.

• RANK (Receptor Activator of Nuclear Factor): produced by osteoclast
• RANKL (Receptor Activator of Nuclear Factor Ligand) and OPG: produced by
osteoblasts and are liberated into tissue, which attaches to the receptors of the
mononuclear/macrophage progenitor cells

Osteoclastogenesis is the result of differentiation of mononuclear/macrophage
progenitor cells and fusion of these cells to become osteoclasts. The commitment of
these cells to become osteoclasts depends on the activation of the RANK receptors
on the surface of RANKL, that is produced by stroma cells and osteoblast
Mononuclear/macrophage cells aggregate, fuse, and form osteoclast.

Inhibition of resorption
OPG binds and neutralizes RANKL, leading to a block in osteoclastogenesis
and decreased survival of osteoclast.

HYPOTHESIS IV
Highly calcified intermediate cementum
Creates a barrier between the dentinal tubules and the
periodontal ligament.
This barrier does not allow irritants such as bacterial by-products to pass
from an infected pulp space to stimulate an inflammatory response in the
adjacent periodontal ligament

Osteoclasts will not adhere to or resorb unmineralized matrix
The most external aspect of cementum is covered by a layer of
cementoblasts over a zone of non-mineralized cementoid, a surface
that provides satisfactory conditions for osteoclast binding is not
present.

DEFINITION
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 ]
Dental resorption is the loss of dental hard tissues as a result of clastic activities. It may occur
as a physiologic or pathologic phenomenon.
[ Cohen ]
Destruction of the cementum or dentin by cementoclastic or osteoclastic activity.
[ Medical Dictionary ]

ANDREASON’S CLASSIFICATION (1970)
Internal
• Inflammatory resorption
• Replacement resorption
External
• Surface resorption
• Inflammatory resorption
CLASSIFICATION

COHEN’S CLASSIFICATION
1.Based on nature
• Pathologic
• Physiologic
2. Based on the anatomical region of occurrence
• Internal root resorption
• External root resorption

3.Based on cause
• Local causes of root resorption
a) Pressure
i. Orthodontic tooth movement
ii. Impacted teeth
iii. Tumours or cysts
b) Inflammation
i. External
• Apical
• Lateral
• Cervical
ii. Internal
c) Dentoalveolar ankylosis and replacement resorption
• Systemic causes
• Idiopathic resorption

WEINE’S CLASSIFICATION
Internal
• Perforating
• Non Perforating
External
• Mild Resorption
• Aggressive Resorption

INGLE’S CLASSIFICATION
Internal Resorption
– Surface Resorption
– Infection Resorption
– Replacement 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

CLASSIFICATION BY AAE
Internal Resorption
– Root Canal Replacement Resorption
– Internal Inflammatory Resorption
– Surface Resorption
– Inflammatory Resorption
– Replacement Resorption
– Dentoalveolar Resorption
Pathologic Root Resorption

Idiopathic Resorption
Inflammatory Resorption
External Root Resorption (Apical, Lateral, Cervical)
Internal Root Resorption
Pressure Resorption
Orthodontic Tooth Movement Resorption
Resorption Due To Impacted Tooth
Resorption Due To Tumours/Cysts
Dentoalveolar Ankylotic Replacement Resorption
Resorption Due To Systemic Causes
CLASSIFICATION BY AAE
(MODIFIED BY COHEN & BURNS –1984)

Internal Resorption
– Root Canal Replacement Resorption
– Internal Inflammatory Resorption
External Resorption
– External Surface Resorption
– External Inflammatory Root Resorption
• Cervical
• Apical
– Ankylosis
– External Replacement Resorption
Transient Apical Breakdown
Combined Internal And External Resorption
GUTMANN’S CLASSIFICATION (1999)
[ QUINTESSCENCE INTERNATIONAL, 1999 ]

Caused By Injury Restricted To External Root Surface
Caused By Injury To External Root Surface + Inflammatory Component
Internal Root Resorption
Resorption Due To Systemic Factors
MARTIN & TROPE’S CLASSIFICATION
(SELTZER AND BENDER)

• Pulpal infection
• Periodontal infection
• Orthodontic pressure
• Impacted tooth or tumor pressure
• Ankylosis
• Idiopathic
CLASSIFICATION BY FUSS ET AL (2003)
(Based on stimulation factors)

Based on anatomical region of occurrence and pathological correlation
 Internal root resorption
Internal replacement resorption (Metaplastic)
Internal inflammatory resorption
Transient
Progressive
 External Root Resorption
Cervical root resorption
With vital pulp
Invasive cervical resorption
 External apical root resorption
HARTSFIELD’S CLASSIFICATION (2004)

II. Based on clinical and histological manifestations
• External surface resorption
• External inflammatory root resorption
• Ankylotic resorption

Trauma Induced Tooth Resorption
• Surface
• Transient
• Pressure
• Orthodontic
• Replacement
Infection Induced Tooth Resorption
• Internal inflammatory (infective) resorption
• External inflammatory resorption
• Communicating internal-external inflammatory resorption
LINDSKOG’S CLASSIFICATION
[ Australian Dental Journal Endodontic Supplement 2007 ]

Hyperplastic Invasive Tooth Resorption
• Internal (invasive) replacement resorption
• Invasive coronal resorption
• Invasive cervical resorption
• Invasive radicular resorption

A NEW ROOT RESORPTION CLASSIFICATION BASED ON CLINICAL FEATURES AND AETIOLOGICAL
EVALUATIONS
HFA, Diogo P, Santos JM. Root Resorption Classifications: A Narrative Review and a Clinical Aid Proposal for Routine
Assessment. Eur Endod J 2018; 3: 134-45

CELLS INVOLVED IN RESORPTION –COHEN
Osteoclasts
 Motile, multinucleated giant cells that are responsible for bone resorption.
 They are formed by the fusion of mononuclear precursor cells of the monocyte-
macrophage lineage derived from the spleen or bone marrow
 Osteoclasts are recruited to the site of injury or irritation by the release of many
proinflammatory cytokines
 To perform their function, osteoclasts must attach themselves to the bone surface.
 On contact with mineralized extracellular matrices, the actin cytoskeleton of an
actively resorbing osteoclast is reorganized to produce an organelle-free zone of
sealing cytoplasm (clear zone/Sealing zone) associated with the osteoclast’s cell
membrane

 This enables the osteoclast to achieve intimate contact with the hard tissue surface
 The clear zone surrounds a series of fingerlike projections (podosomes) of cell
membrane, known as the ruffled border, beneath which bone resorption occurs
 The resorptive area within the clear zone, therefore, is isolated from the extracellular
environment, creating an acidic microenvironment for the resorption of hard tissues.

Odontoclasts
 They are the cells that resorb dental hard tissues are morphologically similar to
osteoclasts.
 Odontoclasts differ from osteoclasts in that they are smaller, have fewer nuclei, and
have smaller sealing zones.
 Osteoclast and odontoclast resorb their target tissues in a similar manner.
 The two cells have similar enzymatic properties,show similar cytological
features,and create resorption depressions termed Howship lacunae on the surface of
the mineralized tissues

ETIOLOGY OF TOOTH RESORPTION
LOCAL CAUSES
– Sharp injuries
– Chronic injuries
– Trauma
– Damage of periodontium after teeth replantation
– Malocclusion
– Improper habits
– Too much force in orthodontic treatment
– Teeth whitening

• Biological treatment with calcium hydroxide
• Delayed or irregular eruption of permanent teeth
• The pressure of the tumor or cyst
• Iatrogenic action, e.g. thermal pulp damage
• Dental abnormalities, e.g. invaginated teeth
• Periodontitis, incorrect execution of periodontal treatment (scaling, root planning)
• Different dental materials (eg. silver nitrate, silicate cements)

SYSTEMIC CASES
– Hormonal disorders, e.g. hyperthyroidism and hypoparathyroidism
– Hypertension
– Atherosclerosis
– Paget’s disease
– Papillon-Lefevre syndrome
– Stevens-Johnson syndrome
– Hepatic impairment
– Kidney disease
– Bone dysplasia
– Genetic disorders

‾ Vitamin A deficiency
‾ Pregnancy
‾ Shingles
‾ Gancher’s disease
‾ Turner’s syndrome
‾ Kabuki syndrome (the presence of a number of external root resorptions of the
lower central incisors and molars)
‾ Radiotherapy

MECHNANISM OF TOOTH RESORPTION
Resorptive process is said to be a BIMODAL PROCESS
• Dissolution of the Inorganic Crystal Structure
• Degradation of the Organic Structure of Collagen, principal Type I

Dissolution of the inorganic crystal structure of hydroxyapatite
• The activated osteoclasts produce an acidic pH (3.0 to 4.5) in their
microenvironment.
• At pH 5.0 or lower, the solubility of hydroxyapatite increases dramatically, and
resorption of hard tissue can occur.
• This acidic environment is primarily achieved through the action of a highly
active polarized proton pump contained within the ruffled border.

• The enzyme carbonic anhydrase II (CA II), which is specific to osteoclasts, also
plays a critical role in establishing a subosteoclastic acidic pH.
• The CA II catalyzes the intracellular conversion of CO2 to H2 CO3, which provides a
readily available source of H+ ions to be pumped into the sub-osteoclastic region
CO2 + H2 O = H2 CO3
H2 CO3 H+ + HCO3 –

Degradation of the organic matrix
The degradation of the organic matrix is accomplished by three groups of proteinase
enzymes:
 Collagenases
 Matrix metalloproteinases (MMP)
Both of which act at neutral or just below neutral pH (7.4), and
 Cysteine proteinase family, which act at an acidic pH

• The cysteine proteinases appear to work closer to the ruffled border, where the pH is
more acidic
• Cysteine proteinases are secreted directly by the osteoclast into the clear zone via the
ruffled border.
• The 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.

 Degradation of inorganic matrix via Carbonic Anhydrase II (CA II)
 Disintegration of organic matrix via Cysteine Proteases (CP), Collagenase
(CL) and MMPs

FACTORS REGULATING TOOTH RESORPTION
• Systemic Regulating Factors:
• Parathyroid Hormone (PTH)
• 1,25-Dihydroxy Vitamin D3
• Calcitonin
• Local Regulating Factors:
• Macrophage Stimulating Factor
• Interleukin 6
• Interleukin 1
• Tumor Necrosis Factor – α
• Prostaglandins
• Bacterial Toxins

Parathyroid hormone (PTH)
Increase in the circulating concentration of PTH promote bone résorption by increasing
both the number of cells present and the rate of activity among individual clastic cells.
The effect of PTH appears to be multifactorial:
• stimulation of osteoblasts using a receptor-mediated,cAMP-dependent pathway
to increase the production of neutral proteases and to decrease the amount of
protease inhibitor and matrix deposition;
• direct action on the osteoclast to increase CA II activity by cAMP-mediated
phosphorylation of the enzyme
• promotion of the fusion of marrow cells, leading to the formation of
multinucleated giant cell of osteoclastic phenotype.

l,25-dihydroxyvitamin D3
• The major effect of l,25-dihydroxyvitamin D3 is to increase the resorbing activity of
osteoclasts already present, without increasing osteoclastic numbers.
• The exact mechanism of action, however, remains unclear

Calcitonin (CT)
Calcitonin inhibits résorption by inhibiting cytoplasmic motility and producing cell
retraction.
• This effect occurs at minimal concentration of CT and is highly sensitive,
prolonged, and modulated through a specific receptor unique to the osteoclast.
• The inhibitory action of calcitonin has also been demonstrated on cells actively
resorbing tooth structure

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

Interleukin 1
 First bone-resorbing cytokines to be identified
 Osteoclast formation, differentiation and activation.
 Stimulates the production and release of prostaglandin E2 (PGE2)
Tumour Necrosis Factor – alpha (TNF-α)
Stimulate osteoclastic activity
Prostaglandins: PGE2
 Stimulates formation of osteoclasts
 Enhancing the fusion of osteoclastic precursors
 Increases the resorbing activity of existing cells

Bacteria’s Role in Tooth Resorption
Two possibilities exist for the mechanism of bacteria induced resorption:
 Bacteria produce acids and proteases that destroy the bone matrix components
 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.

RESORPTIVE FACTORS
 Parathormone
 Vit D3
 Interleukin – 1,6
 Tumor Necrosis Factor
 Leukemia Inhibitory
factors
 Glucocorticoids
ANTIRESORPTIVE FACTORS
 Calcitonin
 Estrogen
 Calcium
 Bone Morphogenic
Protein
 Transforming Growth
factor (TGF)
 Interleukin – 17
 Platelet growth factors
 Bisphosphonates

EXTERNAL ROOT RESORPTION
External resorption is defined as the loss of cementum and/or dentin from the roots of
the teeth originating in the periodontal ligament.
[ Chivian et al 1991 ]
ETIOLOGY
• Periodontal disease
• Luxation injuries
• Hypoparathyroidism
• Hyperthyroidism
• Turners syndrome
• Paget’s disease
• Gaucher’s disease
• Radiation therapy

CLASSIFICATION
According to Cohen, depending on the basis of location, 3 types are:
• Cervical
• Lateral
• Apical
According to Rita F Ne, Guttman et al as given in quintessence International 1999,
Classification is of 3 types by clinical and histologic manifestation.
• Surface resorption.
• External inflammatory root resorption.
• Replacement resorption.

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.
[ Andreason & Hjorting – 1966 ]
Etiology:
Caused by injury restricted to external root surface.
Resorption can occur due to-
ACUTE CAUSES
Concussion
Subluxation
Lateral luxation
Intrusion
Replantation of avulsed teeth
[ Ingle ]

CHRONIC CAUSES
– 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

PRESSURE
Due to excessive forces of
• Orthodontic tooth movement
• Impacted teeth or from tumors or cysts.
Pressure damages the cementum and provides the continuous stimulus for the resorbing
cells.
Removal of the stimulation factor i.e pressure is the treatment of choice for resorption
caused by pressure due to orthodontic tooth movement, impacted tooth or tumor
Fuss et al. Root resorption – Diagnosis, classification and treatment options based on
stimulation factors. Journal of Dental Traumatology, 2003

ORTHODONTIC TOOTH MOVEMENT
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, more the resorption
- Intermittent forces cause less severe root resorption
It mostly affects apical third of the root
Teeth are usually asymptomatic and pulp is mostly vital unless the pressure is high, which disturbs
the apical blood supply
Removal of pressure causes cessation of resorption, thereby root canal treatment is not required

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

PATHOGENESIS:
Injury causes:
• Attachment damage
• Loss of protective layer-serve as inflammatory stimulus
[Seltzer & Bender]
• Injured tissue–adjacent to root and surface cementum– removed by macrophages
& osteoclasts.
• Exposed cementum and dentin release growth factors which trigger periodontal
ligament specific cells to repair the site.
• New cementum is formed with insertion of PDL fibres
[Ingle]

Surface resorption can be transient or progressive.
• In the transient variety, the tooth has a vital, healthy pulp that has recovered
from traumatic event. In such cases, the resorbed area will be restored
completely to normal surface contour by deposition of new cementum.
• In the progressive type, the surface resorption is the beginning of more
destructive resorption, either inflammatory resorption or replacement
resorption

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- slight
cavitation's may be seen on the root surface.
• Most repair related root surface resorption–have limited size and cannot be detected
radiographically.

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
12mm

EXTERNAL INFLAMMATORY TOOTH RESORPTION
• Classically, this type of external root resorption occurs when infection is
superimposed on a traumatic injury – usually following replantation of an avulsed
tooth or a luxation injury.
• It can also be induced in some cases of endodontic pathosis

According to Ingle
• 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 with in few months.
• Most common after intrusion & replantation of avulsed tooth.

• External inflammatory resorption may occur anywhere along the length of the tooth root –
typically it occurs laterally and apically following trauma but when the resorption occurs
as a result of a long-standing infected root canal system, it usually occurs apically.
• It is capable of advancing rapidly such that an entire root surface may be resorbed if left
untreated
According to Cohen,

Traumatic injuries
Contusion injuries to the periodontal ligament
Damage to pericementum
Damaged cementum and bone phagocytosed
Expose underlying dentin & dentinal tubules to osteoclastic
activity
Toxins from bacteria present in the dentinal tubules and/or the
infected root canal diffused via the exposed tubules to the PDL
Pathogenesis (Cohen)

continuation of the osteoclastic process and an associated
inflammation in the PDL,.
Resorption of adjacent alveolar bone
Odontoclast bind to and resorb underlying dentin
Resorption of dentin and exposed root canals

It requires the following two things to occur
1. The root canal system is infected or has been
contaminated with bacteria
2. There has been mechanical damage to the cementum
during the trauma or cementum has been lost as a
result of external surface resorption such that the
dentinal tubules are exposed to the surrounding
periodontal ligament (PDL) and bone
Abott PV, Prevention and management of external inflammatory resorption following trauma to
teeth, Australian Dental Journal 2016; Volume 61: 82-64.

Histologic Features (Cohen)
• Saucer or bowl-shaped areas of resorption in both the cementum and dentin, with
concomitant inflammation in the adjacent periodontal membrane.
• Howship lacunae occupied by odontoclasts.
• Intense inflammatory reaction consists of a mixed-cell infiltrate that includes
plasma cells, lymphocytes, and polymorphonuclear leukocytes in a granulation
tissue matrix.
• Proliferation of capillaries in the areas of inflammation is also a feature
EIR can be identified histologically 1 week after replantation

Clinical Findings:
• Increased mobility
• Dull percussion tone
• Sometimes tooth extruded
• No response to sensitivity testing
• Sometimes sinus tract develop
Radiographic Findings:
• Diagnoses : 2-4 weeks after injury
• Characterized by radiolucent, concave and sometimes ragged bowl shaped excavations
along the root surface with associated radiolucency in the adjacent alveolar bone
• Complete loss of lamina dure in the area of resorption

Prevention and Management
• Treatment for inflammatory resorption is based on removal or reduction of source of
infection – infected necrotic pulp tissue in the root canal space
• This arrests resorption and creates an environment conducive to hard tissue repair of
damaged root surface
• Therefore, it is essential to initiate root canal treatment as soon as radiographic signs
of EIR is identified
• Earlier the diagnosis – better the prognosis
• Extraction – EIR is extensive rendering the tooth unsalvageable

IMMATURE TEETH
Apexification procedures using calcium hydroxide have been performed with good
success.
The disadvantage
 it takes many months to obtain enough of an apical barrier.
 Longterm use (>30 days) of Ca(OH)2 can weaken dentin, possibly by dissolving its
organic component and thereby resulting in cervical root fracture on even slight
impacts or normal use. .(Andreasen et al 2002)
Therefore, MTA as a physical barrier apically, a root canal filling can be placed
immediately without waiting for a biologic response

MATURE TEETH
• Prophylactic extirpation of the pulp in replanted avulsed teeth.
• Biomechanical canal preparation should include the use of sodium hypochlorite
and Ca(OH)2 intracanal medicament placement
• The latter can be expected to have accomplished its task of disinfection so that the
canal can be filled 2 to 3 weeks after treatment

Management strategies
There are two distinct situations when external inflammatory resorption needs to be
managed.
• The first situation is following injuries that are likely to predispose a tooth to
inflammatory resorption where pulp necrosis is very likely to occur and where
there is very likely to be damage to the root surface
• In this situation, the management strategies should be considered as a preventive
approach to reduce the possibility of inflammatory resorption developing.

• The second situation is where external inflammatory resorption has already
commenced and interceptive treatment is required to arrest the resorption and
encourage repair of the PDL and adjacent bone.
• The resorption may occur following trauma (typically on the lateral surfaces of the
root or it may occur as a result of a longstanding infection within any root canal
system, in which case the resorption usually occurs apically
Abott PV, Prevention and management of external inflammatory resorption following
trauma to teeth, Australian Dental Journal 2016; Volume 61: 82-64.

• Systemic antibiotics – start IMMEDIATELY
This preventive treatment should form part of the emergency management of the
tooth as soon as possible after the injury – i.e. once the injuries have been
assessed, the tooth has been repositioned and stabilized(e.g. with a splint) and the
soft tissues have been stabilized (e.g. with sutures).
• Immediate commencement of root canal treatment is recommended in order to
prevent the development of external inflammatory resorption.
• A corticosteroid/antibiotic paste (e.g. Ledermix paste) can be placed as soon as
possible in order to reduce the inflammation and to inhibit bacteria and clastic
cells.
• A corticosteroid/ antibiotic paste (i.e. Ledermix paste) is recommended for the first
3 months
PREVENTIVE MANAGEMENT

• Two dressings for 6 weeks each should be used in fully developed teeth, and three
dressings for 4 weeks each in incompletely developed teeth
• Following the 3-month period for initial healing, a periapical radiograph should be
taken to assess whether external inflammatory resorption is occurring. If there is
inflammatory resorption evident, then Ledermix paste should be used for a further 3
months .
• Calcium hydroxide can be introduced as part of the medicament by using it in a 50:50
(approximately) mixture with Ledermix paste. This combination reduces the toxicity
of the calcium hydroxide and thereby reduces the chance of ankylosis and
replacement resorption occurring

• This combination of materials also increases the antibacterial spectrum compared to
when Ledermix paste is used alone, plus the hard tissue healing effects of calcium
hydroxide can begin to work.
• A further advantage of the mixture is that the calcium hydroxide slows down the
release and diffusion of the active components of Ledermix paste, which results in
them remaining in the root canal system for a longer period of time – up to 3 months
maximum.
• Hence, a period of 2–3 months with the 50:50 mixture of Ledermix paste and calcium
hydroxide can be used to encourage further PDL healing prior to completing the root
canal filling

• If there is no resorption (inflammatory or replacement), then the root canal filling
can be placed in fully developed teeth using gutta percha and cement
• Some cases will require the formation of an apical hard tissue barrier (e.g.
incompletely developed teeth requiring apexification) before the root canal filling
can be completed.
• MTA or Biodentine can be used for apexification

INTERCEPTIVE MANAGEMENT OF ESTABLISHED
INFLAMMATORY RESORPTION
• When external inflammatory resorption is already present, the root canal system will
be pulpless and infected or it may have a previous root canal filling and an infected
root canal system, plus the tooth will have some form of apical periodontitis.
• When external inflammatory resorption is present, root canal treatment is the
treatment of choice in order to salvage the tooth.
• If there is insufficient tooth structure, then the tooth should be extracted.

The general principles are similar to the preventive approach but with two major
differences.
• Firstly, systemic antibiotics are not indicated unless the patient has an acute condition with
systemic signs of infection – such as malaise, increased body temperature, lymph node
involvement, or a rapidly spreading infection (i.e. cellulitis).
In these cases, systemic antibiotics are used to control the systemic manifestations of the
infection only and they will not stop the inflammatory resorption
• Secondly, all cases with established external inflammatory resorption will have already lost
hard tissue – both tooth and bone.

• Hence, one of the aims of interceptive treatment is to encourage repair of the lost hard
tissues and the PDL.
• The most effective material for this is calcium hydroxide as long as it is not used in the early
stages of the treatment.
• It is likely to be needed for periods of 6–12 months, with the medicament being changed
every 3 months, following the initial use of Ledermix paste alone and then the 50:50
mixture of Ledermix with calcium hydroxide.
• Once there are radiographic signs of hard tissue repair, the root canal filling can be
completed and appropriate restoration of the tooth.
• Typically, the average treatment time for the interceptive management of established
external inflammatory resorption is about 12–15 months.

Role of antibiotics in the management of inflammatory resorption
• In 1986, Hammarstreom et al. reported that the immediate use of systemic antibiotics (penicillin and
streptomycin) prevented external inflammatory resorption.
(Hammarstreom L, Bleomlof L, Feiglin B, Andersson L, Lindskog S. Replantation of teeth and
antibiotic treatment. Endodontics & Dental traumatology 1986; 2:51–57.)
• Sae- Lim et al. recommended the use of systemic tetracycline following avulsion
injuries to help prevent inflammatory resorption since tetracyclines inhibit clastic
cells to provide antiresorptive properties in addition to their antibacterial properties
(Sae-Lim V, Wang CY, Trope M. Effect of systemic tetracycline and amoxicillin on inflammatory
root resorption of replanted dogs’ teeth. Endodontics & Dental traumatology 1998; 14:216–220.)

• Tetracyclines also have other properties which make them useful
following trauma, especially when used within the tooth as intracanal
medicaments.
• These properties include substantivity and their bacteriostatic nature
• Tetracyclines also inhibit mammalian collagenases,
which imply that they can help prevent the breakdown of tissues.
Vernillo AT, Ramamurthy NS, Golub LM, Rifkin BR. Nonantimicrobial action of tetracyclines. Current
Opinion in Periodontolgy 1994; 2:111–118

Role of corticosteroids
• Potent inhibitors of inflammation and they also inhibit clastic cells to have
direct antiresorptive action
• When corticosteroids are used as an intracanal medicament during root canal
treatment, they are typically combined with an antibiotic. This combination of
drugs was first reported in 1961
• The effects of a commercially available corticosteroid/ tetracycline intracanal
medicament known as Ledermix paste on inflammatory resorption were
investigated by Pierce and Lindskog.
• This formulation was first recommended for use in endodontics by Schroder
and Triadan in 1960

• Ledermix paste, triamcinolone alone, or demeclocycline alone were placed
immediately into the root canals of replanted teeth and their effects were compared
histologically.
• The root surfaces of the teeth medicated with Ledermix paste, triamcinolone alone,
and demeclocycline alone all had statistically significantly more favourable healing
(75.8% of the root surface, 69.8%, 52.4%, respectively)
• Both Ledermix group and the triamcinolone group were significantly better than the
demeclocycline group
Chen H, Teixeira FB, Ritter AL, Levin L, Trope M. The effect of intracanal anti-inflammatory
medicaments on external root resorption of replanted dog teeth after extended extra-oral dry time.
Dental traumatology 2008;24:74–78.

Bryson E, Levin L, Banchs F, Abbott P, Trope M. Effect of immediate intracanal placement of
Ledermix paste on healing of replanted dog teeth after extended dry times. Dental traumatology
2002;18:316–321
• Studies have demonstrated that the sooner the anti-inflammatory agent is applied,
the more effective it will be – since the inflammatory reaction can be reduced
before it becomes well established with clastic cell activity.
• In addition, if bacteria are prevented from entering the root canal system, then
external inflammatory resorption cannot occur

• When Ledermix paste is placed in the root canal system of teeth, it releases its
active components (triamcinolone and demeclocycline), which then diffuse through
the dentine as well as through any lateral canals and the apical foramen to reach the
periradicular tissues.
• This diffusion increases if the cementum has been removed by trauma or by surface
resorption.
The tetracycline (antibiotic) component works mainly within the root canal system
itself – particularly in the dentine tubules by inhibiting bacterial growth.
The triamcinolone (corticosteroid) component works within the periradicular tissues
by reducing inflammation and inhibiting clastic cells.

• Ledermix paste maintains the release and diffusion process at therapeutic levels
for about 6 weeks in fully developed teeth and for about 4 weeks in incompletely
developed teeth.
• After these periods, the amount of each active component that is being released
is less than their therapeutic levels.
Hence, Ledermix paste intracanal dressings should be removed and replaced after
these time intervals so the treatment can continue to be effective
Abbott PV, Heithersay GS, Hume WR. The release and diffusion through human tooth
roots in vitro of corticosteroid and tetracycline trace molecules from Ledermix paste
Endodontics & Dental traumatology 1988;4:55–62

Role of calcium hydroxide
• It is a powerful antibacterial agent, it has no direct anti-inflammatory action
• When calcium hydroxide is used as a root canal medicament, it releases hydroxyl ion
which diffuse through the dentinal tubules and cementum to reach the PDL
• It can arrest inflammatory resorption by inhibiting the clastic cells

• The pH in the outer dentine can reach levels of approximately 8.0– 9.5, which is higher
than the level at which attachment and growth of human PDL fibroblasts decreases(i.e.
7.8).
• Calcium hydroxide is a relatively toxic material which induces cell necrosis when the
cells come into contact with it.
• Calcium hydroxide can also affect PDL healing in this way and the response favours
ankylosis and replacement resorption

• The loss of the protective cementum layer in the region of the resorption may predispose
the tooth to ankylosis and replacement resorption if calcium hydroxide is used in the
early stages of treatment, as shown by Bryson et al.
• This effect is greatly reduced if calcium hydroxide is applied later, once the
inflammation has resolved through the earlier use of the corticosteroid-antibiotic
compound
Bryson E, Levin L, Banchs F, Abbott P, Trope M. Effect of immediate intracanal placement of
Ledermix paste on healing of replanted dog teeth after extended dry times. Dental traumatology
2002;18:316–321.

• Serious condition for the teeth involved because the teeth become part of the alveolar
bone remodelling process and they are therefore resorbed.
• It occurs most frequently as a result of complication following avulsion in which the
periodontal ligament dries and loses its vitality
EXTERNAL REPLACEMENT RESORPTION

• This PDL complication represents a sequel to a defect in or injury to the PDL cells,
including the cell layer next to the cementum.
• The most frequent cause appears to be acute trauma (severe luxations such as lateral
luxations, intrusions, and replantation of avulsed teeth).
• In those situations, the homeostasis of the PDL is lacking.
• Healing events from the bony alveolus result in creation of a bony bridge between the
socket wall and the root surface

• In situations of moderately sized injuries (1–4 mm2), an initial ankylosis forms.
• If the tooth is allowed functional mobility by the use of a nonrigid splint or no
splinting, small areas of resorption can later be replaced with new cementum and PDL
attachment (transient ankylosis).
• In more extensive injuries (> 4 mm2), a progressive ankylosis takes place. This
implies that the tooth becomes an integral part of the bone remodeling system.
• The entire process includes osteoclastic resorption dependent on remodeling
processes, parathyroid hormone induced resorption, remodeling owing to function and
resorption owing to bacteria present in the gingival area and the root canal.

• All of these processes are very active in children and lead to gradual infraocclusion
and arrested development of the alveolar process.
• As a result, this combination of resorption processes leads to loss of ankylosed teeth
within 1 to 5 years.
• In older individuals, replacement resorption is significantly slower and often allows a
tooth to function for much longer periods of time (ie, 5–20 years), and the position of
the tooth in the arch remains the same (similar to an implant).
Finucane and Kinirons. External inflammatory and replacement resorption of luxated and avulsed
replanted incisors: a review and case presentation. Journal of Dental Traumatology. 2003

CLINICAL FINDINGS
• The tooth appears very firm in its socket, eliciting a high metallic sound on
percussion.
• Patients with replacement resorption are symptom-free.
• This can be demonstrated 4 to 6 weeks post-trauma.
• Infraocclusion and arrested development of the alveolar process.
• In children, replacement resorption leads to loss of ankylosed teeth usually
within 1-5 years. In adults, replacement resorption occurs more slowly, often
allowing the tooth to function for many years

RADIOLOGIC APPEARANCE
• Radiographically there will be total loss of the image of the
periodontal ligament followed by evidence of the
progressive replacement of tooth structure by bone – in time
the image of the tooth root is lost.
• Moth eaten appearance with irregular border, absence of
periodontal ligament and lamina dura is seen.
• Loss of periodontal ligament space with replacement of
bone in association with an uneven contour of root is
indicative of ankylosis

ETIOPATHOGENESIS
• In dentoalveolar ankylosis, the injury results in damage to periodontal ligament
cells and cementum, causing discontinuity in the cementum.
• The cells present in vicinity of the denuded root try to repopulate it.
• Bone precursor cells are more active than the slower moving periodontal ligament
cells.
• They move across the socket wall and populate the damaged root without an
intermediate attachment apparatus.
• Because of this, the bone comes in direct contact with root without an intermediate
attachment apparatus.
• This results in dentoalveolar ankylosis

DIAGNOSIS
• Diagnosis can be made from clinical evaluation and radiographic observation.
• Lack of mobility and high pitched metallic sound on percussion of tooth are often
characteristic feature of ankylosis
• It can usually be diagnosed radiographically within 2 months after injury and
clinically within 1 month by a high percussion sound.

TREATMENT
In adolescents, the ankylosed tooth will fail to erupt and will gradually go
into infraposition. The younger the age, the more pronounced is the infraposition.
Presently, there are five treatment approaches:
1. Decoronation (to maintain and augment the alveolar process)
2. Luxation of the tooth (breaking of ankylosis sites)
3. Vertical distraction
4. Prosthetic elongation
5. Acceptance of the resorbing tooth
Of the above approaches, the decoronation treatment is very suitable in children and
adolescence, when significant remaining alveolar growth is expected.

Decoronation
• The procedure involves removal of the crown of the tooth (leaving what remains of the
root), allowing continued vertical growth of the alveolus
• The extraction of teeth with ankylosis and replacement root resorption promotes greater
post-surgical alveolar bone loss than the extraction of teeth with preserved periodontal
ligament
• With the immediate application of the implants after decoronation, the bone volume and
soft tissue maintenance, vertically and horizontally, is further favored, benefiting the
proper restoration of aesthetics and function
Consolaro A, Ribeiro Júnior PD, Cardoso MA, Miranda DAO, Salfatis M. Decoronation followed by dental
implants placement: fundamentals, applications and explanations. Dental Press J Orthod. 2018

Focal areas of
replacement
ankylosis in the
maxillary second
premolar
Decoronation in the
maxillary second
premolar, with
replacement resorption,
preparing it to receive
an implant in the region.
Installation of an implant in the
region.
The replacement of dental
remnants will follow its natural
course and will not disrupt
osseointegration

• Intentional replantation with the application of Emdogain is a possible treatment
approach to preserve teeth with small areas of ankylosis.
• Emdogain was developed in 1992 with the purpose of regenerating the lost
periodontium.
• When it is applied, amelogenin matrix protein precipitates out of the solution and forms
an insoluble layer on the root surface promoting the attachment of the mesenchymal
cells.
• These cells then produce new matrix component and growth factors, which play major
role in formation of new periodontal attachment.
Filippi A, Pohl Y, Von Arx T, Treatment of replacement resorption by intentional replantation, resection of the
ankylosed sites, and Emdogain – results of a 6-year survey, Dental Traumatology 2006; 22: 307–311.
EMDOGAIN

• Emdogain also inhibits epithelial cell growth which could interfere the regenerative
process.
• It promotes both proliferation and differentiation of osteoblastic cells and inhibits
the formation of osteoclasts by stimulating the effect of osteoprotegrin (OPG).
• Emdogain may also act as growth factor which prolongs the osteoblast growth and
maintains their morphology

Calcitonin
• It is a proven potent inhibitor of clastic cells and has been indicated for the treatment of
external RR.
• The influence of this hormone as an intracanal dressing after tooth replantation has been
investigated, and it has been observed that it causes a decrease in inflammatory RR and better
control of the sequelae of dental trauma even in cases with uncertain prognosis
• The CH/calcitonin combination was seen to be more effective in controlling inflammatory RR
compared to the use of these medications alone.
• This is because of the recognized capacity of reducing the osteoclastic activity, interfering in
the proliferation, motility, and vitality of these cells, and reducing the resorption rate.
Mohammadi et al. Management of Root Resorption Using Chemical Agents: A Review.
Iranian Endodontic Journal, 2016

ALENDRONATE
The mechanism of osteoclast inhibition by alendronate has been attributed to
 Decrease in osteoclast activity with minimal effects on recruitment
 Interference of receptors on the osteoclasts for specific bone matrix proteins
 Promoting the production of an osteoclast-inhibitor by osteoclasts which reduces
the life span and/or the number of differentiated osteoclasts
 Obstruction of resorption by interfering with the ruffled border of the osteoclast
Lustosa-Pereira et al indicated that sodium alendronate was able to reduce the incidence of
radicular resorption, but did not reduce dental ankylosis
Lustosa-Pereira A et al. Evaluation of the topical effect of alendronate on the root surface of extracted and
replanted teeth. Microscopic analysis on rats' teeth. Dent Traumatol. 2006;22(1):30-5.

EXTERNAL CERVICAL ROOT RESORPTION
Also called
 Invasive cervical resorption
 Peripheral inflammatory root resorption (PIRR)
 Supraosseous extracanal invasive resorption
 Subepithelial external root resorption
• Invasive cervical resorption is a clinical term used to describe a relatively uncommon, insidious
and often aggressive form of external tooth resorption, which may occur in any tooth in the
permanent dentition

DEFINITION
According to Heithersay
External root resorption associated with marginal periodontitis without pulpal involvement
is most commonly referred to as cervical invasive root resorption.
According to Cohen
It is a form of root resorption that originates on the external root surface but may invade
root dentin in any direction and to varying degrees.
ECR generally develops immediately apical to the epithelial attachment of the tooth

ETIOLOGY
• Not been fully elucidated
• It is accepted that the resorptive process is the same for ECR as it is for any other type of
resorption
• The anatomic profile of the cementoenamel junction (CEJ) is variable, and the junction
between the enamel and the cementum in this region is not contiguous in all teeth. This
may lead to exposed areas of unprotected dentin, which are vulnerable to osteoclastic
activity, in the cervical region of some teeth
• May possibly be related to a defect in the cementoblast layer in its RANK-RANKL-
OPG system

ORAL SURGERY
PERIODONTAL
THERAPY
ENAMEL
STRIPPING
BLEACHING
DELAYED
ERUPTION
INTRACORONAL
RESTORATION
ORTHODONTIC
TREATMENT
DEVELOPMEN
TAL DEFECTS
BRUXISM
TRAUMA
POTENTIAL
PREDISPOSING
FACTORS

In a large clinical study of 259 teeth with invasive cervical resorption, Heithersay found
that
 23% were related to orthodontic treatment,
 15% to acute trauma,
 14% to a cervical restoration.
 Oral surgery 6%
 Intracoronal bleaching 5%
Other factors:
 Periodontal therapy
 Bruxism,
 Intracoronal restorations,
 Delayed eruption,
Geoffrey S Heithersay. Invasive Cervical Resorption. Journal of Endodontic topics. 2004
Heithersay G, Invasive cervical resorption, Endodontic Topics, Volume 7, Issue 1, March 2004

PATHOGENESIS
• The initial cervical resorption cavity gradually spreads and may progress in both an
apical and a coronal direction, leading eventually to a tooth fracture.
• There are conflicting views on the manner in which the resorptive process is
sustained once the clastic cells have bound to the root dentin in ECR.
• One view is that microorganisms originating from the gingival sulcus provide the
stimulus for continued resorption.
• The opposing hypothesis, by Heithersay, suggests that ECR is a type of “benign
proliferative fibrovascular or fibro-osseous disorder” in which microorganisms
play no active role and are either absent from the site of resorption or invade it only
secondarily.

HEITHERSAY’S CLASSIFICATION
(INVASIVE CERVICAL RESORPTION)
Class 1 Denotes a small invasive resorptive lesion near the
cervical area with shallow penetration into dentine
Class 2
Denotes a well-defined invasive resorptive lesion that
has penetrated close to the coronal pulp chamber but
shows little or no extension into the radicular dentine
Class 3
Denotes a deeper invasion of dentine by resorbing
tissue, not only involving the coronal dentine but also
extending into the coronal third of the root
Class 4 Denotes a large invasive resorptive process that has
extended beyond the coronal third of the root

Frank’ s classification
Based on the location of the portal of entry in the cementum
• Supraosseous- Coronal to the level of alveolar bone.
• Intraosseous- Not accompanied by periodontal breakdown.
• Crestal- At the level of alveolar bone

Three-dimensional classification of ECR
This new clinical classification takes into account the lesion height, circumferential spread and
proximity to the root canal and thus classifying ECR in three dimensions with the use of CBCT
and Periapical Radiograph
Patel et al. External cervical resorption: a three-dimensional classification. International
Endodontic journal, 2018

CLINICAL FEATURES
• The clinical features of ECR are variable .
• The process is very often quiescent and asymptomatic, especially in the earlier
stages, and absence of clinical signs and symptoms is very common;
• The diagnosis is commonly made as a result of a chance radiographic finding.
• A pink or red discoloration may develop at the cervical region of the tooth; when
present, this often is the feature that alerts the patient or clinician to the possible
existence of a problem.
• The discoloration is due to the fibrovascular granulation tissue occupying the
resorptive defect, which has a reduced thickness of enamel and dentin at its
peripheries because of the loss of hard tissue

The granulation tissue imparts a pink hue to the
tooth, through the thinned enamel and dentin, in the
region of the resorption.
The granulation tissue may perforate the enamel or
dentin at the gingival margin, giving the appearance
of mild gingival hyperplasia.
The discoloration, sometimes referred to as a “pink
spot,” can be quite subtle and is often a chance
finding by the patient, or the dentist However, it is a
relatively rare feature of ECR.

• Furthermore, it must occur at a site where it is readily identifiable (e.g., labial
surface of an anterior tooth) to be noticed. Loss of periodontal attachment may
occur in the region of the resorption, and probing of the resorptive defect or the
associated periodontal pocket causes the granulation tissue to bleed profusely.
• As the process progresses, perforation of the root canal wall and bacterial
contamination of the pulp may occur. The affected tooth may develop pulpitis and
the associated clinical symptoms.
• Pulp necrosis and chronic periapical periodontitis may eventually develop.

Histologic Appearance
Similar to that of other forms of resorption, with certain unique features reflecting the
invasive nature of the process.
• In the early stages, granulation (fibrovascular) tissue occupies the resorptive cavity,
and odontoclasts may be evident in lacunae on the resorbing front of the defect.
• Acute inflammatory cells are often absent in the early stages but secondary bacterial
colonization of the site of resorption may occur at a later stage.
• Narrow “channels” of resorption extend through the dentin and may communicate
with the periodontal ligament.

• However, perforation of the root canal wall usually occurs only at a late stage
because the predentin affords protection against the resorbing cells.
• Consequently, the pulpal tissue adjacent to the site of resorption has a normal
histologic appearance until the root canal has been invaded
• As the lesion progresses, bonelike tissue is deposited in the resorptive cavity in
direct contact with the adjacent dentin; this is an attempt to repair the previous
tissue destruction.

RADIOGRAPHIC FEATURES - Cohen
The radiographic appearance of ECR depends on the
location,the extent of invasion, and the relative
proportions of fibroosseous and fibrovascular tissue
occupying the resorptive cavity.
All ECR defects present as a radiolucency of varying
radiodensity, often in but not confined to the cervical
region of the affected tooth or teeth.

• Cervical bowl-shaped lesion is the start of invasive progression of resorption in coronal & apical
direction. Pulp canal not invaded in initial phase.
• The lesion tends to be radiolucent when the defect is predominantly fibrovascular, granulomatous
tissue. However, in cases with some fibro-osseous inclusions (i.e., more longstanding lesions), the
radiolucency may adapt a more cloudy appearance.
• In advanced cases with extensive repair of the tissue destruction, significant deposition of fibro-
osseous tissue gives the defect a mottled radiographic appearance
• The margins of the lesion may vary from poorly to well defined, depending on the depth of the
defect and the proportion and distribution of osseous inclusions in the lesion.
• Although lesions with irregular margins are more common, some ECR defects may have smooth
and/or well-defined margins.

• The radiographic features of ECR are very similar to those of Internal Root Resorption
(IRR) and differentiating between them, especially in the absence of clinical signs,
may be challenging.
• It is useful to trace the outline of the root canal walls as they approach and pass
through the resorption defect on the radiograph.
• In cases of ECR, the outline of the canal wall should be visible and intact and should
maintain its course as it passes through the defect. This is due to the fact that the
resorptive lesion lies on the external surface of the root and is not in communication
with the root canal; it is merely superimposed on the defect radiographically.
• In cases of IRR, it should be possible to trace the outline of the root canal through the
resorptive defect because the defect is an extension of the root canal wall and is
continuous with it.

Although this is a useful diagnostic feature, it does have some shortcomings.
• First, the outline of the root canal wall may be obscured by calcified tissue in the
resorptive defect (ECR or IRR).
• Second, when ECR has resulted in extensive tissue destruction, perforation of the
root canal wall may have allowed communication between the canal wall and the
external defect.

Shift radiographs
 In cases of ECR, the position of the resorptive defect moves relative to the root
canal.
 If the lesion is located palatally/lingually, the defect moves in the same direction as
the x-ray tube shift.
 If the lesion is located buccally, it moves in the opposite direction.
 In contrast, internal resorptive defects maintain their position relative to the root
canal because the defects are an extension of the root canal system

CBCT
3D assessment of the nature, position, and extent of the resorptive defect, eliminating
diagnostic confusion and providing essential information about the restorability and
subsequent management of the tooth.

MANAGEMENT
The
fundamental
treatment
objectives in
ECR
Halt the
resorptive
process
Excavate the
resorptive
defect
Prevent and
monitor the
tooth for
recurrence.
Restore the
hard tissue
defect with an
aesthetic filling
material

Endodontic treatment - when the resorptive process has perforated the
root canal wall.
Surgical access by raising a mucoperiosteal flap
Resorptive cavity is excavated.
Fibrovascular granulomatous tissue removed with a hand excavator.
Fibro-osseous tissue removed with ultrasonic instruments

mucoperiosteal flap is replaced and secured in position.
Cavity is restored with an aesthetically acceptable restorative material, such as
composite resin or glass ionomer cement
Any undermined dentin or enamel removed with a bur in a high-speed
handpiece
The cavity treated with a 90% aqueous solution of trichloracetic acid

• Trichloracetic acid causes coagulation necrosis of the resorptive tissue without
damaging the periodontal tissue.
• The acid also penetrates and treats small channels of resorption that are not accessible
to mechanical instrumentation
• Biodentine may prove to be a particularly suitable material for restoring these defects
because it may combine acceptable aesthetics with the ability to support PDL
attachment.

• The root canal should be prepared in the area of the defect as normal, using saline as an
irrigant.
• A tapered gutta-percha (GP) point then should be placed in the canal to maintain its
patency and to provide a barrier against which the final restoration can be condensed.
• The rubber dam is removed, and surgical treatment of the resorptive defect can be carried
out as described, without any risk of the resorptive debris entering the root canal system.
• After repositioning of the mucoperiosteal flap, root canal treatment can be completed in
the normal manner.

Heithersay advocated a nonsurgical approach to the treatment of ECR. (Heithersay GS:
Invasive cervical resorption, Endod Topics 7:73, 2004.)
• The nonsurgical treatment involved the topical application of a 90% aqueous solution of
trichloracetic acid to the resorptive tissue, curettage, endodontic treatment where necessary,
and restoration with glass-ionomer cement.
• Adjunctive orthodontic extrusion was also employed in some advanced lesions.
• Heithersay by using the nonsurgical protocol referred to previously, related the success rates
for treatment to the classification of the lesion.
• He reported a 100% success rate for class I and class II lesions, a 77.8% success rate for class
III lesions, and a 12.5% success rate for class IV lesions.
• This emphasizes the poorer outcome that can be expected for more advanced cases.

Materials used
Several materials have been used to restore the resorptive defect after curettage, and many
materials continue to be tested for use in such conditions
• Amalgam, glass ionomer cement (GIC) and composite resins have been traditionally used
for restoration.
• However dentin that has been treated with TCA is severely demineralized and therefore
not suitable for bonded restorations like GIC or composite
• The dentin must be refreshed with a bur before bonding procedures.
• Resin modified glass ionomer cement (RMGIC) and composite resin have been used
because they are stronger, bond to tooth structure, and are relatively stable in oral cavity

Newer bioactive materials have been successfully used to treat cases of ICR.
MTA has been recommended because of its biocompatibility, good sealing ability,
moisture tolerance, and the environment it creates for favorable hard-tissue healing .
However, surface of MTA is rough and development of subgingival plaque could be a
problem.
Calcium enriched mixture (CEM cement), a novel bioactive material, has shown
favorable result in repair of resorptive defect as is able to induce hard tissue formation, has
shorter setting time than MTA, good handling characteristics, and produces no tooth
staining.(Asgary S, Ahmadyar M. Gen Dent. 2012

Combinations of different materials have also been used
 A Sandwich technique involving use of MTA, GIC and composite has been
reported.(Kqiku L, Ebeleseder KA, Glockner Oper Dent. 2012 )
 A ‘Reverse Sandwich technique’ has been used in another case where a layer of
microfilled composite is placed in the interior of the lesion, and RMGIC was used to
build-up rest of the defect.(Vinothkumar TS, Tamilselvi R, Kandaswamy D. J
Endod. 2011)
 Geristore is another resin modified glass ionomer that has been used in the
management of ICR (Krishnan U, Moule AJ, Alawadhi A. BMJ Case Reports, 2015)

• IOPAR - an oval radiolucent lesion in the middle third of the root canal of right maxillary
central incisor
• CBCT scan - defect was present at the palatal aspect approaching toward the center of the
canal in the middle third
• As the portal of entry was well within the bone, and could not be located through the root
canal system, extraction of the involved tooth after root canal therapy, followed by
debridement and obturation of the resorption defect, and replantation of the tooth was
planned.

Extraction showing the
resorption defect
Complete debridement of the
resorptive defect
Resorptive defect restored with
Biodentine
Preoperative radiograph
CBCT Sagittal section showing the
extent and location of the
resorption defect
Post-obturation radiograph

• The case was followed up clinically and radiographically, which showed satisfactory
results at 3, 6, 12 and 18 months post-operatively.
• There was no pain on percussion, percussion sound was normal; and radiographically there
was no sign of replacement resorption.
Radiograph at 18 months.

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 [Shafer]

Internal resorption was first reported by Bell in 1830.
Pink tooth of Mummery (1920), so called due to the presence of a pink discoloration on the
crown, is named after the anatomist Mummery
PREVALENCE
• Internal root resorption is considered rare, but the frequency of internal resorption is not
well known.
• The occurrence of internal resorption has been estimated to be between 0.01% and 55%,
depending on the inflammatory status of the pulp.
Nilsson E, BonteBonte E, Bayet F, Management of Internal Root Resorption on Permanent Teeth,
International Journal of Dentistry, 2013

According to Jeanneret, IRR is classified as (Based on location)
Type A (intracoronal resorption),
Type B (intra-root resorption),
Type C (resorption with perforation of the canal wall)
Types of Internal Root Resorption
2 types:-
• Internal root canal inflammatory resorption
• Internal root canal replacement resorption

• In the Inflammatory resorption, the resorptive process
of the intraradicular dentin progresses without adjunctive
deposition of hard tissues adjacent to the resorptive sites.
• The phenomenon is associated with the presence of
granulation tissues in the resorbed area and identifiable
with routine radiographs as a radio clear zone centered on
the root canal.

• In the Replacement Resorption, the resorptive
activity cause defects in the dentin adjacent to the
root canal, with concomitant deposition of bone like
tissue in some regions of the defect.
• It results in an irregular enlargement of the pulp
space with partially or fully obliterated area of the
pulp chamber

Pathogenesis
• For IRR to occur, the outermost protective odontoblast layer and the predentin of the
canal wall must be damaged, resulting in exposure of the underlying mineralized
dentin to odontoclast.
• For IRR to continue, the pulp tissue apical to the resorptive lesion must have a viable
blood supply; this provides clastic cells and their nutrients, and the infected necrotic
coronal pulp tissue provides stimulation for those clastic cells.
• Ultimately, if left untreated, the pulp tissue apical to the resorptive lesion undergoes
necrosis and the bacteria infect the entire root canal system, resulting in apical
periodontitis.

• It is caused by transformation of normal pulp tissue into granulomatous tissue with
giant cells, which resorb dentin.
• This transformation is thought to stem from chronic inflammation of the coronal pulp
caused by continuous bacterial stimulation.
• Trauma, caries and restorative procedures have been suggested to be contributing
factors, but it also occurs as an idiopathic dystrophic changes.

• The vascular changes in the pulp produce hyperaemia, causing an increased oxygen
tension resulting in low pH levels, thus attracting numerous macrophages to the site,
thereby piloting the onset of resorptive process .
• The connective tissue, following the resorptive activity, may undergo metaplasia to form
granulation tissue .
• Predominance of a progressing infection causes necrosis of the entire pulp tissue and
limits the resorptive process and this acts as a protective mechanism preventing its
progression.
• The presence of a collateral blood supply through an accessory canal from the
periodontal ligament to the resorption site can add to maintaining the resorptive process.

ETIOLOGY
• Etiology of internal root resorption (IRR) is quite unclear.
• Persistent infection of the pulp by bacteria causes the colonization of the walls of
the pulp chamber by macrophage-like cells.
• The attachment and spreading of such cells is the primary prerequisite for
initiation of root resorption.
• Trauma and pulpal inflammation/infection are the major contributory factors in
the initiation of internal resorption

Various etiologic factors have been proposed for the loss of predentin including
• Trauma
• caries
• periodontal infections
• excessive heat generated during restorative procedures on vital teeth,
• calcium hydroxide procedures
• vital root resections
• anachoresis
• orthodontic treatment
• cracked teeth
• idiopathic dystrophic changes in normal pulps
• Genetic factors

• The literature also cites the association of herpes zoster with resorption and the
degeneration of odontoblast due to systemic viral infection
• Solomon et al reported a case of internal resorption affecting 21 and 23, with a history of
herpes zoster affecting the maxillary branch of the left trigeminal nerve. (C.S Solomon, M.O
Coffiner and H.E Chalfin. Herpes zoster revisited:implicated in root resorption. JOE, 1986)
• The effect on the dental pulp could be possibly explained by the virus being attracted to the
nerve endings in the pulp .
• Ramchandani and Mellor and Wadden have also accounted cases of internal resorption
linked with herpes zoster infection. (Ramchandani et al. Herpes zoster associated with
tooth resorption and periapical lesions. British journal of oral and maxillofacial surgery.
2007)

Clinical Features
• Common in maxillary central incisors
• Can be found in all areas of root but most commonly found in
cervical region
• Asymptomatic until it has perforated and become necrotic
• Detected mainly through routine radiographs
• In the active stages of resorption, bacterial contamination of vital
pulpal tissue may cause an acute inflammatory response, leading
to clinical symptoms of pulpitis
• With progression, acute or chronic apical periodontitis may
develop.

• Sinus tract(s) may occur and may be associated with suppuration in the periapical tissues
or possibly at the site of a perforation of the root canal wall caused by the hard tissue
destruction.
• Extensive resorption of the coronal pulp may result in a pink or red discoloration visible
through the crown of the affected tooth - this is caused by granulomatous tissue
extending into and occupying the resorptive defect
• Progressive resorptions can result in extensive unrestorable tissue loss.
• At times an external communication can develop between the root canal and the
periodontal ligament, due to perforation of the root

RADIOGRAPHIC FEATURES
• Lesions of IRR present radiographically as radiolucencies of
uniform density that have a smooth outline and are symmetrically
distributed over the root of the affected tooth
• The authors further reported that the outline of the root canal wall
should not be traceable through the resorption defect because the
root canal wall balloons out.
• Other authors have described IRR lesions as oval, circumscribed radiolucencies in continuity
with the root canal wall.

• Internal inflammatory root resorption lesions are more likely be uniformly radiolucent,
whereas in internal replacement (metaplastic) root resorption, the defect has a somewhat
mottled or clouded appearance as a result of the radiopaque nature of the calcified
material occupying the lesion
• In single-rooted teeth with one root canal, the internal resorption starts out as a
symmetrical lesion in coronal pulp/crown area.
• However, in multirooted teeth with a wide pulp chamber, internal resorption begins at
one part of the chamber and spreads locally into the surrounding dentin.
• Diagnosis becomes a major challenge for resorptive defects on the facial/lingual/palatal
aspects, as they are often missed during examination

HISTOLOGIC APPEARANCE
• The pulp tissue next to the resorption showed hyperemia and varying degrees of
inflammation and infiltration of lymphocytes, macrophages, and neutrophilic
leukocytes.
• The odontoblast layer and predentin were absent from the affected dentinal wall
• The bacteria were located either in the dentinal tubules or in the necrotic part of the
coronal root canal.
• Osteoid or cementum-like tissue in some areas of the pulpal wall as well as small
calcifications in the pulp tissue

TREATMENT
Orthograde root canal treatment, with three options depending on the absence or
presence of perforation of the radicular wall
– complete root canal filling with guttapercha on nonperforated lesions
– combined guttapercha in the root canal and MTA fillings for the perforation area
– complete filling with a bioactive material (MTA or Biodentine) on apical
perforated lesions located in a short root length

• Surgical approach is needed when it is not possible to get access to the lesion
through the canal.
• Surgical treatment should always be performed in a second intention, after
orthograde treatment (or retreatment) has been performed, the coronal part of the
canal being filled.
• In these cases, because of the shape of the lesion, surgical approach allows to get
direct access to the lesion and to perform a mechanical cleaning of the resorbed
defect

CHEMOMECHANICAL INSTRUMENTATION
• There is no generally accepted protocol
• A great emphasis must be placed on the chemical dissolution of the vital and necrotic
pulp tissue.
• Therefore, irrigation with sodium hypochlorite is an important part of the treatment of
teeth with internal resorption.
• With large perforations, low-concentration hypochlorite solutions should be used and
other irrigants such as chlorhexidine should be considered.

• Given the inaccessibility of IRR defects to normal instrumentation and passive
irrigation, ultrasonic activation of irrigants should be considered an essential
step in the treatment of these cases
• In the treatment of internal resorption, the use of calcium hydroxide also has two
other important goals
• to control bleeding
• to necrotize residual pulp tissue and to make the necrotic tissue more
soluble to sodium hypochlorite

• In cases where the resorption has not perforated, it is usually enough to use calcium
hydroxide paste in the canal once from 1 to 2 weeks.
• This allows removal of the residual tissue at the next appointment by irrigation and
instrumentation.
• Ultrasonic is recommended both to facilitate tissue removal and for cleaning the
canal from all calcium hydroxide before permanent root filling.
• In perforated internal resorptions, calcium hydroxide treatment has been carried out
for extended time periods for up to 1 year to secure complete healing of the site of
perforation

• Root filling methods using warm guttapercha are generally preferred over other
techniques.
• However, in cases where the resorption has perforated, MTA should be considered
instead of gutta-percha because of its antimicrobial properties and better seal.
• MTA is also very well tolerated by the tissues
• A hybrid technique to obturate canals affected by perforating internal resorption also
may be used.
• In these cases the canal apical to the resorption defect is filled with GP.
• The GP can then be used as a barrier against which the MTA can be packed.

• Clinical situations arise in which a perforating resorptive defect causes extensive
dental hard tissue destruction that fails to respond to or is not amenable to repair with
an orthograde approach.
• Surgical treatment may be needed in these cases.
• MTA would be the material of choice to repair these perforations.
• A well-fitting, tapered GP point or an appropriately sized finger spreader is then
positioned in the canal to occlude it and to provide a barrier against which the MTA
can be packed once surgical access to the defect has been gained.
• The barrier also prevents inadvertent deposition of the MTA into the apical third of the
canal. The perforation is then exposed surgically and repaired with the MTA.

• The canal can be shaped, disinfected, and obturated with thermoplasticized GP
once the MTA has set.
• If the resorptive process has caused sufficient tissue destruction to render the
tooth unrestorable, extraction is the most appropriate treatment option.
• The presence of a perforating resorptive defect is certainly not a
contraindication to treatment, but a perforation of significant size will have a
bearing on the decision to surgically treat or extract the tooth

EXTERNALAPICAL ROOT RESORPTION
External apical root resorption is a pathological condition, characterized by the resorption of hard
tissues (cementum, dentin) and sustained by a local inflammatory reaction, in most cases because
of the presence of infected necrotic dental pulp, which is able to maintain the whole process.
Hammarstrom & Lindskog 1985
Also called
– Inflammatory root resorption of endodontic origin
– Apical inflammatory root resorption
– Apical external root resorption

ETIOLOGY
• Apical periodontitis is the major cause for apical external root resorption.
• Infected necrotic pulp
– Caries (predominant cause)
– Trauma
• Trauma
– Intrusive injuries
– Over instrumentation during endodontic therapy

CLINICAL FEATURES
• External apical root resorption is most frequently observed in the clinical practice.
• Communications are seen primarily through the apical foramina or, occasionally,
through accessory canals.
• It is more severe in the apical third than in the middle and cervical thirds of the root
canal.
• It is usually asymptomatic.
• Clinical symptoms associated with apical periodontitis are present.
• Necrotic pulps are more likely to demonstrate apical resorption

HISTOLOGIC APPEARANCE
Invariably resorption of root at the cementodentinal junction is routinely observed.
It can be of three types.
– Periforaminal resorption -Defined as the area of resorption not comprising the
outline of the foramen, but the surrounding area.
– Foraminal resorption -Defined as the resorption within the outline or perimeter of
the foramen.
– Combined

Apex with periforaminal resorption
involving more than half of the
radicular surface examined. The
resorption displayed a honeycomb
aspect.
Apex with foraminal resorption
involving 1/4-1/2 of the perimeter with
a not well defined, or even absent
outline of the interlacunae crests

PREVALENCE
Apical resorption is present in different degrees in almost all teeth exhibiting apical
periodontitis i.e. 83.2%-87.3% of roots associated with periapical lesions.
Apical internal resorption may also be present as a result of the advancement of
external apical resorption in 74.7% of roots associated with periapical lesions
Chivian N, Root resorption, Pathways of Pulp Cohen 5th edition

RADIOGRAPHIC APPEARANCE
• If there is slight resorption of the root at the cemento-
dentinal junction, radiographic features are usually not
apparent.
• If resorption is extensive, changes in the local anatomy
and loss in the normal apical root shape takes place –
apical remodeling.
• Widening of the periodontal ligament space is seen.
• There will be resorption of adjacent bone, typical of all
inflammatory resorption.

TREATMENT
• The conventional and preferred treatment protocol for a progressive EARR consists
of chemomechanical preparation of the root canal system including a short-term (1
month) dressing of creamy paste of calcium hydroxide (Ca(OH) 2) for bacterial
disinfection of the root canal space.
• The process is followed by a long-term dressing of densely packed Ca(OH)2 to
provide an alkaline pH inside the dentinal tubules to kill the bacteria and neutralize
the endotoxins, which are potent inflammatory stimulators.

• The development of new bioactive materials such as MTA make possible other
therapeutic approaches, including the obturation of the root canal space in complex
cases of iatrogenic or pathologic root perforation.
• It has been shown that intracanal application of MTA can also cause release of
calcium ions through dentinal tubules into external resorption defect, which may
favour the repair potential of the surrounding tissues.

IDIOPATHIC ROOT RESORPTION
• Idiopathic external root resorption is a rarely reported condition which has been observed
in single or multiple teeth.
• There is limited understanding of the causative factors in root resorption rather than the
absence of a causative factor in these cases
• The term IERR was suggested for the first time in 1985 by Belanger & Coke, when they
found that the origin or the cause of this pathology was not related to systemic or local
diseases.

Two types of idiopathic root resorption have been observed; namely,
1. Apical Root Resorption and
2. Cervical Root Resorption
• Cervical root resorption starts in the cervical area of the teeth and progresses toward
the pulp.
• In the apical type the resorption starts apically and progresses coronally causing a
gradual shortening and rounding of the remaining root
Bansal P, Nikhil V, Kapur S, Multiple idiopathic external apical root resorption: A rare case report,
Journal of Conservative Dentistry, Jan-Feb 2015, Vol 18, Issue 1

This type of resorption is infrequent and may appear in localized or multiple forms.
• The localized form occurs in one to three posterior teeth.
• The multiple forms may begin in the molars and bicuspids and eventually involve
most of the dentition in a symmetrical pattern

CLINICAL FEATURES
 The most frequent clinical characteristic of idiopathic root resorption is that patients are
asymptomatic with occasional compromise of tooth mobility.
 Normal clinically appearing teeth and periodontal tissues.
 The idiopathic apical root resorption were slightly more common in the upper jaw and molar
region than in the lower jaw and single root teeth.
 Root resorption may be associated with vital teeth or endodontically treated teeth.
 There will be no periodontal and peri radicular inflammation present and alveolar bone levels
may be within normal limits
Bolhari B, MerajiMeraji N, Nosrat A, Extensive Idiopathic External Root Resorption in First
Maxillary Molar: A Case Report, Iranian Endodontic Journal, 2013 Spring; 8(2): 72–74

• Patients with idiopathic root resorption are commonly asymptomatic clinically with
an occasional complaint of tooth mobility, so the condition is usually found in routine
radiographic examination.
• However, it may cause pain and mobility in severe cases.
• It is sometimes self-limiting or sometimes may progress to tooth loss. There will be
bilaterally symmetrical pattern of root resorption101
Bansal P, Nikhil V, Kapur S, Multiple idiopathic external apical root resorption: A rare case report,
Journal of Conservative Dentistry, Jan-Feb 2015, Vol 18, Issue 1

TREATMENT
• With no absolute etiological factors identified, treatment depends largely on the
presenting symptoms and the extent and severity of root resorption.
• The usual treatment is the extraction of teeth of poor prognosis and long-term
monitoring of the remaining dentition.
• Abutment teeth must be carefully assessed for root resorption.
• A more invasive approach involves endodontic treatment of the affected teeth.
• In the absence of pulpal symptoms, endodontic therapy cannot be indicated for
multiple idiopathic apical root resorption

TRANSIENT APICAL BREAKDOWN (TAB)
• It is a temporary phenomenon in which the apex of the tooth displaces the
radiographic appearance of resorption and invariably followed by surface resorption
and / or obliteration of the pulp canal.
• There have been reports of the healing process known as TAB in cases of subluxation
due to trauma.
• This series of healing processes also includes the gradual recovery of crown color
following injury-induced discoloration

Transient resorption of root and bone at the apex
Enlarging apical foramina
Vascular regeneration – Recovery of pulp vitality
Calcification of regenerated tissue
Pulp obliteration
This comprises of

Usually, it occurs after moderate injuries to the tooth which includes
• Subluxation
• Extrusion
• Lateral luxation
• Other causes include
– Infections
– orthodontic treatment
– trauma from occlusion

CLINICAL FEATURES
• It is commonly seen in matured teeth with completely closed apex.
• The breakdown causes is related to the type of injury and stage of root development.
• The injured periradicular tissue generally returns to normal following repair one year
after trauma

RADIOGRAPHIC FEATURES
• Radiographically it shows semicircular radiolucency with transient localized change
in the size of the apical periodontal ligament space.
• There will be blunting of the apex of the surface resorption.
• Obliteration of the pulp canal may also be seen

TREATMENT
• In the event of subluxation or other relatively mild luxation injury, if the tooth root is still
immature, the vasculature may regenerate through the wide apical foramen.
• However, if injury degree is low, vascular regeneration may occur similarly even in teeth
with complete roots.
• In teeth with complete roots, however, vascular regeneration is extremely rare, and pulp
necrosis occurs in most cases. However, there have been reports of the healing process
known as TAB in cases of subluxation due to trauma.

• Normally, pulp necrosis is suspected and root canal treatment is started in almost
all cases when a change in crown color is evident and pulp vital reaction is absent.
• Conservative monitoring must also be considered in light of factors such as patient
age, type of injury and patient consent.
• When change of a crown color and absence of the vital reaction of a pulp continue
six months or more or accept the radiolucency of the apical area to continue to it, a
necrosis of pulp is considered, and it is thought that root canal treatment should be
started immediately

CONCLUSION
• The etiology of root resorption is multifactorial.
• The mechanism of hard dental tissue resorption is similar to that which occurs in bone
tissue.
• Tooth resorption is a perplexing problem for all dental practitioners.
• The etiologic factors are vague, diagnoses are educated guesses, and often the chosen
treatment does not prevent the rapid disappearance of the calcified dental tissues

Sincetheetiologicfactors,diagnosis,treatment,andprognosisis differentforthese
varioustypesof resorptivedefects,thepractitionermustbeableto diagnose
resorptionradiographicallyor clinically,distinguishinternalfromexternal
resorption,andcommenceappropriatetreatmentto halttheresorptiveprocess

REFERENCES
 Pathways of pulp- Cohen 11th edition
 Ingle’s Endodontics- 6th edition
 Seltzer and Bender's Dental Pulp
 Heithersay GS. Invasive cervical resorption: an analysis of potential predisposing factors.
Quintessence Int. 1999
 Heithersay GS. Treatment of invasive cervical resorption: an analysis of results using
topical application of trichloroacetic acid, curettage and restoration. Quintessence Int.
1999
 Vinothkumar TS, Tamilselvi R, Kandaswamy D. Reverse sandwich restoration for the
management of invasive cervical resorption: A case report. J Endod. 2011
 Kqiku L, Ebeleseder KA, Glockner K.Treatment of invasive cervical resorption with
sandwich technique using mineral trioxide aggregate: a case report. Oper Dent. 2012

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