THE VARIOUS

FORMS OF
TOOTH
RESORPTION
Blum JS. The various forms of tooth
resorption. Aust Endod J. 2024
Aug;50(2):191-201. doi:
10.1111/aej.12857. Epub 2024 May
27. PMID: 38798140.

Presented by Dr. Anisha

Dept of Conservative Dentistry and
Endodontics
 INTRODUCTION

• In dentistry, tooth resorption refers to the loss of organic and inorganic components
of tooth structure undertaken by clastic cells . Loss of enamel, dentine and cementum
has an array of implications, ranging from structural compromise to the tooth with
attendant risk of tooth loss, to possible infection of the root canal system and
potential periodontal consequences.
Heithersay GS. External root resorption. Ann R Australas Coll Dent Surg. 1994;12:46–59.

• A correct diagnosis and understanding of the aetiology involved in tooth resorption

is critical for effective management.
Lin S, Moreinos D, Kaufman AY, Abbott PV. Tooth resorption– Part 1: the evolvement, rationales and

controversies of tooth resorption. Dent Traumatol. 2022;38(4):253–66.

 DEFINITIONS
Root resorption is the
progressive loss of dentine and Root resorption is resorption
cementum through the affecting the cementum or
continued action of osteoclastic dentin of the root of a tooth.
cells.
Patel S, Ford T P. Is the resorption external or internal? [Cohen]
Dent Update 2007; 34: 218–229

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]
 HISTORY
• Bell in 1829 recognized the external and internal “absorptive” defects.
• Tomes & Nowell (1906) studied the process of resorption and repair (hollow
cavities due to dentino-clastic action followed by the deposition of new
cementum).
• Tomes termed the process absorption in 1859.
• In 1920 Mummery described pink areas on teeth (internal resorptive lesions).
• Ingle in 1965 classified into idiopathic types of resorption, both internal and
external.
• In 1963 Penick provided guidelines for the clinical management of root
resorption.
 CLASSIFICATION

Inflammatory

Internal

Replacement

Andreason
(1970)
Inflammatory

External Replacement

Surface
 COHEN

BASED ON
CAUSES

BASED ON
ANATOMICAL REGION
BASED ON NATURE OF OCCURRENCE
LOCAL
-INFLAMMATORY
-PRESSURE
-REPLACEMENT/ANKYLOTIC

Internal
Physiologic

SYSTEMIC

External
Pathologic
IDIOPATHIC
 ACCORDING to
AAE (1984)

DENTOALVEOLAR
RESORPTION DUE
ANKYLOTIC PRESSURE
INFLAMMATORY IDIOPATHIC TO SYSTEMIC
REPLACEMNT RESORPTION
CASUSES
RESORPTION

ORTHODONTIC
RESORPTION DUE RESORPTION DUE
TOOTH
INTERNAL EXTERNAL TO IMPACTED TO
MOVEMENT
TOOTH TUMORS/CYSTS
RESORPTION
LINDSKOG 2006
SEQUENCE OF EVENTS LEADING TO
ROOT RESORPTION
 Mechanism of 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
Dissolution of inorganic crystal structure:
• Enzymes - acid phosphatase and carbonic anhydrase II
• The carbonic anhydrase II catalyzes the conversion of CO2 to
H2CO3,providing a source of H+ ions in the clear zone via the proton pump
associated with the ruffled border. (ph < 5).
• Simultaneously, Cl- enters the vacuolar space through the Cl channel in the ruffled
border.
• H+ combines with Cl- ions to form hydrochloric acid (HCl) which leads to
dissolution of the mineralized matrix and exposes the organic phase of the root
• The disintegration of the organic matrix is brought about by cysteine proteinase,
collagenase and matrix metalloproteinase enzymes.
• The cysteine proteinase enzymes act at an acidic pH closer to the ruffled border,
while collagenase and matrix metalloproteinase enzymes are active at the resorbing
surface where the pH is closer to neutral due to the buffering capacity of the
dissolving mineral salts.
• This leads to disintegration of organic structure.
• This paper aims to provide practitioners with a detailed summary of the various forms of
tooth resorption, focusing on a classification scheme and management strategies that are
aetiologically based. This review categorises tooth resorption into three main groups; trauma
induced, infection induced and hyperplastic invasive as proposed by Lindskog et al.
• Trauma induced resorptions result from a physical force acting on the tooth in the absence
of infection. Infection induced resorptions occur due to inflammation that is mounted in
response to infection of the root canal system. Hyperplastic invasive resorptions occur as a
result of aggressive invasion of resorbing granulation tissue. The subdivisions of each
resorption will be discussed, with an emphasis on their pathophysiology along with
appropriate methods that facilitate their diagnosis and management.
TRAUMA INDUCED RESORPTION

Surface
resorption

Pressure
and Replacem

Orthdonti ent

c resorption

resorption
 Surface resorption

• Surface resorption is a self-limiting and reparative

process defined by shallow areas of resorption of
either cementum or dentine often resulting from minor
trauma.
• Damage to cementum or dentine attracts clastic cells to
the area and resorption occurs as part of the normal
inflammatory response to tissue injury. In the absence
of infection, the inflammatory response is transient and
repair often occurs with cementum-like tissue.

Abbott PV, Lin S. Tooth resorption—part 2: a clinical classifica- tion. Dent Traumatol. 2022;38(4):267–85.

Gunraj MN. Dental root resorption. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999;88(6):647–53
External
Internal

• Surface resorption may be further

divided into internal or external
surface resorption, depending on its
location
 Internal Surface Resorption

• Internal surface resorption is a rare condition that

is defined as minor areas of resorption of the
dentin walls of the root canal.

• It is believed to be a transient and self-limiting

process. The term “surface” is used to designate
this type of resorption as it indicates the minor
and shallow nature of the resorption.
Histological Features:
• Loss of odontoblasts and predentin in the
affected area.
• Presence of inflammatory cells (neutrophils,
macrophages) attracted to the exposed dentin.
• Formation of resorption lacunae, where
dentinoclasts are actively resorbing dentin.
• The process is self-limiting and typically lasts
only 2–3 weeks unless the irritant persists.

Clinical and Radiographic Detection:

• Clinically undetectable: Since it occurs on the
inner walls of the root canal, there are no symptoms or
external signs.
• Radiographically undetectable: The defects are
too shallow to be visualized on standard radiographs.
Clinical Importance:
• Although self-limiting, internal surface resorption can act as
a precursor to internal inflammatory resorption if the causative
factor (e.g., bacterial infection from caries) remains.
• In cases where it progresses, internal inflammatory resorption
becomes detectable and requires intervention (e.g., root canal
treatment).
Management Considerations:
• Since internal surface resorption is self-limiting, no treatment
is required unless it progresses to internal inflammatory resorption.
• If associated with caries, addressing the bacterial infection is
crucial to prevent further damage.
In summary, internal surface resorption is a transient, mild resorptive
process that is difficult to diagnose but can progress if the irritant persists.
Understanding its etiology helps clinicians recognize its role in the
development of more aggressive resorptive conditions.
External surface resorption
External surface resorption is defined
as small areas of resorption of the
cementum. Occasionally it may extend
into the dentin. The term “surface” is
used to describe this type of resorption
because it usually only involves the
external surface of the tooth.
• Clinically, external surface resorption is
asymptomatic and does not present any
noticeable signs. However, a recent history of
trauma may suggest its temporary presence
within a few weeks of the injury.
Radiographically, this type of resorption is
usually undetectable due to the shallow nature
of the resorptive defect, and it is typically
identified only through histological
examination.

• Because external surface resorption is self-

limiting, treatment is not required as long as the
irritation is temporary and bacterial
contamination has not occurred. However, if
the root canal system becomes infected during
the injury, the condition can progress into
external inflammatory resorption
Transient apical internal resorption
• Although rare, a special case of surface resorption
(sometimes referred to as transient apical internal
resorption) may be found in association with transient
apical breakdown subsequent to trauma, typically
after luxation injuries.
• The resorption observed is considered to be an
adaptive response allowing ingress of a greater
vascular network to aid in the healing process.
• Diagnosis is made primarily through radiographic
appearance of a confined periapical radiolucency, and
spontaneous remission is often observed provided the
root canal remains uninfected.
 Pressure and orthodontic resorption

• Pressure-related resorption occurs when a physical force is applied to a tooth,

leading to the loss of dental hard tissue.
• This process can be classified into three etiological categories: physiological,
pathological, and orthodontic.

Abbott PV, Lin S. Tooth resorption—part 2: a clinical classifica- tion. Dent Traumatol. 2022;38(4):267–85.
 Physiological Pressure-Related Resorption
• Physiological resorption is a natural process that
occurs as part of normal dental development,
most notably in primary teeth. As permanent
successors erupt, they exert pressure on the roots
of primary teeth, leading to progressive
resorption until exfoliation occurs.
• This type of resorption is typically asymptomatic
and diagnosed radiographically, showing
extensive root resorption in primary teeth at the
site of pressure from the developing permanent
tooth.
 Pathological Pressure-Related Resorption
• Pathological resorption occurs when external
pressure is exerted on a tooth due to abnormal
conditions such as impacted or ectopic teeth,
expansile tumors, or cysts. Slow-growing
lesions, such as cysts, ameloblastomas, giant
cell tumors, and fibro-osseous lesions, can
apply persistent pressure on adjacent teeth,
triggering resorptive changes.
• Management involves identifying and
removing the underlying pathological cause to
halt further resorption.
 Orthodontic Resorption
• Orthodontic-induced resorption affects the apical portion
of roots due to the application of sustained orthodontic
forces.
• Excessive or prolonged force activates molecular pathways
that upregulate inflammatory cytokines, leading to
increased activity of clastic cells responsible for root
resorption. Additionally, orthodontic forces may stimulate
pulpal inflammation and increased blood flow, further
enhancing the activity of resorptive cells.

Several factors influence the extent of orthodontic resorption,

including:
• Patient factors (age, root morphology)
• Local factors (tooth position, surrounding
structures)
• Orthodontic factors (magnitude and direction of
forces applied)
 Diagnosis and Management
• Orthodontic resorption is typically asymptomatic
unless it progresses to an extent that causes tooth
mobility. Diagnosis is primarily radiographic, with
periapical radiographs and orthopantomograms
showing characteristic shortening and blunting of
root tips.
• Management involves halting orthodontic
treatment for at least six months, as resorption
ceases once mechanical forces are removed.
Careful force application and monitoring during
orthodontic treatment are crucial in preventing
excessive root resorption.
 Replacement resorption

• Replacement resorption is a pathological process where the resorbed root

structure is replaced by bone.
• It can be classified into two types based on location: external replacement
resorption and internal replacement resorption.
 External Replacement Resorption
1.1 Pathogenesis

External replacement resorption occurs due to extensive

necrosis of the periodontal ligament (PDL), which leads to
direct fusion between the tooth and the alveolar bone,
establishing ankylosis. This fusion prevents normal tooth
mobility and allows normal skeletal bone turnover to
progressively replace the root structure with bone.

1.2 Etiology
• Severe luxation injuries
• Delayed replantation of avulsed teeth
• Prolonged drying or compression of the PDL cells

1.3 Clinical Presentation

• Ankylosis precedes the radiographic appearance of
resorption
 • Progressive replacement of root structure by bone
• Resorption typically becomes evident within one year
of the injury
• No associated periapical radiolucency, as the process is
not infection-driven

1.5 Management

There is no curative treatment for external replacement

resorption, making prevention and early intervention essential:

1. Prevention Strategies
◦ Use of mouthguards and protective wear in
contact sports
◦ Public education on first aid for avulsed teeth
(timely replantation and proper storage medium)

2. Management of Ankylosed Teeth

◦ In growing patients, decoronation during puberty
helps maintain alveolar ridge development and prevent
2.1 Pathogenesis

Internal replacement resorption is a rare condition that

originates within the root canal system. It is believed to
result from metaplasia of pulp tissues following trauma,
leading to the production of cancellous-like bone within
the pulp space, replacing pulp and dentin.

2.2 Clinical Presentation

• Usually asymptomatic
• No notable clinical signs unless associated with
other pathology

2.3 Radiographic Features

• Irregular enlargement of the pulp chamber
• Mottled radiopaque interior resembling
calcified bone instead of dentin

2.4 Management
• No treatment is indicated, as the condition is
INTERNAL INFLAMMATORY
RESORPTION

INFECTION INDUCED RESORPTION

EXTERNAL INFLAMMATORY
RESORPTION
 INTERNAL INFLAMMATORY RESORPTION

• Internal inflammatory resorption is a pathological process characterized by the

progressive loss of dentin from within the root canal system due to the activity
of dentinoclasts and granulation tissue. This resorption occurs only in teeth
where the coronal pulp tissue is necrotic and infected, allowing bacterial
penetration into the dentin tubules.
Cellular and Tissue Changes
• The pulpal tissue becomes necrotic and lacks odontoblasts and predentin,
which normally protect against resorption.
• The necrotic pulp is replaced by periodontal-like connective tissue, although it
remains unclear whether this occurs before or after the onset of resorption.
• Active resorption is characterized by:
◦ Inflamed pulp tissue in the root canal apical to the defect
◦ Dentinoclasts and granulation tissue within the defect
• As bacterial infection progresses toward the apical end, the remaining pulp
tissue undergoes necrosis, leading to a pulpless and infected root canal system.
• When infection spreads beyond the resorptive defect, the blood supply is lost,
leading to the cessation of resorption. At this stage, apical periodontitis develops.
Etiology
The main contributing factors for internal inflammatory resorption include:
• Dental trauma
• Caries (most commonly associated)
• A combination of caries and trauma
• A combination of caries and periodontal disease
Since this resorptive process only occurs in the presence of bacterial infection, the
role of microorganisms is clear, explaining why caries is a frequent factor.
Symptoms and SignsThe presentation of internal inflammatory resorption varies
depending on its stage of progression:
Radiographic Features

Radiographic examination is essential for diagnosing internal

inflammatory resorption. The typical features include:
• Oval-shaped enlargement of the pulp chamber or
root canal space
• Variability in shape and size of the resorptive
defect
• Horizontal tube shift technique can help
differentiate it from external resorption
• CT scans may be useful in complex cases but are
generally not required
 Management
The goal of treatment is to eliminate infection, stop the resorptive process, and restore
the tooth. The standard approach involves root canal treatment with specific
medicaments.

Root Canal Treatment Protocol

1. Disinfection of the Root Canal System

◦ Antibiotic-corticosteroid pastes (e.g., Ledermix paste)
▪ Triamcinolone: Anti-inflammatory, inhibits resorptive cells
▪ Tetracycline antibiotics:
▪ Directly inhibit bacteria
▪ Suppress clastic (resorbing) cell activity
◦ Calcium hydroxide (Ca(OH)₂) application
▪ Antibacterial effect
▪ Inhibits resorption
▪ Dissolves necrotic tissue trapped in the resorptive defect

2. Final Root Canal Filling

◦ Once resorption has ceased, the canal is obturated with an appropriate
EXTERNAL INFLAMMATORY RESORPTION

• External Inflammatory Resorption (EIR) occurs when

the tooth has an infected root canal system along
with damage to the external root surface
(cementum and/or periodontal ligament). This allows
bacteria and their endotoxins to escape into the
surrounding tissues, triggering an inflammatory
response and subsequent activation of clastic cells,
which resorb both the tooth structure and adjacent
bone.
• This condition is also referred to as infection-related
resorption, as infection plays a key role, but it is not
the sole factor—damage to the root surface or another
pathway for bacterial escape is also required.
• Inflammation persists as long as the infection remains
untreated, making the term "inflammatory"
appropriate.
Types of External Inflammatory
Resorption
EIR can occur in two locations along
the root:
1. External Apical
Inflammatory Resorption
(EAIR) – Occurs at the apex of
the root.
2. External Lateral
Inflammatory Resorption
(ELIR) – Occurs along the lateral
surface of the root
Clinical Presentation
The symptoms and signs of EIR depend on the underlying cause:
• Post-trauma Cases:
◦ Patient history reveals a previous traumatic injury.
◦ No immediate symptoms related to resorption, but symptoms may arise from
the injury itself.
• Long-standing Infected Root Canal System:
◦ May be asymptomatic if associated with chronic apical periodontitis.
◦ Pain on biting/percussion if there is acute apical periodontitis.
◦ Swelling if an acute apical abscess develops.
◦ Draining sinus if there is a chronic apical abscess.
◦ The affected tooth will have no response to pulp sensibility tests,
indicating pulp necrosis.
◦ The cause (caries, cracks, failing restoration, etc.) is usually apparent.
External Inflammatory Resorption has distinct radiographic characteristics:
• Radiolucency within the tooth root due to external tooth substance loss.
• Radiolucency in adjacent bone at the resorptive site.
• Loss of lamina dura at the resorption site.
• Lateral Resorption (ELIR):
◦ Often appears as a bowl-shaped radiolucency, though shape and size may vary.
• Apical Resorption (EAIR):
◦ Root apex appears irregular or moth-eaten due to destruction.
◦ Open apical foramen with periapical radiolucency.
 Manage
ment
Strategie
s
The treatment
approach
depends on
whether EIR is
= anticipated
(preventive
approach) or
already
present
(interceptive
approach).
CERVICAL INVASIVE
RESOPRTION

HYPERPLASTIC INVASIVE RESORPTION

CORONAL INVASIVE
RESOPRTION
 CERVICAL INVASIVE RESOPRTION

Definition
• Cervical invasive resorption (CIR) is characterized by the progressive invasion of
destructive resorptive tissue at the cervical region of the tooth, leading to the
replacement of mineralized tooth structure.
Etiology (Causes and Risk Factors)

The exact cause remains unclear; however, the following have been suggested as
predisposing factors:
• Damage to the Cementoenamel Junction (CEJ): Due to acute trauma,
parafunction, excessive occlusal forces, or orthodontic treatment.
• Anatomical Variations: In cases where the enamel and cementum do
not unite at the CEJ, exposed dentin may become susceptible to resorptive
activity.
• Infection: Persistent infection and plaque accumulation may sustain the
resorption process.
• Hypoxia and Mechanical Stresses in the Periodontal Ligament
(PDL): These conditions may stimulate osteoclast activity and accelerate
resorption.
Pathogenesis (Disease Progression)
1. Resorptive fibrovascular granulation tissue invades the CEJ.
2. Connective tissue and inflammatory cells form a resorption cavity.
3. If untreated, fibro-osseous tissue may infiltrate the defect, depositing
abnormal calcifications.
4. The lesion progresses circumferentially towards the pulp but typically does
not penetrate the pulp chamber due to the protective pericanalar resorption-
resistant sheet (PRRS).
 Clinical Features
• Pink Spot Lesion: Highly vascular resorptive
tissue becomes visible through the enamel.
• Asymptomatic Nature: Patients usually do not
experience pain unless the resorptive process reaches
the pulp.
• Possible Pulpal Symptoms: If communication
occurs between the resorptive defect and the root canal
system.

Diagnostic Methods
• Medical & Dental History: Identifies
predisposing factors such as trauma, orthodontic
treatment, or bruxism.
• Radiographic Examination:
◦ 2D Radiographs (Periapical & Bitewing
X-rays): Commonly used but limited by
superimposition.
◦ CBCT (Cone-Beam Computed
Tomography): Superior in determining the true
extent of the resorption by avoiding anatomic
distortion.
2D Imaging)
◦ Class 1: Small, well-defined
resorptive lesion.
◦ Class 2: Larger resorptive defect
with minimal extension into dentin.
◦ Class 3: Deep resorptive invasion
reaching coronal third of the root.
◦ Class 4: Extensive resorption beyond
the coronal third, compromising the
prognosis.
2. Patel et al. 3D Classification (Based on
CBCT)
◦ Provides a more accurate assessment
by overcoming limitations of 2D imaging.
◦ Accounts for the true depth,
circumferential spread, and proximity to
vital structures.
 Treatment Strategies
al is to remove or inactivate the resorptive tissue and restore the defect while preserving the tooth's stru
 CORONAL INVASIVE RESOPRTION

Definition
Coronal invasive resorption, also known as pre-eruptive intracoronal
resorption (PEIR), is a pathological process occurring in developing
teeth. It is characterized by the invasion of fibrovascular resorptive
granulation tissue into a localized defect within the coronal enamel
before the tooth has fully erupted.
Etiology and Pathogenesis
• The exact cause is not well understood, but recent histopathological
findings suggest that what was previously termed "occult caries" or "pre-
eruptive caries" in pediatric dentistry may actually be coronal invasive
resorption.
• The presence of clastic (resorptive) cells in the lesions indicates an
active resorptive process rather than a bacterial infection (as seen in caries).
• The resorption process begins within the crown of an unerupted tooth
and progresses due to fibrovascular invasion, leading to mineral loss and
potential pulp exposure.
Clinical Features
• Pink Spot Lesion: A localized pink
discoloration may be observed on the crown due
to the underlying vascular tissue.
• Asymptomatic Presentation: Most cases
are discovered incidentally during routine
radiographic examinations, as they do not
cause pain until pulp involvement occurs.

4. Radiographic Features
• Irregular margins surrounding the
resorptive defect.
• The lesion is often radiolucent, indicating
demineralization of enamel and dentin.
Management and Treatment
 CONCLUSION

Classification of tooth resorption based on aetiology allows

clinicians to understand, diagnose and manage the various
forms of tooth resorption. This paper provides clinicians with
an overview of each resorption, and approaches to accurately
diagnose and manage each [Link] research is required,
particularly to understand the pathogenesis of cervical
invasive resorption and to investigate potential therapeutics to
arrest replacement resorption.
THANKYOU